Increased TV watching is dangerous to your CV health. What about other sedentary activities, such as reading? In particular, reading medical journal articles?
The study is clearly an explanatory sequential design using a QUANT and a QUAL phase. However, the title and the abstract design states that this is an exploratory study. Looking further down at the methods section, the authors state that "This mixed-methods study used an explanatory sequential design and involved two phases "
We thank professor Kawada for the constructive remarks.
Indeed, women presented with more subthreshold or clinical insomnia than men (14.9% and 6.3%, vs. 11.6% and 4.4%, p=0.003, while men presented more frequently with depression (14.0% vs 10.1%, p=0.001). We ran the multivariable models stratifying on gender, and we assessed possible interactions between gender and insomnia / depression. The results show no significant (p<0.05) interaction, although a trend for a higher OR among women was noted for depression when fatigue was categorized using the threshold of 5 of the fatigue scale questionnaire (Table provided upon request). Hence, we believe that the results obtained using the model adjusting for gender are adequate.
Regarding sleep duration, we agree it is an important issue and that future studies on fatigue should include an adequate estimation of the mean sleep duration.
I read the recently published systematic review on Injection therapy for base of thumb osteoarthritis: a systematic review and meta-analysis published in BMJ Open[1] with interest. It follows hot on the heels of 6 other previous published systematic reviews on the same subject, 3 on exactly the same subject of injection therapy in base of thumb osteoarthritis[2–5] and 3 others that included injections amongst all non-surgical or conservative therapies[6–8]. The conclusion of all 7 reviews is, not surprisingly, consistent in determining the level of evidence is poor, a conclusion which we can all agree on, however the other conclusion that there is no evidence steroid injections confer any benefit, is in contrast to the outcomes of non-randomised studies and with clinical experience.
I believe the disconnect occurs due to the long-term outcome measures used in the assessment of outcomes usually recorded at 26 weeks. Longitudinal studies of the effect of steroid injections in base of thumb osteoarthritis (CMCJ OA) accord with clinical experience in that that the best outcomes were measured at 4 weeks (76% better at 4 weeks[9], with 2/3 better at 8 weeks, ½ at 12 weeks but only 1/6 at 26 weeks[5],. So, by assessing outcomes at 26 weeks, the pain-relieving effects of steroid have already dissipated.
Another variation that needs to be considered but was not discussed is the different formulations and doses of corticosteroids used in the study as these vary in anti-i...
I read the recently published systematic review on Injection therapy for base of thumb osteoarthritis: a systematic review and meta-analysis published in BMJ Open[1] with interest. It follows hot on the heels of 6 other previous published systematic reviews on the same subject, 3 on exactly the same subject of injection therapy in base of thumb osteoarthritis[2–5] and 3 others that included injections amongst all non-surgical or conservative therapies[6–8]. The conclusion of all 7 reviews is, not surprisingly, consistent in determining the level of evidence is poor, a conclusion which we can all agree on, however the other conclusion that there is no evidence steroid injections confer any benefit, is in contrast to the outcomes of non-randomised studies and with clinical experience.
I believe the disconnect occurs due to the long-term outcome measures used in the assessment of outcomes usually recorded at 26 weeks. Longitudinal studies of the effect of steroid injections in base of thumb osteoarthritis (CMCJ OA) accord with clinical experience in that that the best outcomes were measured at 4 weeks (76% better at 4 weeks[9], with 2/3 better at 8 weeks, ½ at 12 weeks but only 1/6 at 26 weeks[5],. So, by assessing outcomes at 26 weeks, the pain-relieving effects of steroid have already dissipated.
Another variation that needs to be considered but was not discussed is the different formulations and doses of corticosteroids used in the study as these vary in anti-inflammatory effect and duration. In these reviews the seven studies used 6 different variations of methylprednisolone 40mg, betamethasone- high solubility/ short acting (1.5mg or 1 ml), or triamcinolone- low solubility/ long acting ( 5 , 10 and 20mg), and this variation must have a bearing on results. I use triamcinolone 40mg ( equivalent to 8mg or 3mls of betamethasone or 40mg methylprednisolone) per injection with reliably good effect for 6-12 weeks. Is this choice of corticosteroid and dosage another reason the clinical effect exceeds the study effects?
