title: No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake.
abstract: OBJECTIVE
  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.
  
  
  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%, (P<0.001). 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.
authors.affiliation: Department of Medicine and Clinical Research Centre, University of California San Francisco, San Francisco, CA 94143-0126, USA. frassett@gcrc.ucsf.edu
authors.forename: L A
authors.initials: LA
authors.lastname: Frassetto
authors.forename: A C
authors.initials: AC
authors.lastname: Hardcastle
authors.forename: A
authors.initials: A
authors.lastname: Sebastian
authors.forename: L
authors.initials: L
authors.lastname: Aucott
authors.forename: W D
authors.initials: WD
authors.lastname: Fraser
authors.forename: D M
authors.initials: DM
authors.lastname: Reid
authors.forename: H M
authors.initials: HM
authors.lastname: Macdonald
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000468:Alkalies / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure; D015519:Bone Density / Q000187:drug effects*; D001862:Bone Resorption; D002140:California; D002712:Chlorides / Q000378:metabolism / Q000494:pharmacology; D004032:Diet; D019587:Dietary Supplements; D005260:Female; D006801:Humans; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000209:etiology / Q000378:metabolism; D017419:Potassium, Dietary / Q000494:pharmacology*; D012189:Retrospective Studies; D012606:Scotland; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D017673:Sodium Chloride, Dietary / Q000378:metabolism / Q000494:pharmacology*; D013131:Spine / Q000187:drug effects*
chemical_list: D000468:Alkalies; D015415:Biomarkers; D002712:Chlorides; D017419:Potassium, Dietary; D017673:Sodium Chloride, Dietary; D012964:Sodium