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High-Protein Meat Diet has No Adverse Effects on Bone in Postmenopausal Women

Abstract

A diet high in meat protein and potential renal acid load increases fractional calcium absorption and urinary calcium excretion without affecting markers of bone resorption or formation in postmenopausal women.

Our objective in this study was to determine the effects of a high-protein and high-potential renal acid load (PRAL) diet on calcium (Ca) absorption and retention and markers of bone metabolism. In a randomized crossover design, 16 postmenopausal women consumed 2 diets: 1 with low protein and low PRAL (LPLP; total protein: 61 g/d; PRAL: -48 mEq/d) and 1 with high protein and high PRAL (HPHP; total protein: 118 g/d; PRAL: 33 mEq/d) for 7 wk each separated by a 1-wk break. Ca absorption was measured by whole body scintillation counting of radio-labeled (47)Ca. Compared with the LPLP diet, the HPHP diet increased participants’ serum IGF-I concentrations (P < 0.0001), decreased serum intact PTH concentrations (P < 0.001), and increased fractional (47)Ca absorption (mean ± pooled SD: 22.3 vs. 26.5 ± 5.4%; P < 0.05) and urinary Ca excretion (156 vs. 203 ± 63 mg/d; P = 0.005). The net difference between the amount of Ca absorbed and excreted in urine did not differ between 2 diet periods (55 vs. 28 ± 51 mg/d). The dietary treatments did not affect other markers of bone metabolism. In summary, a diet high in protein and PRAL increases the fractional absorption of dietary Ca, which partially compensates for increased urinary Ca, in postmenopausal women. The increased IGF-I and decreased PTH concentrations in serum, with no change in biomarkers of bone resorption or formation, indicate a high-protein diet has no adverse effects on bone health.

Cao JJ, Johnson LK, Hunt JR
J. Nutr. Mar 2011
PMID: 21248199 | Free Full Text

The present study detected no change in potential biomarkers of osteoclast activity, such as blood TRAP, CTX, and sRANKL and urinary DPD, or biomarkers of osteoblast activity, such as blood OPG and OC. The observed changes in IGF-I and PTH were apparently insufficient to elicit detectable changes in biomarkers of osteoclast or osteoblast activity.

Many epidemiological observations have shown that long-term protein intakes are positively associated with bone mineral density (9, 11, 13, 53). Several recent meta-analyses have concluded that protein is beneficial to bone health (54) and protein-induced acid load does not promote skeletal bone mineral loss or contribute to the development of osteoporosis (55, 56). The results from this study are in agreement with those findings.

In conclusion, in postmenopausal women, a diet high in both protein and PRAL increased Ca absorption, at least partially compensating for an increase in urinary excretion. No change in either bone resorption or formation biomarkers was observed, indicating that a high-protein diet is not detrimental. However, the increased serum IGF-I combined with decreased serum PTH concentrations suggest that a high-protein diet could be beneficial to bone health.

Review: Low Protein Intake and Bones – 2003

Abstract

Low protein intake: the impact on calcium and bone homeostasis in humans.

Increasing dietary protein results in an increase in urinary calcium. Despite over 80 y of research, the source of the additional urinary calcium remains unclear. Because most calcium balance studies found little effect of dietary protein on intestinal calcium absorption, it was assumed that the skeleton was the source of the calcium. The hypothesis was that the high endogenous acid load generated by a protein-rich diet would increase bone resorption and skeletal fracture. However, there are no definitive nutrition intervention studies that show a detrimental effect of a high protein diet on the skeleton and the hypothesis remains unproven. Recent studies from our laboratory demonstrate that dietary protein affects intestinal calcium absorption. We conducted a series of short-term nutrition intervention trials in healthy adults where dietary protein was adjusted to either low, medium or high. The highest protein diet resulted in hypercalciuria with no change in serum parathyroid hormone. Surprisingly, within 4 d, the low protein diet induced secondary hyperparathyroidism that persisted for 2 wk. The secondary hyperparathyroidism induced by the low protein diet was attributed to a reduction in intestinal calcium absorption (as assessed by dual stable calcium isotopes). The long-term consequences of these low protein-induced changes in calcium metabolism are not known, but they could be detrimental to skeletal health. Several recent epidemiological studies demonstrate reduced bone density and increased rates of bone loss in individuals habitually consuming low protein diets. Therefore, studies are needed to determine whether low protein intakes directly affect rates of bone resorption, bone formation or both.

