Anders Bach-Mortensen PhD , Benjamin Goodair MSc , Michelle Degli Esposti PhD
{"title":"Involuntary closures of for-profit care homes in England by the Care Quality Commission","authors":"Anders Bach-Mortensen PhD , Benjamin Goodair MSc , Michelle Degli Esposti PhD","doi":"10.1016/S2666-7568(24)00008-4","DOIUrl":"10.1016/S2666-7568(24)00008-4","url":null,"abstract":"<div><p>Adult social care services in England are struggling, and sometimes failing, to supply the quality of care deserved by the most vulnerable people in society. The Care Quality Commission (CQC) is responsible for protecting the recipients of this crucial public service. Their strongest enforcement is the ability to cancel the registration—the legal right to operate—of a health or social care provider. Using novel data from the CQC, we show that the proportion of care home closures due to CQC enforcements, relative to all closures, is increasing. Since 2011, 816 care homes (representing 19 918 registered beds) have been involuntarily closed by the CQC. Our results show that effectively all involuntary closures (804/816) occurred in for-profit care homes. This data emphasises the need for a comprehensive assessment of the impact of for-profit provision on the quality and sustainability of adult social care in England.</p></div>","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 4","pages":"Pages e297-e302"},"PeriodicalIF":13.1,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000084/pdfft?md5=a9aa35d516035b1845f62591e51e415c&pid=1-s2.0-S2666756824000084-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kathryn Nicholson PhD , Winnie Liu BSc , Daire Fitzpatrick MD , Kate Anne Hardacre BMSc , Sarah Roberts MD , Jennifer Salerno PhD , Prof Saverio Stranges MD PhD , Martin Fortin MD MSc , Prof Dee Mangin MBCHB DPH
{"title":"Prevalence of multimorbidity and polypharmacy among adults and older adults: a systematic review","authors":"Kathryn Nicholson PhD , Winnie Liu BSc , Daire Fitzpatrick MD , Kate Anne Hardacre BMSc , Sarah Roberts MD , Jennifer Salerno PhD , Prof Saverio Stranges MD PhD , Martin Fortin MD MSc , Prof Dee Mangin MBCHB DPH","doi":"10.1016/S2666-7568(24)00007-2","DOIUrl":"10.1016/S2666-7568(24)00007-2","url":null,"abstract":"<div><p>Multimorbidity (multiple conditions) and polypharmacy (multiple medications) are increasingly common, yet there is a need to better understand the prevalence of co-occurrence. In this systematic review, we examined the prevalence of multimorbidity and polypharmacy among adults (≥18 years) and older adults (≥65 years) in clinical and community settings. Six electronic databases were searched, and 87 studies were retained after two levels of screening. Most studies focused on adults 65 years and older and were done in population-based community settings. Although the operational definitions of multimorbidity and polypharmacy varied across studies, consistent cut-points (two or more conditions and five or more medications) were used across most studies. In older adult samples, the prevalence of multimorbidity ranged from 4·8% to 93·1%, while the prevalence of polypharmacy ranged from 2·6% to 86·6%. High heterogeneity between studies indicates the need for more consistent reporting of specific lists of conditions and medications used in operational definitions.</p></div>","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 4","pages":"Pages e287-e296"},"PeriodicalIF":13.1,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000072/pdfft?md5=8a7dd41890037b965e15a057ab456b6c&pid=1-s2.0-S2666756824000072-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Scott T Chiesa PhD , Tom Norris PhD , Victoria Garfield PhD , Prof Marcus Richards PhD , Prof Alun D Hughes PhD
{"title":"Early-life cumulative exposure to excess bodyweight and midlife cognitive function: longitudinal analysis in three British birth cohorts","authors":"Scott T Chiesa PhD , Tom Norris PhD , Victoria Garfield PhD , Prof Marcus Richards PhD , Prof Alun D Hughes PhD","doi":"10.1016/S2666-7568(24)00005-9","DOIUrl":"https://doi.org/10.1016/S2666-7568(24)00005-9","url":null,"abstract":"<div><h3>Background</h3><p>Excess bodyweight (BMI >25 kg/m<sup>2</sup>) in midlife (age 40–65 years) has been linked to future cognitive decline and an increased risk of dementia. Whether chronic exposure to excess bodyweight in the early decades of life (<40 years) is associated with compromised cognitive function by midlife, however, remains unclear. This study therefore aimed to test potential bidirectional direct and indirect pathways linking cumulative exposure to excess bodyweight and cognitive function in the early decades of life.