I believe that systematic reviews should include a section about the correlation of the review’s findings with clinical experience, and non-randomised literature, and current practice. An uncritical reading of this and other reviews on the subject suggest that intra-articular steroid injections should not be used as no beneficial effect is demonstrated, on the contrary every practicing hand surgeon and majority of patients injected will affirm that steroid injections provide pain relief albeit only for a temporary period.
1 Riley N, Vella-Baldacchino M, Thurley N, et al. Injection therapy for base of thumb osteoarthritis: A systematic review and meta-Analysis. BMJ Open 2019;9:1–13. doi:10.1136/bmjopen-2018-027507
2 Kroon FPB, Rubio R, Schoones JW, et al. Intra-Articular Therapies in the Treatment of Hand Osteoarthritis: A Systematic Literature Review. Drugs and Aging 2016;33:119–33. doi:10.1007/s40266-015-0330-5
3 Trellu S Fautrel B, Gossec L DS. Intra-Articular injections in thumb osteoarthritis. A systematic review and meta-analysis of randomized controlled trials. Ann Rheum Dis 2014;73. doi:10.1016/j.jbspin.2015.02.002
4 Trellu S, Dadoun S, Berenbaum F, et al. Intra-articular injections in thumb osteoarthritis: A systematic review and meta-analysis of randomized controlled trials. Jt Bone Spine 2015;82:315–9. doi:10.1016/j.jbspin.2015.02.002
5 Fowler A, Swindells MG, Burke FD. Intra-articular corticosteroid injections to manage trapeziometacarpal osteoarthritis—a systematic review. Hand 2015;10:583–92. doi:10.1007/s11552-015-9778-3
6 Lue S, Koppikar S, Shaikh K, et al. Systematic review of non-surgical therapies for osteoarthritis of the hand: an update. Osteoarthr Cartil 2017;25:1379–89. doi:10.1016/j.joca.2017.05.016
7 Spaans AJ, Van Minnen LP, Kon M, et al. Conservative treatment of thumb base osteoarthritis: A systematic review. J Hand Surg Am 2015;40:16-21.e6. doi:10.1016/j.jhsa.2014.08.047
8 Hamasaki T, Laprise S, Harris PG, et al. Efficacy of non‐surgical interventions for trapeziometacarpal (thumb base) osteoarthritis: A systematic review. Arthritis Care Res (Hoboken) 2019;:0–2. doi:10.1002/acr.24084
9 Maarse W, Watts AC, Bain GI. Medium-term outcome following intra-articular corticosteroid injection in first CMC joint arthritis using fluoroscopy. Hand Surg 2009;14:99–104. doi:10.1142/S0218810409004311
Hackett et al. conducted a prospective study to evaluate the association between disability discrimination and well-being (1). Adjusted odds ratio (95% confidence interval [CI]) of disability discrimination for depression and fair/poor self-rated health were 5.40 (3.25 to 8.97) and 2.05 (1.19 to 3.51), respectively. In addition, standardized regression coefficients (95% CI) of disability discrimination for psychological distress, mental functioning, and life satisfaction were 3.28 (2.41 to 4.14), -7.35 (-9.70 to -5.02) and -1.27 (-1.66 to -0.87), respectively. Prospectively, disability discrimination was also significantly associated with increased psychological distress and poorer mental functioning by adjusting for baseline scores. I have some concerns about their study.
Gill et al. conducted a prospective study to evaluate potential risk factors for severe disability (2). Hazard ratio (HR) (95% CI) of persons with ≥85 years old, hearing impairment, frailty, cognitive impairment, low functional self-efficacy and low peak flow for progressive disability were 1.6 (1.1-2.4), 1.7 (1.0-2.8), 2.4 (1.6-3.7), 2.0 (1.3-3.1), 1.8 (1.2-2.8), and 1.7 (1.2-2.4), respectively. In addition, HR (95% CI) of persons with visual impairment, hearing impairment, poor physical performance, and low peak flow for catastrophic disability were 1.4 (1.1-1.8), 1.3 (1.0-1.7), 1.8 (1.3-2.5), 1.3 (1.0-1.7), respectively. To avoid severe disability, appropriate interventions for modifiable facto...
