title: Comparison of 2 weight-loss diets of different protein content on bone health: a randomized trial.
abstract: BACKGROUND
  It has been hypothesized that hip-fracture rates are higher in developed than in developing countries because high-protein (HP) Western diets induce metabolic acidosis and hypercalciuria. Confounders include interactions between dietary protein and calcium, sodium, and potassium.
  
  
  OBJECTIVE
  We determined whether an HP or a high-normal-protein (HNP) weight-loss diet caused greater loss in bone mineral density (BMD) over 24 mo.
  
  
  METHODS
  The Weight Loss, Protein and Bone Density Study was conducted from 2008 to 2011 in 323 overweight [body mass index (BMI; in kg/m(2)) >27] postmenopausal women, with a total hip BMD t score less than -2.0. Subjects were randomly assigned to receive an isocaloric calcium-replete HP (≥90 g protein/d) or HNP (<80 g protein/d) weight-loss diet, with the aim of a difference of 20 g protein/d. A total of 186 subjects (90 subjects in the HP group, 96 subjects in the HNP group) completed 12 mo, and 137 subjects (69 subjects in the HP group, 68 subjects in the HNP group) completed 24 mo.
  
  
  RESULTS
  Biomarkers confirmed a difference in protein intake of 16 and 13.1 g at 12 and 24 mo, respectively. Mean (±SE) weight loss was equal; HP subjects lost 7.9 ± 0.9 kg and HNP subjects lost 8.9 ± 0.9 kg at 24 mo. Subjects lost 1-2% BMD annually at lumbar spine vertebrae 2-4, the forearm, the femoral neck, and hip. ANCOVA showed no effect of the HP or HNP diet (P > 0.05 for diet and diet-time interactions). A diet-by-time analysis showed that the HNP diet increased C-terminal telopeptide and osteocalcin (P ≤ 0.001 for each) despite hypercalciuria (P = 0.029).
  
  
  CONCLUSIONS
  High dietary protein intake during weight loss has no clinically significant effect on bone density but slows bone turnover. This trial was registered at the Australian and New Zealand Clinical Trials Registry (http://www.anzctr.org.au) as ACTRN12608000229370.
authors.affiliation: From Food and Nutritional Sciences, Commonwealth Scientific and Industrial Research Organisation, Adelaide, Australia (DJ, JK, and PC); the Centre of Clinical Research Excellence in Human Nutrition, University of Adelaide, Adelaide, Australia (DJ and PC); the Endocrinology Department, The Queen Elizabeth Hospital, Adelaide, Australia (DJ); Clinical Chemistry, South Australia Pathology, Adelaide, Australia (BECN); and the University of South Australia, Frome Road, Adelaide, Australia (JK and PC).
authors.forename: David
authors.initials: D
authors.lastname: Jesudason
authors.forename: Be Christopher
authors.initials: BC
authors.lastname: Nordin
authors.forename: Jennifer
authors.initials: J
authors.lastname: Keogh
authors.forename: Peter
authors.initials: P
authors.lastname: Clifton
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D001806:Blood Urea Nitrogen; D001823:Body Composition; D015992:Body Mass Index; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000652:urine; D002136:Calcium, Dietary / Q000008:administration & dosage; D003906:Developing Countries; D004038:Diet, Reducing; D004044:Dietary Proteins / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D008875:Middle Aged; D009520:New Zealand; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010349:Patient Compliance; D010710:Phosphates / Q000097:blood; D017698:Postmenopause / Q000187:drug effects / Q000378:metabolism; D012964:Sodium / Q000652:urine; D011795:Surveys and Questionnaires; D014807:Vitamin D / Q000097:blood
chemical_list: D002136:Calcium, Dietary; D004044:Dietary Proteins; D010281:Parathyroid Hormone; D010710:Phosphates; D015675:Osteocalcin; D014807:Vitamin D; D012964:Sodium; D000469:Alkaline Phosphatase; D002118:Calcium