Kerstetter JE, O’Brien KO, Insogna KL
J. Nutr. Mar 2003
PMID: 12612169 | Free Full Text

The subject is complicated with a lot of conflicting data. The full article is great.

When BMD is the primary outcome, most (39–48), but not all (49–53), epidemiological studies show a positive relationship between protein intake and BMD. Stated another way, most of the epidemiological evidence shows that when other known dietary factors are controlled, those individuals who consume low protein diets have lower BMD. Using the National Health and Nutrition Examination Survey (NHANES) III database, we found that in 1882 non-Hispanic white women 50 y old and older, after adjusting for age and body weight, a low protein intake was associated with a significantly lower hip bone mineral density (Fig. 5) (47). Consistent with these data, Hannan and colleagues (46) studied 615 participants in the Framingham Osteoporosis Study over a 4-y period and found that lower levels of protein intake were associated with significantly higher rates of bone loss at the hip and spine. These findings confirm the earlier work of Freudenheim et al. (39), who reported that a low protein intake was associated with greater loss in bone density from the wrist in 35- to 65-y-old women. Most recently, Promislow et al. (48) found a positive association between total dietary protein intake and BMD in elderly men and women participating in the Rancho Bernardino study. Therefore, there is substantial agreement in those studies in which BMD is the primary outcome. Munger et al. (59), reporting data from the Iowa Women’s Health Study, found an increased risk of hip fracture in 55- to 69-y-old women consuming the lowest amounts of protein.

Adequate dietary protein may also help in fracture healing and in preventing bone loss after fracture. Bonjour and colleagues (73) studied the effects of 6 mo of protein supplementation, after osteoporotic hip fracture, in a group of elderly subjects. These patients had self-selected protein intakes that were very low (∼40 g). The administration of additional protein (+20 g) was associated with significant attenuation of proximal femur bone loss in the fractured hip such that, at 1 y, bone loss rates were 50% lower in the protein-supplemented individuals. The correction of poor protein nutrition also improved serum prealbumin and insulin-like growth factor 1 (IGF-1) concentrations and decreased the length of rehabilitation (73).

There is agreement that diets moderate in protein (in the approximate range of 1.0 to 1.5 g protein/kg) are associated with normal calcium metabolism and presumably do not alter skeletal homeostasis. Approximately 30–50% of adults in the United States consume dietary protein that could be considered moderate. At low protein intakes, intestinal calcium absorption is reduced, resulting in increases in serum PTH and calcitriol that persist for at least 2–4 wk. The long-term implications of these findings are unknown; however, recent epidemiological data suggest increased rates of bone loss in individuals consuming such diets. Individuals consuming high protein intakes, particularly from omnivorous sources, develop hypercalciuria that is attributable for the most part to an increase in intestinal calcium absorption. Whether high protein diets result in an increase in bone resorption and higher fracture rates remains uncertain.

 

Potassium Bicarbonate Decreases Resorption and Increases Bone Formation in Postmenopausal Women

Abstract

Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate.