Hackett et al. conducted a prospective study to evaluate the association between disability discrimination and well-being (1). Adjusted odds ratio (95% confidence interval [CI]) of disability discrimination for depression and fair/poor self-rated health were 5.40 (3.25 to 8.97) and 2.05 (1.19 to 3.51), respectively. In addition, standardized regression coefficients (95% CI) of disability discrimination for psychological distress, mental functioning, and life satisfaction were 3.28 (2.41 to 4.14), -7.35 (-9.70 to -5.02) and -1.27 (-1.66 to -0.87), respectively. Prospectively, disability discrimination was also significantly associated with increased psychological distress and poorer mental functioning by adjusting for baseline scores. I have some concerns about their study.
Gill et al. conducted a prospective study to evaluate potential risk factors for severe disability (2). Hazard ratio (HR) (95% CI) of persons with ≥85 years old, hearing impairment, frailty, cognitive impairment, low functional self-efficacy and low peak flow for progressive disability were 1.6 (1.1-2.4), 1.7 (1.0-2.8), 2.4 (1.6-3.7), 2.0 (1.3-3.1), 1.8 (1.2-2.8), and 1.7 (1.2-2.4), respectively. In addition, HR (95% CI) of persons with visual impairment, hearing impairment, poor physical performance, and low peak flow for catastrophic disability were 1.4 (1.1-1.8), 1.3 (1.0-1.7), 1.8 (1.3-2.5), 1.3 (1.0-1.7), respectively. To avoid severe disability, appropriate interventions for modifiable factors are needed. Although Gill et al. presented some physical factors, Hackett et al. pointed out the effect of disability discrimination on psych-social outcomes such as psychological distress, mental functioning, and life satisfaction. These well-being-related factors might affect quality of life in older inhabitants.
Regarding the query, I experienced two cases of older inhabitants in a local city. Male subjects, aged 86 years and 9 months, has hearing impairment, frailty, mild-to-moderate cognitive impairment, low functional self-efficacy and low peak flow caused by thoracic operation in his 50s. For 60 years, he has been taking anti-psychiatric medications, and his stature is strong kyphosis. In combination with the lack of disability discrimination, perception of psychological distress and poorer mental functioning is low. Female subjects, aged 84 years and 9 months, is a wife of the previous case and has hearing impairment, frailty, mild-to-moderate cognitive impairment, low functional self-efficacy caused by lumbar disc compression fracture in her 80 years old. For 12 years, she has been taking anti-depressant medication, and her stature is moderate to severe kyphosis. She also lacks the ability of disability discrimination, and perception of psychological distress and poorer mental functioning is also low. Stressful events frequently emerge in everyday life of their family members, and appropriate management is needed to keep quality of life in the target inhabitants.
Finally, ethnic and sex difference on the association between disability discrimination and well-being should be specified by further studies.
References
1. Hackett RA, Steptoe A, Lang RP, Jackson SE. Disability discrimination and well-being in the United Kingdom: a prospective cohort study. BMJ Open. 2020;10(3):e035714. doi:10.1136/bmjopen-2019-035714
2. Gill TM, Han L, Gahbauer EA, Leo-Summers L, Murphy TE. Risk factors and precipitants of severe disability among community-living older persons. JAMA Netw Open. 2020;3(6):e206021. doi:10.1001/jamanetworkopen.2020.6021
Barker et al. conducted a review to investigate risk-benefit assessment of aspirin for fracture (1). Pooled odds ratio (95% CI) of aspirin use for any fracture was 0.83 (0.70 to 0.99). There was a tendency of the association between aspirin use and total hip bone mineral density (BMD). Similar results were observed for lumbar spine BMD. I have some concerns about their study.
I understand that fracture risk includes BMD, but other psycho-physiological factors also attribute to fracture such as physical balance, muscle strength and mental instability. Aspirin use might modify the level of physical fitness and lead to the benefits of reduced fracture risk and increased trend of BMD. Barker et al. included a cross-sectional study by Bonten et al., to evaluate the effect of low-dose aspirin on BMD (2). There was no difference between aspirin users and non-users for vertebral BMD in men and women. They speculated that the risk of fractures observed in aspirin users in previous studies might not be directly related to BMD.
Chin summarized the effect of aspirin use on bone health (3). Although aspirin could prevent bone loss in animal models of osteoporosis, human epidemiological studies regarding aspirin used and fracture risk were limited, and the effect of aspirin use on fracture prevention has been inconclusive. On this point, Barker et al. presented precise information on the relationship. Each component of a meta-analysis should be added for stable estimation....
