We aim to explore the association between caffeine and its metabolites and bone mineral density (BMD) in postmenopausal women. Data of 4286 postmenopausal women were extracted from the National Health and Nutrition Examination Survey (NHANES) database in 2009–14 in this cross-sectional study. Weighted linear regression and stepwise regression analyses were used to screen the covariates. Weighted univariate and multivariate linear regression analyses were used to explore the associations between caffeine and its metabolites and BMD. The evaluation index was estimated value (β) with 95 % confidence intervals (CIs). We also explored these relationships in age subgroups. The median BMD level among the eligible women was 0⋅7 gm/cm2. After adjusting for covariates including age, body mass index (BMI), fat intake, Calcium (Ca) supplements, diabetes mellitus (DM), angina pectoris, parental history of osteoporosis (OP), anti-osteoporosis therapy, poverty income ratio (PIR), vitamin D (VD) supplements, coronary heart disease (CHD), and previous fracture, we found that caffeine intake was not significantly related to the BMD reduction (β = 0, P = 0⋅135). However, caffeine metabolites, including MethyluricAcid3, MethyluricAcid7, MethyluricAcid37, Methylxanthine3, and Methylxanthine37, were negatively associated with the BMD (all P < 0⋅05). In addition, MethyluricAcid37 and Methylxanthine37 were negatively associated with BMD in females aged <65 years old, while MethyluricAcid3 and Methylxanthine3 were noteworthy in those who aged ≥65 years old. The roles of caffeine and its metabolites in BMD reduction and OP in postmenopausal women needed further exploration.

The influence of the source of dietary fat on postprandial thermogenesis and substrate oxidation rates, was examined in twelve postmenopausal women aged 57–73 years, with BMI 21·9–38·3 kg/m2. A single blind, randomised, paired comparison of two high-fat, isoenergetic, mixed test meals was conducted. The major source of fat was either cream (CREAM) or extra virgin olive oil (EVOO). RMR, diet-induced thermogenesis (DIT) and substrate oxidation rates over 5 h were measured by indirect calorimetry. There were no differences in body weight, RMR, fasting carbohydrate or fat oxidation rates between the two occasions. DIT (EVOO 97 (sd 46) v. CREAM 76 (sd 69) kJ/5 h and EVOO 5·2 (sd 2·5) v. CREAM 4·1 (sd 3·7)% energy) did not differ between the two test meals. The postprandial increase in carbohydrate oxidation rates, relative to their respective fasting values (ΔCOX), was significantly lower following the EVOO meal (EVOO 10·6 (sd 8·3) v. CREAM 17·5 (sd 10) g/5 h; paired t test, P=0·023), while postprandial fat oxidation rates (ΔFOX) were significantly higher (EVOO 0·0 (sd 4·4) v. CREAM -3·6 (sd 4·0) g/5 h; P=0·028). In the eight obese subjects, however, DIT was significantly higher following the EVOO meal (EVOO 5·1 (sd 2·0) v. CREAM 2·5 (sd 2·9) %; P=0·01). This was accompanied by a significantly lower ΔCOX (EVOO 10·9 (sd 9·9) v. CREAM 17·3 (sd 10·5) g/5 h; P=0·03) and significantly higher ΔFOX (EVOO 0·11 (sd 4·4) v. CREAM −4·1 (sd 4·5) g/5 h, P=0·034). The present study showed that olive oil significantly promoted postprandial fat oxidation and stimulated DIT in abdominally obese postmenopausal women.