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Review: Nutrients for Bone Health

Abstract

Essential Nutrients for Bone Health and a Review of their Availability in the Average North American Diet.

Osteoporosis and low bone mineral density affect millions of Americans. The majority of adults in North America have insufficient intake of vitamin D and calcium along with inadequate exercise. Physicians are aware that vitamin D, calcium and exercise are essential for maintenance of bone health. Physicians are less likely to be aware that dietary insufficiencies of magnesium, silicon, Vitamin K, and boron are also widely prevalent, and each of these essential nutrients is an important contributor to bone health. In addition, specific nutritional factors may improve calcium metabolism and bone formation. It is the authors’ opinion that nutritional supplements should attempt to provide ample, but not excessive, amounts of factors that are frequently insufficient in the typical American diet. In contrast to dietary insufficiencies, several nutrients that support bone health are readily available in the average American diet. These include zinc, manganese, and copper which may have adverse effects at higher levels of intake. Some multivitamins and bone support products provide additional quantities of nutrients that may be unnecessary or potentially harmful. The purpose of this paper is to identify specific nutritional components of bone health, the effects on bone, the level of availability in the average American diet, and the implications of supplementation for each nutritional component. A summary of recommended dietary supplementation is included.

Price CT, Langford JR, Liporace FA
Open Orthop J 2012
PMID: 22523525 | Free Full Text

Oral intake of 2 gm/day of strontium ranelate have improved bone strength and reduced fracture rates in women with osteoporosis, but there are reports of increased risks of venous blood clots and memory loss [82, 87].

Alcohol Reduces Bone Resorption Markers

Abstract

Moderate ingestion of alcohol is associated with acute ethanol-induced suppression of circulating CTX in a PTH-independent fashion.

The “J shape” curve linking the risk of poor bone health to alcohol intake is now well recognized from epidemiological studies. Ethanol and nonethanol components of alcoholic beverages could influence bone remodeling. However, in the absence of a solid underlying mechanism, the positive association between moderate alcoholic intake and BMD remains questionable because of confounding associated social factors. The objective of this work was to characterize the short-term effects of moderate alcohol consumption on circulating bone markers, especially those involved in bone resorption. Two sequential blood-sampling studies were undertaken in fasted healthy volunteers (age, 20-47 yr) over a 6-h period using beer of different alcohol levels (<0.05-4.6%), solutions of ethanol or orthosilicic acid (two major components of beer), and water +/- calcium chloride (positive and negative controls, respectively). Study 1 (24 subjects) assessed the effects of the different solutions, whereas study 2 (26 subjects) focused on ethanol/beer dose. Using all data in a “mixed effect model,” we identified the contributions of the individual components of beer, namely ethanol, energy, low-dose calcium, and high-dose orthosilicic acid, on acute bone resorption. Markers of bone formation were unchanged throughout the study for all solutions investigated. In contrast, the bone resorption marker, serum carboxy terminal telopeptide of type I collagen (CTX), was significantly reduced after ingestion of a 0.6 liters of ethanol solution (>2% ethanol; p <or= 0.01, RM-ANOVA), 0.6 liters of beer (<0.05-4.6% ethanol; p < 0.02), or a solution of calcium (180 mg calcium; p < 0.001), but only after calcium ingestion was the reduction in CTX preceded by a significant fall in serum PTH (p < 0.001). Orthosilicic acid had no acute effect. Similar reductions in CTX, from baseline, were measured in urine after ingestion of the test solutions; however, the biological variability in urine CTX was greater compared with serum CTX. Modeling indicated that the major, acute suppressive effects of moderate beer ingestion (0.6 liters) on CTX were caused by energy intake in the early phase (approximately 0-3 h) and a “nonenergy” ethanol component in the later phase (approximately 3 to >6 h). The early effect on bone resorption is well described after the intake of energy, mediated by glucagon-like peptide-2, but the late effect of moderate alcohol ingestion is novel, seems to be ethanol specific, and is mediated in a non-calcitonin- and a non-PTH-dependent fashion, thus providing a mechanism for the positive association between moderate alcohol ingestion and BMD.

Sripanyakorn S, Jugdaohsingh R, Mander A, Davidson SL…
J. Bone Miner. Res. Aug 2009
PMID: 19257829 | Free Full Text

Taurine Inhibits Osteoblast Apoptosis in Mouse Cells

Abstract

Taurine inhibits serum deprivation-induced osteoblast apoptosis via the taurine transporter/ERK signaling pathway.