Barker et al. conducted a review to investigate risk-benefit assessment of aspirin for fracture (1). Pooled odds ratio (95% CI) of aspirin use for any fracture was 0.83 (0.70 to 0.99). There was a tendency of the association between aspirin use and total hip bone mineral density (BMD). Similar results were observed for lumbar spine BMD. I have some concerns about their study.
I understand that fracture risk includes BMD, but other psycho-physiological factors also attribute to fracture such as physical balance, muscle strength and mental instability. Aspirin use might modify the level of physical fitness and lead to the benefits of reduced fracture risk and increased trend of BMD. Barker et al. included a cross-sectional study by Bonten et al., to evaluate the effect of low-dose aspirin on BMD (2). There was no difference between aspirin users and non-users for vertebral BMD in men and women. They speculated that the risk of fractures observed in aspirin users in previous studies might not be directly related to BMD.
Chin summarized the effect of aspirin use on bone health (3). Although aspirin could prevent bone loss in animal models of osteoporosis, human epidemiological studies regarding aspirin used and fracture risk were limited, and the effect of aspirin use on fracture prevention has been inconclusive. On this point, Barker et al. presented precise information on the relationship. Each component of a meta-analysis should be added for stable estimation. I suspect that aspirin users are generally older people and have a risk of frailty and cognitive impairment. Not only bone quantity and quality, but also other physio-psycho-social factors might contribute to fracture.
References
1. Barker AL, Soh SE, Sanders KM, et al. Aspirin and fracture risk: a systematic review and exploratory meta-analysis of observational studies. BMJ Open. 2020;10(2):e026876. Published 2020 Feb 20. doi:10.1136/bmjopen-2018-026876
2. Bonten TN, de Mutsert R, Rosendaal FR, et al. Chronic use of low-dose aspirin is not associated with lower bone mineral density in the general population. Int J Cardiol. 2017;244:298-302. doi:10.1016/j.ijcard.2017.06.089
3. Chin KY. A Review on the relationship between aspirin and bone health. J Osteoporos. 2017;2017:3710959. doi:10.1155/2017/3710959
We thank Professor Kawada for his interest in our study.(1) We agree that the three recent papers he quotes are interesting studies that make important contributions. We do not agree with his expression of concerns about our study as they seem to reflect an assumption that different reporting to the papers he quoted were the concerns; these studies are not comparable to ours.
Oppewal et al. studied only elderly people,(2) whilst our study was of adults aged 16 years and over; their study included people using three care providers, whilst ours was population based. Oppewal et al. gathered cause of death information from medical case-files, and acknowledged, amongst other limitations, that information on cause of death in these files was sometimes limited which was beyond their control. Indeed they reported immediate and primary (underlying) cause of death, but not contributing causes of death, raising the question of whether it was possible for them to distinguish underlying and contributing causes of death from the case-files. We found the most common underlying causes of death for the adults with Down syndrome were dementia (35.1%), then other infection (12.3%); but when considering all contributing causes of death (not just the underlying cause), we found the most common after Down syndrome to be dementia (42.1%), and respiratory infection (38.6%) (reported in our table 5).
In a study published in the same month as ours, De Campos Gomes et al. reported hig...
We thank Professor Kawada for his interest in our study.(1) We agree that the three recent papers he quotes are interesting studies that make important contributions. We do not agree with his expression of concerns about our study as they seem to reflect an assumption that different reporting to the papers he quoted were the concerns; these studies are not comparable to ours.
Oppewal et al. studied only elderly people,(2) whilst our study was of adults aged 16 years and over; their study included people using three care providers, whilst ours was population based. Oppewal et al. gathered cause of death information from medical case-files, and acknowledged, amongst other limitations, that information on cause of death in these files was sometimes limited which was beyond their control. Indeed they reported immediate and primary (underlying) cause of death, but not contributing causes of death, raising the question of whether it was possible for them to distinguish underlying and contributing causes of death from the case-files. We found the most common underlying causes of death for the adults with Down syndrome were dementia (35.1%), then other infection (12.3%); but when considering all contributing causes of death (not just the underlying cause), we found the most common after Down syndrome to be dementia (42.1%), and respiratory infection (38.6%) (reported in our table 5).