In normal subjects, a low level of metabolic acidosis and positive acid balance (the production of more acid than is excreted) are typically present and correlate in degree with the amount of endogenous acid produced by the metabolism of foods in ordinary diets abundant in protein. Over a lifetime, the counteraction of retained endogenous acid by base mobilized from the skeleton may contribute to the decrease in bone mass that occurs normally with aging.
To test that possibility, we administered potassium bicarbonate to 18 postmenopausal women who were given a constant diet (652 mg [16 mmol] of calcium and 96 g of protein per 60 kg of body weight). The potassium bicarbonate was given orally for 18 days in doses (60 to 120 mmol per day) that nearly completely neutralized the endogenous acid.
During the administration of potassium bicarbonate, the calcium and phosphorus balance became less negative or more positive–that is, less was excreted in comparison with the amount ingested (mean [+/- SD] change in calcium balance, +56 +/- 76 mg [1.4 +/- 1.9 mmol] per day per 60 kg; P = 0.009; change in phosphorus balance, +47 +/- 64 mg [1.5 +/- 2.1 mmol] per day per 60 kg; P = 0.007) because of reductions in urinary calcium and phosphorus excretion. The changes in calcium and phosphorus balance were positively correlated (P < 0.001). Serum osteocalcin concentrations increased from 5.5 +/- 2.8 to 6.1 +/- 2.8 ng per milliliter (P < 0.001), and urinary hydroxyproline excretion decreased from 28.9 +/- 12.3 to 26.7 +/- 10.8 mg per day (220 +/- 94 to 204 +/- 82 mumol per day; P = 0.05). Net renal acid excretion decreased from 70.9 +/- 10.1 to 12.8 +/- 21.8 mmol per day, indicating nearly complete neutralization of endogenous acid.
In postmenopausal women, the oral administration of potassium bicarbonate at a dose sufficient to neutralize endogenous acid improves calcium and phosphorus balance, reduces bone resorption, and increases the rate of bone formation.

Sebastian A, Harris ST, Ottaway JH, Todd KM…
N. Engl. J. Med. Jun 1994
PMID: 8190153 | Free Full Text

Potassium Citrate, but not Chloride, Increases Bone Density in Postmenopausal Women

Abstract

Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia.

Chronic acid loads are an obligate consequence of the high animal/grain protein content of the Western diet. The effect of this diet-induced metabolic acidosis on bone mass is controversial. In a randomized, prospective, controlled, double-blind trial, 161 postmenopausal women (age 58.6 +/- 4.8 yr) with low bone mass (T score -1 to -4) were randomly assigned to 30 mEq of oral potassium (K) citrate (Kcitrate) or 30 mEq of K chloride (KCl) daily. The primary end point was the intergroup difference in mean percentage change in bone mineral density (BMD) at lumbar spine (L2 through L4) after 12 mo. Compared with the women who received KCl, women who received Kcitrate exhibited an intergroup increase in BMD (+/-SE) of 1.87 +/- 0.50% at L2 through L4 (P < 0.001), of 1.39 +/- 0.48% (P < 0.001) at femoral neck, and of 1.98 +/- 0.51% (P < 0.001) at total hip. Significant secondary end point intragroup changes also were found: Kcitrate increased L2 through L4 BMD significantly from baseline at months 3, 9, and 12 and reached a month 12 increase of 0.89 +/- 0.30% (P < 0.05), whereas the KCl arm showed a decreased L2 through L4 BMD by -0.98 +/- 0.38% (P < 0.05), significant only at month 12. Intergroup differences for distal radius and total body were NS. The Kcitrate-treated group demonstrated a sustained and significant reduction in urinary calcium excretion and a significant increase in urinary citrate excretion, with increased citrate excretion indicative of sustained systemic alkalization. Urinary bone resorption marker excretion rates were significantly reduced by Kcitrate, and for deoxypyridinoline, the intergroup difference was significant. Urinary net acid excretion correlated inversely and significantly with the change in BMD in a subset of patients. Large and significant reductions in BP were observed for both K supplements during the entire 12 mo. Bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as citrate, and the effect is independent of reported skeletal effects of K.

Jehle S, Zanetti A, Muser J, Hulter HN…
J. Am. Soc. Nephrol. Nov 2006
PMID: 17035614 | Free Full Text

Despite more than 70 yr of sustained interest in the possibility that chronic metabolic acidosis might decrease bone mass, central questions regarding the effect of acid-base alterations on human bone physiology and pathophysiology remain unanswered (4,27,28). First, does chronic metabolic acidosis of any magnitude decrease bone mass? Second, does the low-grade chronic metabolic acidosis that is induced by the acidogenic Western diet result in osteoporosis? Third, can neutralization of dietary acid result in increased bone mass in normal humans or those with osteopenia?