Taurine has positive effects on bone metabolism. However, the effects of taurine on osteoblast apoptosis in vitro have not been reported. The aim of this study was to investigate the activity of taurine on apoptosis of mouse osteoblastic MC3T3-E1 cells. The data showed that 1, 5, 10, or 20 mM taurine resulted in 16.7, 34.2, 66.9, or 63.75% reduction of MC3T3-E1 cell apoptosis induced by the serum deprivation (serum-free α-MEM), respectively. Taurine (1, 5, or 10 mM) also reduced cytochrome c release and inhibited activation of caspase-3 and -9, which were measured using fluorogenic substrates for caspase-3/caspase-9, in serum-deprived MC3T3-E1 cells. Furthermore, taurine (10 mM) induced extracellular signal-regulated kinase (ERK) phosphorylation in MC3T3-E1 cells. Knockdown of the taurine transporter (TAUT) or treatment with the ERK-specific inhibitor PD98059 (10 μM) blocked the activation of ERK induced by taurine (10 mM) and abolished the anti-apoptotic effect of taurine (10 mM) in MC3T3-E1 cells. The present results demonstrate for the first time that taurine inhibits serum deprivation-induced osteoblast apoptosis via the TAUT/ERK signaling pathway.

Zhang LY, Zhou YY, Chen F, Wang B…
Braz. J. Med. Biol. Res. Jul 2011
PMID: 21710101 | Free Full Text

IP-6 Inhibits Osteoclastogenesis and Increases Resorption of Mature Osteoclasts In Vitro

Abstract

Inositol hexakisphosphate inhibits osteoclastogenesis on RAW 264.7 cells and human primary osteoclasts.

Inoxitol hexakisphosphate (IP6) has been found to have an important role in biomineralization and a direct effect inhibiting mineralization of osteoblasts in vitro without impairing extracellular matrix production and expression of alkaline phosphatase. IP6 has been proposed to exhibit similar effects to those of bisphosphonates on bone resorption, however, its direct effect on osteoclasts (OCL) is presently unknown. The aim of the present study was to investigate the effect of IP6 on the RAW 264.7 monocyte/macrophage mouse cell line and on human primary osteoclasts. On one hand, we show that IP6 decreases the osteoclastogenesis in RAW 264.7 cells induced by RANKL, without affecting cell proliferation or cell viability. The number of TRAP positive cells and mRNA levels of osteoclast markers such as TRAP, calcitonin receptor, cathepsin K and MMP-9 was decreased by IP6 on RANKL-treated cells. On the contrary, when giving IP6 to mature osteoclasts after RANKL treatment, a significant increase of bone resorption activity and TRAP mRNA levels was found. On the other hand, we show that 1 µM of IP6 inhibits osteoclastogenesis of human peripheral blood mononuclear cells (PBMNC) and their resorption activity both, when given to undifferentiated and to mature osteoclasts.
Our results demonstrate that IP6 inhibits osteoclastogenesis on human PBMNC and on the RAW264.7 cell line. Thus, IP6 may represent a novel type of selective inhibitor of osteoclasts and prove useful for the treatment of osteoporosis.

Arriero Mdel M, Ramis JM, Perelló J, Monjo M
PLoS ONE 2012
PMID: 22905230 | Free Full Text

Phytate Associated with Bone Density in Posmenopausal Women of Mallorca

Abstract

[The influence of consumption of phytate on the bone mass in posmenopausal women of Mallorca].

Osteoporosis is a serious health problem in the population, mainly for postmenopausal women. Therefore, it is important to develop programs to decrease prevalence. The main objective of this study is to determine the influence of phytate consumption on bone mineral density.
The bone mineral density was evaluated in postmenopausal women by means of dual X-ray double energy absorptiometry for calcaneous (C), lumbar spine (LS) and femoral neck (FN). The results obtained were related to the consumption of phytate by means of a dietary questionnaire.
In the three different areas (C, LS, FN) we observed significantly higher values of T-score in women that consumed adequate amounts of phytate as opposed to those that did not, (C 0.1 vs. -0.5, LS -1.2 and -2.5 and FN -0.2 and -1.2). There is also an increase in the T-score as more phytate is consumed, up to a maximum of two times a week (C -0.7 in non consumers, -0.2 in those that consume phytate once a week and 0.2 in those that consume phytate twice a week; LS -2.8, -1.7 and 1.1 and finally, CF -1.3, -0.6 and -0.1).
The results obtained seem to indicate that the adequate consumption of phytate may play an important role in the prevention of bone mineral density loss in postmenopausal women.

López-González AA, Grases F, Marí B, Vicente-Herrero MT…
Reumatol Clin
PMID: 21794821 | Free Full Text

Iron Deficiency Causes Lower Bone Density in Rats

Abstract

Iron deficiency negatively affects vertebrae and femurs of rats independently of energy intake and body weight.