In a study published in the same month as ours, De Campos Gomes et al. reported higher mortality in some regions of Brazil than others, in indigenous women, in people with no years of schooling, and that in some regions mortality was related to years of schooling.(3) They attributed these findings to regional differences in access to and quality of health services. We did not study these factors as our study was located in Scotland, and schooling is universal for all in Scotland to age 16 years. These are between-country differences.
For ethical reasons, statistical disclosure controls precluded us reporting types of congenital heart malformations, as <5 of the adults with Down syndrome had congenital heart malformations identified amongst the all contributory causes of death (reported in our table 5). Results of course are different for children; in a Scotland-wide study our group published earlier this year, we reported that between 1990-2015 there were 1,235 live births with Down syndrome, of whom 92 (7.4%) had died (18.5 times more than age-sex-neighbourhood deprivation matched controls), and for 33 (34.4%) this was from congenital heart malformations.(4) This was particularly so in the first month and first year of life.
The study by Hithersay et al. is important, as the high rate of dementia in people with Down syndrome has been known for several decades. They focused on how dementia status influences mortality in older adults with Down syndrome, rather than causes of death in all adults with intellectual disabilities with, and without, Down syndrome.(5) They did not report underlying and contributory causes of death as that was not their aim. Our study is not therefore comparable with theirs. Their secondary aim was to investigate factors that influenced age at death separately for those with, and those without, dementia (unlike our methods). In their multivariable models, they reported that only late-onset epilepsy was associated with mortality in the older adults without dementia, and only APOE genotype was associated in the older adults with dementia (Professor Kawada quoted from the univariate analyses).
These studies are on different populations, and have different aims, and so different results. None of these studies investigated standardised mortality rates, nor causes of death in adults of all ages with intellectual disabilities, with and without Down syndrome, nor avoidable deaths. We hope our reply has allayed the correspondent’s concerns.
References
1. Cooper S-A, Allan L, Greenlaw N, et al. Rates, causes, place and predictors of mortality in adults with intellectual disabilities with and without Down syndrome: cohort study with record linkage. BMJ Open 2020;10(5):e036465 doi:10.1136/bmjopen-2019-036465
2. Oppewal A, Schoufour JD, van der Maarl HJK, et al. Causes of mortality in older people with intellectual disability: results fromt eh HA-ID study. Am J Intellect Dev Disabil 2018;123(1):61-71. doi:10.1352/1944-7558-123.1.61
3. De Campos Gomes F, de Melo-Neto JS, Goloni-Bertollo EM, et al. Trends and predictions for survival and mortality in individuals with Down syndrome in Brazil: a 21-year analysis. J Intellectl Disabil Res 2020 May 7. doi:10.1111/jir.12735
4. Hughes-McCormack LA, McGowan R, Pell JP, et al. Birth incidence, deaths and hospitalisations of children and young people with Down syndrome, 1990–2015: birth cohort study. BMJ Open 2020;10:e033770. doi:10.1136/ bmjopen-2019-033770
5. Hithersay R, Startin CM, Hamburg S, Association of dementia with mortality among adults with Down syndrome older than 25 years. JAMA Neurol. 2019;76(2):152-160. doi:10.1001/jamaneurol.2018.3616
Aslam et al. conducted a prospective study to assess the association between milk/total dairy consumption and major osteoporotic fracture (MOF) in women (1). The authors handled women aged ≥50 years, and MOFs (hip, forearm, clinical spine and proximal humerus) were confirmed radiologically. Consuming >500 mL/d of milk was not significantly associated with increased HR for MOF. In addition, adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of Non-milk drinkers against drinkers consuming <250 mL/d of milk and consumption of ≥800 g/d total dairy against 200-399 g/d of total dairy for MOF were 1.56 (0.99 to 2.46) and 1.70 (0.99 to 2.93), respectively. They concluded that there was a trend for increased MOF in women with zero milk and higher total dairy consumption. I want to present results from recent meta-analyses.
Malmir et al. summarized the association of milk and dairy intake with risk of osteoporosis and hip fracture (2). There was an inverse relationship of milk and dairy intake with risk of osteoporosis and hip fracture in cross-sectional and case-control studies. By meta-regression analysis, every additional 200-gram intake of dairy and milk were associated with a 22% and 37% reduced risk of osteoporosis, respectively. In addition, milk consumption was associated with a 25% reduced risk of hip fracture. In contrast, the significance disappeared in cohort studies, and a greater intake of milk and dairy products did not reduce the risk of osteo...