Indirect support for a possible role of chronic metabolic acidosis to reduce bone mass comes from small, uncontrolled studies in humans with nonazotemic renal disease (distal renal tubular acidosis [29,30]). Chronic dietary acid loads were shown to result in significant and reversible negative calcium balance (6), and experimental increases in animal protein intake or its chief acidogenic constituent, methionine, within the range that is characteristic of the Western diet were shown to cause both negative calcium balance and increased systemic acid load (31,32). Compatible with and strongly supportive of these observations, short-term neutralization of endogenous acid production by oral ingestion of bicarbonate for 7 to 18 d in both postmenopausal women and young healthy adults resulted in calcium retention and—on the basis of analysis of bone markers—in inhibition of bone resorption (13,14).

[…]

This study establishes that bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as Kcitrate and that this effect is independent of reported in vitro skeletal effects of co-administered K. The magnitude of the effect is large, and the safety profile was found to be excellent, albeit based on a limited sample size. The results strongly support the thesis that neutralization of the modern Western diet will promote skeletal health. The associated BP effects of the K supplement provide additional incentive to move forward with controlled outcome trials using long-term Kcitrate treatment.

Potassium Citrate or Fruits + Veggies, No Benefit Over 2 Years

Abstract

Effect of potassium citrate supplementation or increased fruit and vegetable intake on bone metabolism in healthy postmenopausal women: a randomized controlled trial.

Alkali provision may explain why fruit and vegetables benefit bone health.
We aimed to determine the effects of alkali-providing potassium citrate (double-blind) and fruit and vegetable intake (single-blind) on bone turnover over 2 y.
We conducted a randomized placebo-controlled trial in 276 postmenopausal women (aged 55-65 y). Women were randomly assigned to 4 groups: high-dose potassium citrate (55.5 mEq/d), low-dose potassium citrate (18.5 mEq/d), placebo, and 300 g additional fruit and vegetables/d (equivalent of 18.5 mEq alkali). Serum and fasted urine for bone markers were collected at baseline and at 3, 6, 12, 18, and 24 mo. An additional urine sample was collected at 4-6 wk. Bone mineral density (BMD) was measured at baseline and 2 y.
Repeated-measures ANOVA showed no difference between groups for urinary free deoxypyridinoline cross-links relative to creatinine (fDPD/Cr), serum N-terminal propeptide of type 1 collagen, or beta C-terminal telopeptide, although, at 4-6 wk, fDPD/Cr was lower in the high-dose potassium citrate group (P = 0.04). Mean +/- SD spine BMD loss in the placebo group (1.8 +/- 3.9%) did not differ significantly from that in the treatment groups (2.1 +/- 3.2%; P = 0.88). Hip BMD loss in the placebo and low-dose potassium citrate groups was 1.3 +/- 2.3% and 2.2 +/- 2.3%, respectively (P = 0.14).
Two-year potassium citrate supplementation does not reduce bone turnover or increase BMD in healthy postmenopausal women, which suggests that alkali provision does not explain any long-term benefit of fruit and vegetable intake on bone.

Macdonald HM, Black AJ, Aucott L, Duthie G…
Am. J. Clin. Nutr. Aug 2008
PMID: 18689384 | Free Full Text

In summary, neither potassium citrate at 18.5 or 55.6 mEq/d nor 300 g self-selected fruit and vegetables/d influenced bone turnover or prevented BMD loss over 2 y in healthy postmenopausal women. Further work is required to investigate whether particular fruit and vegetables are important and how much of each is optimal for bone health.

Bicarbonate, but Not Potassium, Decreases Resorption

Abstract

Treatment with potassium bicarbonate lowers calcium excretion and bone resorption in older men and women.