The question of whether iron deficiency has direct adverse effects on vertebral trabecular bone and long bones was answered by this study. Four groups of female weanling rats were fed for 5 wk diets that were 1) control; 2) calcium restricted, 1.0 g Ca/kg diet; 3) iron deficient, <8 mg Fe/kg diet; or 4) control, pair-fed to the iron-deficient group. Whole body and femur DEXA analysis revealed that calcium-restricted and iron-deficient rats had lower bone mineral density (BMD) and content (BMC) than pair-fed and control rats. However, pair-fed rats also had decreased BMD and BMC compared to control rats. The third lumbar trabecular bone microarchitecture in both diet-restricted groups had decreased bone volume fraction (BV/TV) and trabecular number and thickness, a less favorable structural model index, and increased trabecular separation compared with the controls and the pair-fed groups as determined by microcomputer tomography. The control and pair-fed groups did not differ from one another, suggesting that iron deficiency and calcium restriction affected vertebrae independently of food intake and body weight. Finite element analysis revealed lower force to compress the vertebrae and lower stiffness but greater von Mises stress in calcium-restricted and iron-deficient groups compared to the control and pair-fed groups. Urinary deoxypyridinium crosslinks, serum osteocalcin, and cholcalciferol were increased in calcium-restricted rats compared to the other 3 groups. Using micro-CT imaging technology, this study demonstrated microarchitectural pathology due to iron deficiency upon vertebral trabecular bone compared to the control and pair-fed rats, although not to the same extent as severe calcium restriction.

Medeiros DM, Stoecker B, Plattner A, Jennings D…
J. Nutr. Nov 2004
PMID: 15514276 | Free Full Text

Zinc-Carnosine Prevents Bone Loss in Ovariectomized Rats

Abstract

Prolonged administration of beta-alanyl-L-histidinato zinc prevents bone loss in ovariectomized rats.

The effect of beta-alanyl-L-histidinato zinc (AHZ), in which zinc is chelated to beta-alanyl-L-histidine, on bone metabolism was investigated in the femoral diaphysis of ovariectomized rats. AHZ (10, 30 and 100 mg/kg body weight/day) was orally administered to ovariectomized rats for 3 months. Ovariectomy significantly decreased the estradiol concentration in the serum as compared with that from sham-operated rats. This decrease was not altered by the dose of AHZ. The bone volume and dry weight in the femur of ovariectomized rats significantly decreased in comparison with those from sham-operated rats. Moreover, alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents in the femoral diaphysis were significantly decreased by ovariectomy. The decreases of the femoral volume and dry weight, the femoral-diaphyseal alkaline phosphatase activity, DNA and calcium contents by ovariectomy were completely prevented by the tested doses of AHZ (10, 30 and 100 mg/kg/day). AHZ in the dose range of 10-100 mg/kg/day caused a significant increase in zinc content in the femoral diaphysis of ovariectomized rats. The present study suggests that the prolonged administration of AHZ can prevent bone loss by ovariectomy.

Yamaguchi M, Kishi S
Jpn. J. Pharmacol. Oct 1993
PMID: 8283831 | Free Full Text

Zinc Intake and Plasma Level Associated with Bone Density in Men with Osteoporosis

Abstract

Zinc intakes and plasma concentrations in men with osteoporosis: the Rancho Bernardo Study.

Low zinc intakes and reduced blood zinc concentrations have been reported to be associated with osteoporosis in women.
The objective was to examine the independent association between dietary zinc and plasma zinc and the association of each with bone mineral density (BMD) and 4-y bone loss in community-dwelling older men.
Of the original Rancho Bernardo Study subjects, 396 men (age: 45-92 y) completed BMD measurements at baseline in 1988-1992 and 4 y later. Osteoporosis was defined as a BMD > or = 2.5 SDs below the mean for young women (a T-score < or = -2.5). At baseline, dietary intake data were collected by using a standard food-frequency questionnaire, and plasma zinc concentrations were measured by using inductively coupled plasma spectroscopy.
The mean dietary zinc intake was 11.2 mg, and the mean plasma zinc concentration was 12.7 micromol/L. Plasma zinc was correlated with total zinc intake (diet plus supplements). Dietary zinc intake and plasma zinc concentrations were lower in men with osteoporosis at the hip and spine than in men without osteoporosis at those locations. BMDs for the hip, spine, and distal wrist were significantly lower in men in the lowest plasma zinc quartile (<11.3 micromol/L) than in men with higher plasma zinc concentrations. The association between plasma zinc and BMD was cross-sectional, longitudinal, and independent of age or body mass index. However, plasma zinc did not predict bone loss during the 4-y interval.
Dietary zinc intake and plasma zinc each have a positive association with BMD in men.