Aslam et al. conducted a prospective study to assess the association between milk/total dairy consumption and major osteoporotic fracture (MOF) in women (1). The authors handled women aged ≥50 years, and MOFs (hip, forearm, clinical spine and proximal humerus) were confirmed radiologically. Consuming >500 mL/d of milk was not significantly associated with increased HR for MOF. In addition, adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of Non-milk drinkers against drinkers consuming <250 mL/d of milk and consumption of ≥800 g/d total dairy against 200-399 g/d of total dairy for MOF were 1.56 (0.99 to 2.46) and 1.70 (0.99 to 2.93), respectively. They concluded that there was a trend for increased MOF in women with zero milk and higher total dairy consumption. I want to present results from recent meta-analyses.
Malmir et al. summarized the association of milk and dairy intake with risk of osteoporosis and hip fracture (2). There was an inverse relationship of milk and dairy intake with risk of osteoporosis and hip fracture in cross-sectional and case-control studies. By meta-regression analysis, every additional 200-gram intake of dairy and milk were associated with a 22% and 37% reduced risk of osteoporosis, respectively. In addition, milk consumption was associated with a 25% reduced risk of hip fracture. In contrast, the significance disappeared in cohort studies, and a greater intake of milk and dairy products did not reduce the risk of osteoporosis and hip fracture. These results were statistically consistent with data by Aslam et al.
Hidayat et al. evaluated the association between dairy consumption (milk, yogurt, and cheese) and the risk of hip fracture (3). Pooled relative risks (RRs) (95% CIs) of the highest versus lowest category of yogurt, milk, and cheese consumptions for hip fracture were 0.78 (0.68 to 0.90), 0.86 (0.73 to 1.02), and 0.85 (0.66 to 1.08), respectively. Protective effect of milk consumption for hip fracture was only observed in USA study, presenting pooled RR (95% CI) of 0.75 (0.65 to 0.87). The study in USA also presented that pooled RR (95% CI) of milk consumption per 1 glass/day for hip fracture was 0.93 (0.88 to 0.98). Discrepancy of results in different countries and different types of dairy products might need further study to verify the association. Stratified meta-analysis by sex and age are recommended, such as women aged ≥50 years old (1).
References
1. Aslam H, Holloway-Kew KL, Mohebbi M, Jacka FN, Pasco JA. Association between dairy intake and fracture in an Australian-based cohort of women: a prospective study. BMJ Open. 2019;9(11):e031594. Published 2019 Nov 21. doi:10.1136/bmjopen-2019-031594
2. Malmir H, Larijani B, Esmaillzadeh A. Consumption of milk and dairy products and risk of osteoporosis and hip fracture: a systematic review and Meta-analysis. Crit Rev Food Sci Nutr. 2020;60(10):1722‐1737. doi:10.1080/10408398.2019.1590800
3. Hidayat K, Du X, Shi BM, Qin LQ. Systematic review and meta-analysis of the association between dairy consumption and the risk of hip fracture: critical interpretation of the currently available evidence. Osteoporos Int. 2020 May 7. doi:10.1007/s00198-020-05383-3
Cooper et al. investigated clinical predictors of mortality in adults with intellectual disabilities (1). Standardized mortality ratios (SMRs) (95% confidence interval [CI]) in Down syndrome adults and adults without Down syndrome were 5.28 (3.98, 6.57) and 1.93 (1.68, 2.18), respectively. In addition, SMRs in males and females were 1.69 (1.42, 1.95) and 3.48 (2.90, 4.06), respectively. Aspiration/reflux/choking and respiratory infection were the most common causes of mortality in adults without Down syndrome, and dementia was the most common causes of mortality in Down syndrome adults. Mortality risk related to percutaneous endoscopic gastrostomy/tube fed, Down syndrome, diabetes, lower respiratory tract infection at cohort-entry, smoking, epilepsy, hearing impairment, increasing number of prescribed drugs, increasing age were related to mortality in adults with intellectual disabilities. I have some concerns about their study.
First, Oppewal et al. also reported the cause-specific mortality of older Down syndrome adults with intellectual disability (2). The common cause of mortality was respiratory disease (51.1%), followed by dementia (22.2%), and this information was not consistent with data by Cooper et al. Methodological difference of survey, including definition, might contribute to the statistical information.