Bicarbonate has been implicated in bone health in older subjects on acid-producing diets in short-term studies.
The objective of this study was to determine the effects of potassium bicarbonate and its components on changes in bone resorption and calcium excretion over 3 months in older men and women. Design, Participants, and Intervention: In this double-blind, controlled trial, 171 men and women age 50 and older were randomized to receive placebo or 67.5 mmol/d of potassium bicarbonate, sodium bicarbonate, or potassium chloride for 3 months. All subjects received calcium (600 mg of calcium as triphosphate) and 525 IU of vitamin D(3) daily.
Twenty-four-hour urinary N-telopeptide and calcium were measured at entry and after 3 months. Changes in these measures were compared across treatment groups in the 162 participants included in the analyses.
Bicarbonate affected the study outcomes, whereas potassium did not; the two bicarbonate groups and the two no bicarbonate groups were therefore combined. Subjects taking bicarbonate had significant reductions in urinary N-telopeptide and calcium excretion, when compared with subjects taking no bicarbonate (both before and after adjustment for baseline laboratory value, sex, and changes in urinary sodium and potassium; P = 0.001 for both, adjusted). Potassium supplementation did not significantly affect N-telopeptide or calcium excretion.
Bicarbonate, but not potassium, had a favorable effect on bone resorption and calcium excretion. This suggests that increasing the alkali content of the diet may attenuate bone loss in healthy older adults.

Dawson-Hughes B, Harris SS, Palermo NJ, Castaneda-Sceppa C…
J. Clin. Endocrinol. Metab. Jan 2009
PMID: 18940881 | Free Full Text

Supplementation with potassium did not significantly alter calcium excretion or markers of bone turnover in this study. This is in contrast to earlier reports of Lemann et al. (19) and Jones et al. (20) who found that increasing potassium intake decreased urinary calcium excretion. The apparently conflicting observation that higher potassium intake is associated with higher BMD in healthy perimenopausal women (21) may result from the fact that potassium-rich diets tend to be alkali-producing, in that they are rich in fruits and vegetables. Treatment with potassium did enhance sodium excretion, as has been documented widely.

In conclusion, we have found that reducing the acidogenicity of the diet into the alkali-producing range with bicarbonate lowers calcium excretion and the bone resorption rate in healthy older men and women consuming rather typical acid-producing American diets. Treatment with 67.5 mmol/d of potassium bicarbonate was safe and well tolerated in this population. Increasing intake of alkali merits further consideration as a safe and low-cost approach to improving skeletal health in older men and women.

Review: Potassium and Osteoporosis

Abstract

Potassium and health.

Potassium was identified as a shortfall nutrient by the Dietary Guidelines for Americans 2010 Advisory Committee. The committee concluded that there was a moderate body of evidence of the association between potassium intake and blood pressure reduction in adults, which in turn influences the risk of stroke and coronary heart disease. Evidence is also accumulating of the protective effect of adequate dietary potassium on age-related bone loss and reduction of kidney stones. These benefits depend on organic anions associated with potassium as occurs in foods such as fruits and vegetables, in contrast to similar blood pressure-lowering benefits of potassium chloride. Benefits to blood pressure and bone health may occur at levels below current recommendations for potassium intake, especially from diet, but dose-response trials are needed to confirm this. Nevertheless, intakes considerably above current levels are needed for optimal health, and studies evaluating small increases in fruit and vegetable intake on bone and heart outcomes for short periods have had disappointing results. In modern societies, Western diets have led to a decrease in potassium intake with reduced consumption of fruits and vegetables with a concomitant increase in sodium consumption through increased consumption of processed foods. Consumption of white vegetables is associated with decreased risk of stroke, possibly related to their high potassium content. Potatoes are the highest source of dietary potassium, but the addition of salt should be limited. Low potassium-to-sodium intake ratios are more strongly related to cardiovascular disease risk than either nutrient alone. This relationship deserves further attention for multiple target tissue endpoints.