Hyun TH, Barrett-Connor E, Milne DB
Am. J. Clin. Nutr. Sep 2004
PMID: 15321813 | Free Full Text

Too Much Zinc Reduces Bone Density in Rats

Abstract

Marginal zinc deficiency exacerbates bone lead accumulation and high dietary zinc attenuates lead accumulation at the expense of bone density in growing rats.

Environmental lead exposure is associated with reduced bone growth and quality, which may predispose to osteoporosis. Zinc supplementation may reduce lead accumulation; however, effects on bone development have not been addressed. Our objective was to investigate the effects of marginal zinc (MZ) and supplemental zinc (SZ) intakes on bone lead deposition and skeletal development in lead-exposed rats. In a factorial design, weanling Sprague-Dawley rats were assigned to MZ (8 mg/kg diet); zinc-adequate control (CT; 30 mg/kg); zinc-adequate, diet-restricted (DR; 30 mg/kg); or SZ (300 mg/kg) groups, with and without lead acetate-containing drinking water (200 mg Pb/l) for 3 weeks. Excised femurs were analyzed for bone mineral density (BMD) by dual-energy x-ray absorptiometry, morphometry, and mineral content. MZ had higher femur lead and lower femur zinc concentrations and impaired skeletal growth and mineralization than CT. DR inhibited growth but did not result in higher femur lead concentrations than CT. SZ had higher femur zinc and lower femur lead concentrations than the other treatments. DR and SZ had impaired BMD versus CT and MZ. Lead also retarded skeletal growth and impaired BMD, but an interaction between lead and MZ was only found for femoral knee width, which was lower in MZ exposed to lead. In summary, while MZ deficiency exacerbated bone lead concentration, it generally did not intensify lead toxicity. SZ was protective against bone lead but was detrimental to BMD, suggesting that the optimal level of SZ to reduce lead absorption, while supporting growth and bone development, requires further investigation.

Jamieson JA, Taylor CG, Weiler HA
Toxicol. Sci. Jul 2006
PMID: 16624848 | Free Full Text

Review: Alkaline Diets and the Acid Load Theory are Bunk – 2013

Abstract

Nutritional disturbance in acid-base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney.

The nutritional acid load hypothesis of osteoporosis is reviewed from its historical origin to most recent studies with particular attention to the essential but overlooked role of the kidney in acid-base homeostasis. This hypothesis posits that foods associated with an increased urinary acid excretion are deleterious for the skeleton, leading to osteoporosis and enhanced fragility fracture risk. Conversely, foods generating neutral or alkaline urine would favour bone growth and Ca balance, prevent bone loss and reduce osteoporotic fracture risk. This theory currently influences nutrition research, dietary recommendations and the marketing of alkaline salt products or medications meant to optimise bone health and prevent osteoporosis. It stemmed from classic investigations in patients suffering from chronic kidney diseases (CKD) conducted in the 1960s. Accordingly, in CKD, bone mineral mobilisation would serve as a buffer system to acid accumulation. This interpretation was later questioned on both theoretical and experimental grounds. Notwithstanding this questionable role of bone mineral in systemic acid-base equilibrium, not only in CKD but even more in the absence of renal impairment, it is postulated that, in healthy individuals, foods, particularly those containing animal protein, would induce ‘latent’ acidosis and result, in the long run, in osteoporosis. Thus, a questionable interpretation of data from patients with CKD and the subsequent extrapolation to healthy subjects converted a hypothesis into nutritional recommendations for the prevention of osteoporosis. In a historical perspective, the present review dissects out speculation from experimental facts and emphasises the essential role of the renal tubule in systemic acid-base and Ca homeostasis.

Bonjour JP
Br. J. Nutr. Oct 2013
PMID: 23551968 | Free Full Text

…experiments carried out among patients suffering from severe metabolic acidosis caused by renal insufficiency, or among healthy subjects made acidotic by administering NH4Cl, suggested the involvement of bone tissue in maintaining the acid–base balance. This hypothesis was later refuted on the basis of both theoretical and experimental arguments. Despite this rebuttal, the hypothesis was put forward that bone could play a buffering role, with the consideration that nutrients, particularly animal proteins with their acid load, could be a major cause of osteoporosis. Several recent human studies have shown that there is no relationship between nutritionally induced variations of urinary acid excretion and Ca balance, bone metabolism and the risk of osteoporotic fractures. Variations in human diets across a plausible range of intakes have been shown to have no effect on blood pH. Consistent with this lack of a mechanistic basis, long-term studies of alkalinising diets have shown no effect on the age-related change in bone fragility. Consequently, advocating the consumption of alkalinising foods or supplements and/or removing animal protein from the human diet is not justified by the evidence accumulated over the last several decades.