</p></div><div><h3>Methods</h3><p>In this longitudinal analysis, harmonised measures of BMI and cognitive function were available in 19 742 participants aged 47–53 years recruited to the 1946 National Survey of Health and Development (n=2131), the 1958 National Child Development Study (n=9385), and the 1970 British Cohort Study (n=8226). Individual BMI trajectories spanning three decades from age 10–40 years were created for each participant and excess bodyweight duration, BMI change between ages, and cumulative excess bodyweight exposure were calculated. Harmonised measures of verbal and non-verbal ability, mathematical ability, and reading ability were used to create a latent factor for childhood cognitive function, and immediate and delayed recall, animal naming, and letter-search speed tests were used for midlife cognitive function. Multivariable linear regression and structural equation models (SEM) were used to test for potential bidirectional relationships between cognition and excess bodyweight in both individual cohorts and pooled datasets while accounting for other potential early-life confounders.</p></div><div><h3>Findings</h3><p>Increases in BMI during adolescence and greater cumulative exposure to excess bodyweight across early life were associated with lower midlife cognitive function in all cohorts (eg, pooled difference in cognitive function per 10 years excess bodyweight duration –0·10; 95% CI –0·12 to –0·08; p<0·001). Further adjustment for childhood cognitive function attenuated many of these associations towards the null (eg, pooled difference in cognitive function per 10 years excess bodyweight duration –0·04; 95% CI –0·06 to –0·02; p=0·001), however, with any remaining associations then fully attenuating once further adjusted for other early-life factors (eg, pooled difference in cognitive function per 10 years excess bodyweight duration 0, –0·03 to 0·01; p=0·38). In the reverse direction, low childhood cognition was associated with greater cumulative exposure to excess bodyweight over the next four decades, although much of this relationship was found to probably be explained via other potentially modifiable upstream early-life factors such as childhood disadvantage. SEM in all cohorts suggested the presence of modest direct and indirect pathways connecting earlier cognitive function to later excess bodyweight, but scarce evidence for an effect of early-life excess bodyweight on c","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 3","pages":"Pages e204-e213"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000059/pdfft?md5=58dedd6dbb989655c2147d4b4a88df1b&pid=1-s2.0-S2666756824000059-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140000021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Active vitamin D treatment in the prevention of sarcopenia in adults with prediabetes (DPVD ancillary study): a randomised controlled trial","authors":"Tetsuya Kawahara MD , Prof Gen Suzuki MD , Shoichi Mizuno PhD , Naoki Tominaga MD , Mikio Toda MD , Nagahiro Toyama MD , Prof Tetsuya Inazu MD , Chie Kawahara MD , Yosuke Okada MD , Prof Yoshiya Tanaka MD","doi":"10.1016/S2666-7568(24)00009-6","DOIUrl":"10.1016/S2666-7568(24)00009-6","url":null,"abstract":"<div><h3>Background</h3><p>Observational studies show inverse associations between serum 25-hydroxyvitamin D concentrations and sarcopenia incidence; however, it remains unclear whether treatment with vitamin D prevents its development. We aimed to assess whether treatment with active vitamin D (eldecalcitol [0·75 μg per day]) can reduce the development of sarcopenia among adults with prediabetes.</p></div><div><h3>Methods</h3><p>This randomised, double-blind, placebo-controlled, multicenter trial as an ancillary study was conducted at 32 clinics and hospital sites in Japan. Participants were assigned (1:1) by using a central randomisation method in which a randomisation list was made for each hospital separately using a stratified permuted block procedure. The primary endpoint was sarcopenia incidence during 3 years in the intention-to-treat population defined as weak handgrip strength (<28 kg for men and <18 kg for women) and low appendicular skeletal muscle index (<7·0 kg/m<sup>2</sup> for men and <5·7 kg/m<sup>2</sup> for women in bioelectrical impedance analysis). Although the usual criterion of hypercalcaemia was 10·4 mg/dL (2·6 mmol/L) or higher, hypercalcaemia that was enough to discontinue the study was defined as 11·0 mg/dL or higher. This study is registered with the UMIN clinical trials registry, UMIN000005394.