Weaver CM
Adv Nutr May 2013
PMID: 23674806 | Free Full Text

The full text includes several pages about osteoporosis. This is just the final summary at the end of that section:

In summary, benefits of potassium on bone are seen typically when given as organic salts at relatively high doses of 60 to 90 mmol/d (2400–3600 mg/d). Organic salts of potassium reduce urinary calcium loss and improve calcium balance at these levels. But whether that is related to protection against skeletal buffering of an acidogenic diet is still a topic for debate. Perhaps acid-base balance is not the mechanism in healthy kidneys, but as kidney function declined with age, it may be an important mechanism. The glomerular filtration rate declines by as much as 50% from age 20 to 80 y (68), or perhaps excess acid only affects bone through interaction with receptors on bone cells to stimulate bone turnover, and this process is reduced by the alkaline organic salts of potassium.

 

Sodium Associated with Lower Bone Density in Young Women

Abstract

Higher urinary sodium, a proxy for intake, is associated with increased calcium excretion and lower hip bone density in healthy young women with lower calcium intakes.

We assessed 24-h urinary sodium (Na) and its relationship with urinary calcium (Ca) and areal bone mineral density (aBMD) at the whole body, lumbar spine and total hip in a cross-sectional study. 102 healthy non-obese women completed timed 24-h urine collections which were analyzed for Na and Ca. Dietary intakes were estimated using a validated food frequency questionnaire. Participants were grouped as those with lower vs. higher calcium intake by median split (506 mg/1000 kcal). Dietary Na intake correlated with 24-h urinary loss. Urinary Na correlated positively with urinary Ca for all participants (r = 0.29, p < 0.01) and among those with lower (r = 0.37, p < 0.01) but not higher calcium intakes (r = 0.19, p = 0.19). Urinary Na was inversely associated with hip aBMD for all participants (r = -0.21, p = 0.04) and among women with lower (r = -0.36, p < 0.01) but not higher (r = -0.05, p = 0.71) calcium intakes. Urinary Na also entered a regression equation for hip aBMD in women with lower Ca intakes, contributing 5.9% to explained variance. In conclusion, 24-h urinary Na (a proxy for intake) is associated with higher urinary Ca loss in young women and may affect aBMD, particularly in those with lower calcium intakes.

Bedford JL, Barr SI
Nutrients Nov 2011
PMID: 22254088 | Free Full Text

The potential implications of sodium-induced calciuria for bone are likely to be more serious in those with low calcium intakes, who may be unable to increase calcium absorption to fully compensate for increased urinary losses. For example, Heaney [3] noted that to offset the average urinary calcium loss of 1 mmol (40 mg) associated with an increased sodium intake of 100 mmol (2300 mg), gross calcium absorption efficiency would need to increase to 34% (from 25%) in those with intakes of 600 mg/day, and to about 50% (from 37%) in those with intakes of 300 mg/day-and that this may not be possible. However, at intakes of 1200 mg/day, absorption efficiency would only need to increase from to 23% (from 20%) [3]. Empirical support for the idea that high calcium intakes may protect against high sodium intakes is provided by the study of Ilich et al. [20]. In a 3-year prospective study, postmenopausal women were randomly assigned to maintain usual sodium intake of about 3000 mg/day or to reduce intake to 1500 mg/day. All women also received calcium supplements, and total calcium intake averaged over 1300 mg/day. Because compliance with the sodium intervention was not high, results were reported by tertile of observed urinary sodium excretion rather than by initial group assignment. No negative associations between urinary sodium and bone density were observed [20]. This suggests that, at least in postmenopausal women with high calcium intakes, sodium intake does not adversely affect bone.

DASH Diet and Sodium Reduction Improve Bone in Adults

Abstract

The DASH diet and sodium reduction improve markers of bone turnover and calcium metabolism in adults.

