No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake

L. A. Frassetto* (Corresponding Author), A. C. Hardcastle, A. Sebastian, L. Aucott, W. D. Fraser, D. M. Reid, H. M. MacDonald

*Corresponding author for this work

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background/Objectives: In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture.Subjects/Methods:We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n=266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low-or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined.Results:Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: 0.6±2.8% and 1.5±2.4%, respectively (P=0.027); spine: 0.5±3.4% and 2.6±3.5%, (P0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium-or potassium-lowering effects on blood pressure did not alter the results.Conclusions:Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.

Original languageEnglish
Pages (from-to)1315-1322
Number of pages8
JournalEuropean Journal of Clinical Nutrition
Volume66
Issue number12
DOIs
Publication statusPublished - 24 Oct 2012

Fingerprint

Alkalies
Sodium Chloride
Potassium
Bone Density
Blood Pressure
Bone and Bones
Salts
Bone Remodeling
Scotland
Bone Resorption
Arterial Pressure
Dietary Sodium Chloride
Diet Therapy
Osteoporosis
Hip
Spine
Placebos
Diet
Calcium
Acids

Keywords

  • blood pressure
  • diet
  • osteoporosis
  • potassium
  • sodium chloride

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake. / Frassetto, L. A. (Corresponding Author); Hardcastle, A. C.; Sebastian, A.; Aucott, L.; Fraser, W. D.; Reid, D. M.; MacDonald, H. M.

In: European Journal of Clinical Nutrition, Vol. 66, No. 12, 24.10.2012, p. 1315-1322.

Research output: Contribution to journalArticle

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abstract = "Background/Objectives: In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture.Subjects/Methods:We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n=266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low-or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined.Results:Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: 0.6±2.8{\%} and 1.5±2.4{\%}, respectively (P=0.027); spine: 0.5±3.4{\%} and 2.6±3.5{\%}, (P0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium-or potassium-lowering effects on blood pressure did not alter the results.Conclusions:Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.",
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author = "Frassetto, {L. A.} and Hardcastle, {A. C.} and A. Sebastian and L. Aucott and Fraser, {W. D.} and Reid, {D. M.} and MacDonald, {H. M.}",
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T1 - No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake

AU - Frassetto, L. A.

AU - Hardcastle, A. C.

AU - Sebastian, A.

AU - Aucott, L.

AU - Fraser, W. D.

AU - Reid, D. M.

AU - MacDonald, H. M.

N1 - This work was funded in part by the UK Food Standards Agency (UK) and in part by Armand Hammer (USA).

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N2 - Background/Objectives: In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture.Subjects/Methods:We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n=266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low-or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined.Results:Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: 0.6±2.8% and 1.5±2.4%, respectively (P=0.027); spine: 0.5±3.4% and 2.6±3.5%, (P0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium-or potassium-lowering effects on blood pressure did not alter the results.Conclusions:Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.

AB - Background/Objectives: In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture.Subjects/Methods:We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n=266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low-or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined.Results:Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: 0.6±2.8% and 1.5±2.4%, respectively (P=0.027); spine: 0.5±3.4% and 2.6±3.5%, (P0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium-or potassium-lowering effects on blood pressure did not alter the results.Conclusions:Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.

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