</p></div><div><h3>Findings</h3><p>A total of 1094 participants (548 in the eldecalcitol group and 546 in the placebo group; 44·2% [484 of 1094] women; mean age 60·8 [SD 9·2] years) were followed up for a median of 2·9 (IQR 2·8–3·0) years. Eldecalcitol treatment as compared with placebo showed statistically significant preventive effect on sarcopenia incidence (25 [4·6%] of 548 participants in the eldecalcitol group and 48 [8·8%] of 546 participants in the placebo group; hazard ratio 0·51; 95% CI 0·31 to 0·83; p=0·0065). The incidence of adverse events did not differ between the two groups.</p></div><div><h3>Interpretation</h3><p>We found that treatment with eldecalcitol has the potential to prevent the onset of sarcopenia among people with prediabetes via increasing skeletal muscle volume and strength, which might lead to a substantial risk reduction of falls.</p></div><div><h3>Funding</h3><p>Kitakyushu Medical Association.</p></div><div><h3>Translation</h3><p>For the Japanese translation of the abstract see Supplementary Materials section.</p></div>","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 4","pages":"Pages e255-e263"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000096/pdfft?md5=1097e8a64c8b845163d6a6e0bad59385&pid=1-s2.0-S2666756824000096-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140029186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ATEMPTing to navigate between “lower is better” and “less is more”","authors":"Nicholas M Pajewski , Jordana B Cohen","doi":"10.1016/S2666-7568(24)00024-2","DOIUrl":"10.1016/S2666-7568(24)00024-2","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 3","pages":"Pages e164-e165"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000242/pdfft?md5=757b23fdbc3ae9c64f5acc3815320a8b&pid=1-s2.0-S2666756824000242-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139717944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cancer survivorship and bone health","authors":"Peter KK Wong , Weiwen Chen","doi":"10.1016/S2666-7568(24)00022-9","DOIUrl":"10.1016/S2666-7568(24)00022-9","url":null,"abstract":"","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 3","pages":"Pages e168-e169"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756824000229/pdfft?md5=67e11c00a7453540c9b81dfc09e68e5e&pid=1-s2.0-S2666756824000229-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139713182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva Buzasi MSc , Helena Carreira PhD , Garth Funston PhD , Kathryn E Mansfield PhD , Harriet Forbes PhD , Helen Strongman PhD , Prof Krishnan Bhaskaran PhD
{"title":"Risk of fractures in half a million survivors of 20 cancers: a population-based matched cohort study using linked English electronic health records","authors":"Eva Buzasi MSc , Helena Carreira PhD , Garth Funston PhD , Kathryn E Mansfield PhD , Harriet Forbes PhD , Helen Strongman PhD , Prof Krishnan Bhaskaran PhD","doi":"10.1016/S2666-7568(23)00285-4","DOIUrl":"10.1016/S2666-7568(23)00285-4","url":null,"abstract":"<div><h3>Background</h3><p>A history of multiple myeloma, prostate cancer, and breast cancer has been associated with adverse bone health, but associations across a broader range of cancers are unclear. We aimed to compare the risk of any bone fracture and major osteoporotic fractures in survivors of a wide range of cancers versus cancer-free individuals.</p></div><div><h3>Methods</h3><p>In this population-based matched cohort study, we used electronic health records from the UK Clinical Practice Research Datalink linked to hospital data. We included adults (aged ≥18 years) eligible for linkage, and we restricted the study start to Jan 2, 1998, onwards and applied administrative censoring on Jan 31, 2020. The cancer survivor group included survivors of the 20 most common cancers. Each individual with cancer was matched (age, sex, and general practice) to up to five controls (1:5) who were cancer-free. The primary outcomes were any bone fracture and any major osteoporotic fracture (pelvic, hip, wrist, spine, or proximal humeral fractures) occurring more than 1 year after index date (ie, the diagnosis date of the matched individual with cancer). We used Cox regression models, adjusted for shared risk factors, to estimate associations between cancer survivorship and bone fractures.