Second, de Campos Gomes et al. analyzed mortality and related factors in individuals with Down syndrome in Brazil (3). They concluded that ethn...
Cooper et al. investigated clinical predictors of mortality in adults with intellectual disabilities (1). Standardized mortality ratios (SMRs) (95% confidence interval [CI]) in Down syndrome adults and adults without Down syndrome were 5.28 (3.98, 6.57) and 1.93 (1.68, 2.18), respectively. In addition, SMRs in males and females were 1.69 (1.42, 1.95) and 3.48 (2.90, 4.06), respectively. Aspiration/reflux/choking and respiratory infection were the most common causes of mortality in adults without Down syndrome, and dementia was the most common causes of mortality in Down syndrome adults. Mortality risk related to percutaneous endoscopic gastrostomy/tube fed, Down syndrome, diabetes, lower respiratory tract infection at cohort-entry, smoking, epilepsy, hearing impairment, increasing number of prescribed drugs, increasing age were related to mortality in adults with intellectual disabilities. I have some concerns about their study.
First, Oppewal et al. also reported the cause-specific mortality of older Down syndrome adults with intellectual disability (2). The common cause of mortality was respiratory disease (51.1%), followed by dementia (22.2%), and this information was not consistent with data by Cooper et al. Methodological difference of survey, including definition, might contribute to the statistical information.
Second, de Campos Gomes et al. analyzed mortality and related factors in individuals with Down syndrome in Brazil (3). They concluded that ethnic factors and years of schooling influenced mortality across the administrative regions. Different region has ethnic difference and different races, which would contribute to educational difference and medical service. These factors would relate each other, and contribute mortality in individuals with Down syndrome.
Regarding complication in Down syndrome, congenital heart defects (CHDs) should be classified to typical and atypical CHDs for mortality risk (4). Atypical CHDs include aortic coarctation and univentricular hearts, and survival rate at 10 and 40 years in patients with typical CHDs were 99% and 98%, which were significantly higher than those in patients with atypical CHDs, presenting 91% and 84%. Complication might contribute to prognosis in individuals of Down syndrome, which had been also recognized (1, 5).
Finally, Hithersay et al. examined factors associated with dementia in Down syndrome adults (6). Hazard ratio (HR) (95% CI) of APOE ε4 carriers for mortality in Down syndrome adults with dementia was 6.91 (1.756, 27.195). In addition, HR (95% CI) of epilepsy for mortality in Down syndrome adults without dementia was 9.66 (1.59, 58.56). Furthermore, HRs (95% CIs) of APOE ε4 carriers, adults with early-onset epilepsy, multiple health comorbidities, and those living with family for earlier dementia diagnoses were 4.91 (2.53, 9.56), 3.61 (1.12, 11.60), 1.956 (1.087, 3.519), and 2.14 (1.08, 4.20), respectively. Dementia was the most common causes of mortality in Down syndrome adults (1), and factors of earlier dementia diagnoses were specified.
References
1. BMJ Open. 2020;10(5):e036465. doi:10.1136/bmjopen-2019-036465
2. Am J Intellect Dev Disabil. 2018;123(1):61-71. doi:10.1352/1944-7558-123.1.61
3. J Intellect Disabil Res. 2020 May 7. doi:10.1111/jir.12735
4. Am J Med Genet A. 2020 Apr 22. doi:10.1002/ajmg.a.61586
5. J Appl Res Intellect Disabil. 2020;33(3):420-429. doi:10.1111/jar.12684
6. JAMA Neurol. 2019;76(2):152-160. doi:10.1001/jamaneurol.2018.3616
Increased TV watching is dangerous to your CV health. What about other sedentary activities, such as reading? In particular, reading medical journal articles?
The study is clearly an explanatory sequential design using a QUANT and a QUAL phase. However, the title and the abstract design states that this is an exploratory study. Looking further down at the methods section, the authors state that "This mixed-methods study used an explanatory sequential design and involved two phases "
We thank professor Kawada for the constructive remarks.
Indeed, women presented with more subthreshold or clinical insomnia than men (14.9% and 6.3%, vs. 11.6% and 4.4%, p=0.003, while men presented more frequently with depression (14.0% vs 10.1%, p=0.001). We ran the multivariable models stratifying on gender, and we assessed possible interactions between gender and insomnia / depression. The results show no significant (p<0.05) interaction, although a trend for a higher OR among women was noted for depression when fatigue was categorized using the threshold of 5 of the fatigue scale questionnaire (Table provided upon request). Hence, we believe that the results obtained using the model adjusting for gender are adequate.