Dietary strategies to prevent and treat osteoporosis focus on increased intake of calcium and vitamin D. Modification of whole dietary patterns and sodium reduction may also be effective. We examined the effects of two dietary patterns and three sodium levels on bone and calcium metabolism in a randomized feeding study. A total of 186 adults, aged 23-76 y, participated. After a 2-wk run-in period, participants were assigned randomly to diets containing three levels of sodium (50, 100 and 150 mmol/d) to be consumed for 30 d in random order. Serum osteocalcin (OC), C-terminal telopeptide of type I collagen (CTX), fasting serum parathyroid hormone (PTH), urinary sodium, potassium, calcium and cAMP were measured at baseline and at the end of each sodium period. The Dietary Approaches to Stop Hypertension (DASH) diet reduced serum OC by 8-11% and CTX by 16-18% (both P < 0.001). Urinary calcium excretion did not differ between subjects that consumed the DASH and control diets. Reducing sodium from the high to the low level significantly decreased serum OC 0.6 microg/L in subjects that consumed the DASH diet, fasting serum PTH 2.66 ng/L in control subjects and urinary calcium 0.5 mmol/24 h in both groups. There were no consistent effects of the diets or sodium levels on urinary cAMP. In conclusion, the DASH diet significantly reduced bone turnover, which if sustained may improve bone mineral status. A reduced sodium intake reduced calcium excretion in both diet groups and serum OC in the DASH group. The DASH diet and reduced sodium intake may have complementary, beneficial effects on bone health.

Lin PH, Ginty F, Appel LJ, Aickin M…
J. Nutr. Oct 2003
PMID: 14519796 | Free Full Text

Taurine No Benefit in Calcium Deficient Rats

Abstract

Effects of taurine supplementation on bone mineral density in ovariectomized rats fed calcium deficient diet.

Taurine supplementation has been shown to have a beneficial effect on femur bone mineral content in ovariectomized rats. It therefore seemed desirable to find out whether the beneficial effect of taurine on ovariectomized rats fed calcium deficient diet could also be reproduced. Forty female Sprague-Dawley rats were divided into two groups. One group was OVX and the other group received sham operation (SHAM), and received either control diet or a taurine supplemented diet for 6 weeks. All rats were fed on calcium deficient diet (AIN-93: 50% level of calcium) and deionized water. Bone mineral density (BMD) and bone mineral content (BMC) were measured in spine and femur. The serum and urine concentrations of calcium and phosphorus were determined. Bone formation was measured by serum osteocalcin and alkaline phosphatase (ALP) concentrations. Bone resorption rate was measured by deoxypyridinoline (DPD) crosslinks immunoassay and corrected for creatinine. Urinary calcium and phosphorus excretion, osteocalcin in blood and cross link value were not significantly different among the groups. Within the OVX group, the taurine supplemented group had not higher femur bone mineral content than the control group. This study established the need for a study on the taurine effect on bone with different calcium levels.

Choi MJ
Nutr Res Pract 2009
PMID: 20016710 | Free Full Text

This experiment was originally designed to test the ability of a taurine supplement to minimize bone loss during postmenopausal model with low calcium intake. Sulfur is predominantly responsible for determining the net endogenous acid production from protein because it is the acid precursor that is oxidized to sulfuric acid (Frassetto et al., 1998). It would therefore make sense that a dietary supplement with excess sulfur-containing amino acids (taurine) could yield increased sulfuric acid production in the body. However, these data suggest that bone mineral density per weight was increased, without changes in bone resorption and bone formation, in the taurine supplemented group, and therefore have the potential to increase bone mineral density if either the study is extended or more taurine is supplemented. The beneficial effect of taurine on ovariectomized rats fed calcium deficient diet was not reproduced. Because in this study, the control and taurine groups consumed identical diets as in the previous study (besides the calcium content), and we do not know whether intestinal calcium absorption will be increased by more taurine supplement. These results indicate that no significant differences in spine and femur BMD were found due to 2% taurine diet in OVX rats fed calcium deficient diet for 6 weeks. No positive effects of taurine on bone mineral density were found in the present study. Our failure to see an association between taurine supplementation and bone mineral density may have been related to the fact that we used calcium deficient diet and the same amount of taurine. Further investigations of the relation between taurine and calcium intake level for bone mineral density are warranted.