</p></div><div><h3>Findings</h3><p>578 160 adults with cancer diagnosed in 1998–2020 were matched to 3 226 404 cancer-free individuals. Crude incidence rates of fractures in cancer survivors ranged between 8·39 cases (95% CI 7·45–9·46) per 1000 person-years for thyroid cancer and 21·62 cases (20·18–23·18) per 1000 person-years for multiple myeloma. Compared with cancer-free individuals, the risk of any bone fracture was increased in 15 of 20 cancers, and of major osteoporotic fractures in 17 of 20 cancers. Effect sizes varied: adjusted hazard ratios (HRs) were largest for multiple myeloma (1·94, 95% CI 1·77–2·13) and prostate cancer (1·43, 1·39–1·47); HRs in the range 1·20–1·50 were seen for stomach, liver, pancreas, lung, breast, kidney, and CNS cancers; smaller associations (HR <1·20) were observed for malignant melanoma, non-Hodgkin lymphoma, leukaemia, and oesophageal, colorectal, and cervical cancers. Increased risks of major osteoporotic fracture were noted most substantially in multiple myeloma (2·25, 1·96–2·58) and CNS (2·12, 1·56–2·87), liver (1·62, 1·01–2·61), prostate (1·60, 1·53–1·67), and lung cancers (1·60, 1·44–1·77). Effect sizes tended to reduce over time since diagnosis but remained elevated for more than 5 years in several cancers, such as multiple myeloma and stomach, lung, breast, prostate, and CNS cancers.</p></div><div><h3>Interpretation</h3><p>Survivors of most types of cancer were at increased risk of bone fracture for several years after cancer, with variation by cancer type. These findings can help to inform mitigation and prevention strategies.</p></div><div><h3>Funding</h3><p>Wellcome Trust.</p></div>","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 3","pages":"Pages e194-e203"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756823002854/pdfft?md5=6a950dff74083763add0b191a0e8c9ae&pid=1-s2.0-S2666756823002854-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139713183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peter Hanlon PhD , Heather Wightman BSc , Marina Politis BSc , Stella Kirkpatrick BSc , Caitlin Jones MBChB , Melissa K Andrew PhD , Davide L Vetrano PhD , Elsa Dent PhD , Emiel O Hoogendijk PhD
{"title":"The relationship between frailty and social vulnerability: a systematic review","authors":"Peter Hanlon PhD , Heather Wightman BSc , Marina Politis BSc , Stella Kirkpatrick BSc , Caitlin Jones MBChB , Melissa K Andrew PhD , Davide L Vetrano PhD , Elsa Dent PhD , Emiel O Hoogendijk PhD","doi":"10.1016/S2666-7568(23)00263-5","DOIUrl":"https://doi.org/10.1016/S2666-7568(23)00263-5","url":null,"abstract":"<div><p>Both frailty (reduced physiological reserve) and social vulnerability (scarcity of adequate social connections, support, or interaction) become more common as people age and are associated with adverse consequences. Analyses of the relationships between these constructs can be limited by the wide range of measures used to assess them. In this systematic review, we synthesised 130 observational studies assessing the association between frailty and social vulnerability, the bidirectional longitudinal relationships between constructs, and their joint associations with adverse health outcomes. Frailty, across assessment type, was associated with increased loneliness and social isolation, perceived inadequacy of social support, and reduced social participation. Each of these social vulnerability components was also associated with more rapid progression of frailty and lower odds of improvement compared with the absence of that social vulnerability component (eg, more rapid frailty progression in people with social isolation <em>vs</em> those who were not socially isolated). Combinations of frailty and social vulnerability were associated with increased mortality, decline in physical function, and cognitive impairment. Clinical and public health measures targeting frailty or social vulnerability should, therefore, account for both frailty and social vulnerability.</p></div>","PeriodicalId":34394,"journal":{"name":"Lancet Healthy Longevity","volume":"5 3","pages":"Pages e214-e226"},"PeriodicalIF":13.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666756823002635/pdfft?md5=b12c0286decea331e46e55947087cd58&pid=1-s2.0-S2666756823002635-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139998893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}