The effect of coffee consumption on functional disability has been scarcely investigated. Thus, this study aimed to examine the association between coffee consumption and functional disability in older American adults. Participants (≥60 years old, n 7704) were from the National Health and Nutrition Examination Survey 2007–2016. Coffee consumption was assessed through two 24-h dietary recall interviews. Five domains of functional disability including lower extremity mobility (LEM), general physical activity (GPA), leisure and social activities (LSA), activities of daily living (ADL) and instrumental activities of daily living (IADL) were self-reported. Age- and multivariate-adjusted logistic regression models and restricted cubic spline analyses were used. Total coffee consumption was inversely associated with LEM, GPA, LSA and IADL disability. Compared with non-drinkers of total coffee, those who consumed ≥2 cups/d reported lower odds of LEM (OR 0·67, 95 % CI 0·50, 0·91), GPA (OR 0·65, 95 % CI 0·47, 0·88), LSA (OR 0·61, 95 % CI 0·45, 0·83) and IADL (OR 0·59, 95 % CI 0·44, 0·78) disability. The dose–response analyses confirmed these relationships. Intake of ≥2 cups/d caffeinated coffee was also inversely linked to GPA (OR 0·67, 95 % CI 0·48, 0·92), LSA (OR 0·66, 95 % CI 0·46, 0·93) and IADL (OR 0·57, 95 % CI 0·43, 0·75) disability, whereas the inverse association of 2+ cups/d decaffeinated coffee was only on LEM (OR 0·43, 95 % CI 0·23, 0·81) and LSA (OR 0·39, 95 % CI 0·16, 0·94) disability. The present study suggested that coffee consumption was inversely associated with functional disability in older American adults. Those associations of diverse coffee types differed across domains of functional disability.

Only one previous study has examined the association between coffee consumption and risk of acute pancreatitis, and it found a reduced risk for alcohol-related episodes among high consumers of coffee. Therefore, we examined (1) the association between coffee consumption and risk of non-gallstone-related acute pancreatitis and (2) whether this association was modified by alcohol intake. Data were obtained from two prospective cohorts, the Cohort of Swedish Men and the Swedish Mammography Cohort, including 76 731 men and women (born 1914–1952). Coffee consumption was assessed at baseline with a FFQ, and the cohorts were followed up between 1998 and 2012 via linkage to national health registries. Hazard ratios were estimated using Cox models, with adjustment for potential confounding factors. During 1 035 881 person-years of total follow-up, 383 cases (246 in men and 137 in women) of incident non-gallstone-related acute pancreatitis were identified. Overall, and irrespective of whether a categorical or a continuous exposure model was used, we observed no association between coffee consumption and risk of non-gallstone-related acute pancreatitis (e.g. the multivariable-adjusted hazard ratio for each 1 cup/d increase in coffee consumption was 0·97; 95 % CI 0·92, 1·03). There was no evidence of effect modification by alcohol intake (Pinteraction=0·77). In conclusion, coffee consumption was not associated with risk of non-gallstone-related acute pancreatitis in this large prospective cohort study. Because of the limited number of epidemiological studies and their conflicting results, further research is needed to elucidate this potential association.

To investigate the effect of coffee consumption on hip fracture risk, a meta-analysis was conducted. The PubMed database was screened for all published studies about coffee consumption and hip fracture through to November 2011. Reviews, PubMed option ‘related articles’ and references of retrieved papers were also searched for potentially relevant papers. Only studies that contained OR with 95 % CI for the association between coffee consumption and hip fracture risk were included. The summary risk estimates were calculated by fixed- and random-effects models. Subgroup analyses were carried out stratified by study designs and participant characteristics, respectively. A total of six prospective cohort studies and six case–control studies were included in the final analysis. The pooled OR displayed increased risk of hip fracture by 29·7 % (95 % CI 0·960, 1·751; P = 0·09) for the highest compared with the lowest coffee consumption by the random-effects model (P for heterogeneity = 0·000; I2 = 84·0 %), but the result had no statistical significance. Subgroup analyses showed that coffee consumption significantly increased hip fracture risk by 54·7 % (95 % CI 1·152, 2·077; P = 0·004) among women, by 40·1 % (95 % CI 1·015, 1·935; P = 0·040) for elderly participants aged over 70 years, and by 68·3 % for Northern Americans (95 % CI 1·492, 1·899; P = 0·000). Other subgroup analyses according to data published before the year 2000 showed a positive association between coffee and hip fracture risk, and follow-up duration also positively affected hip fracture risk, especially when the follow-up length was less than 13 years. Although our meta-analysis has provided insufficient evidence that coffee consumption significantly increases hip fracture risk, coffee intake may increase hip fracture risk among women, elderly participants and Northern Americans. No dose–response pattern was observed.

Habitual coffee consumption is associated with the prevention of type 2 diabetes, which often accompanies diabetic nephropathy. However, the relationship between coffee consumption and kidney function is unclear. Therefore, we investigated the associations between habitual coffee consumption and kidney function and damage assessed by the estimated glomerular filtration rate (eGFR) and proteinuria using dipstick urinalysis, respectively, in a cross-sectional study of 342 apparently healthy adults. Habitual coffee consumption was defined as drinking one or more cups of coffee per d. eGFR in coffee consumers (n 182; 80·1 (sd 15·0) ml/min per 1·73 m2) was significantly higher than that in non-coffee consumers (n 160; 76·9 (sd 12·6) ml/min per 1·73 m2) (P < 0·05). Multivariate logistic analysis showed that, compared with non-coffee consumption, coffee consumption was significantly associated with normal or increased eGFR (NIGFR) ( ≥ 90 ml/min per 1·73 m2), but not proteinuria, which was not attenuated, even after adjustment for age, sex, smoking, tea consumption and other cardiovascular risks (OR 2·91; 95 % CI 1·51, 5·61; P = 0·001). When we took into account eGFR measured 1 year before in a subgroup of the subjects (n 262), coffee consumption (n 142) had a significant relationship with eGFR, which was consistently higher with a difference of 4·0 ml/min per 1·73 m2 compared with non-coffee consumption (P = 0·01; two-way repeated ANOVA). Similar associations were observed in both sexes when data were reanalysed according to sex. In conclusion, our findings suggest that habitual coffee consumption is associated with NIGFR independently of clinical confounders. Further studies are needed to confirm this association and to explore whether the effect of coffee consumption on eGFR is beneficial for the kidney.