Regarding sleep duration, we agree it is an important issue and that future studies on fatigue should include an adequate estimation of the mean sleep duration.
Pedro Marques-Vidal, on behalf of all authors
I read the recently published systematic review on Injection therapy for base of thumb osteoarthritis: a systematic review and meta-analysis published in BMJ Open[1] with interest. It follows hot on the heels of 6 other previous published systematic reviews on the same subject, 3 on exactly the same subject of injection therapy in base of thumb osteoarthritis[2–5] and 3 others that included injections amongst all non-surgical or conservative therapies[6–8]. The conclusion of all 7 reviews is, not surprisingly, consistent in determining the level of evidence is poor, a conclusion which we can all agree on, however the other conclusion that there is no evidence steroid injections confer any benefit, is in contrast to the outcomes of non-randomised studies and with clinical experience.
Show MoreI believe the disconnect occurs due to the long-term outcome measures used in the assessment of outcomes usually recorded at 26 weeks. Longitudinal studies of the effect of steroid injections in base of thumb osteoarthritis (CMCJ OA) accord with clinical experience in that that the best outcomes were measured at 4 weeks (76% better at 4 weeks[9], with 2/3 better at 8 weeks, ½ at 12 weeks but only 1/6 at 26 weeks[5],. So, by assessing outcomes at 26 weeks, the pain-relieving effects of steroid have already dissipated.
Another variation that needs to be considered but was not discussed is the different formulations and doses of corticosteroids used in the study as these vary in anti-i...
Hackett et al. conducted a prospective study to evaluate the association between disability discrimination and well-being (1). Adjusted odds ratio (95% confidence interval [CI]) of disability discrimination for depression and fair/poor self-rated health were 5.40 (3.25 to 8.97) and 2.05 (1.19 to 3.51), respectively. In addition, standardized regression coefficients (95% CI) of disability discrimination for psychological distress, mental functioning, and life satisfaction were 3.28 (2.41 to 4.14), -7.35 (-9.70 to -5.02) and -1.27 (-1.66 to -0.87), respectively. Prospectively, disability discrimination was also significantly associated with increased psychological distress and poorer mental functioning by adjusting for baseline scores. I have some concerns about their study.
Gill et al. conducted a prospective study to evaluate potential risk factors for severe disability (2). Hazard ratio (HR) (95% CI) of persons with ≥85 years old, hearing impairment, frailty, cognitive impairment, low functional self-efficacy and low peak flow for progressive disability were 1.6 (1.1-2.4), 1.7 (1.0-2.8), 2.4 (1.6-3.7), 2.0 (1.3-3.1), 1.8 (1.2-2.8), and 1.7 (1.2-2.4), respectively. In addition, HR (95% CI) of persons with visual impairment, hearing impairment, poor physical performance, and low peak flow for catastrophic disability were 1.4 (1.1-1.8), 1.3 (1.0-1.7), 1.8 (1.3-2.5), 1.3 (1.0-1.7), respectively. To avoid severe disability, appropriate interventions for modifiable facto...
Show MoreBarker et al. conducted a review to investigate risk-benefit assessment of aspirin for fracture (1). Pooled odds ratio (95% CI) of aspirin use for any fracture was 0.83 (0.70 to 0.99). There was a tendency of the association between aspirin use and total hip bone mineral density (BMD). Similar results were observed for lumbar spine BMD. I have some concerns about their study.
I understand that fracture risk includes BMD, but other psycho-physiological factors also attribute to fracture such as physical balance, muscle strength and mental instability. Aspirin use might modify the level of physical fitness and lead to the benefits of reduced fracture risk and increased trend of BMD. Barker et al. included a cross-sectional study by Bonten et al., to evaluate the effect of low-dose aspirin on BMD (2). There was no difference between aspirin users and non-users for vertebral BMD in men and women. They speculated that the risk of fractures observed in aspirin users in previous studies might not be directly related to BMD.
Chin summarized the effect of aspirin use on bone health (3). Although aspirin could prevent bone loss in animal models of osteoporosis, human epidemiological studies regarding aspirin used and fracture risk were limited, and the effect of aspirin use on fracture prevention has been inconclusive. On this point, Barker et al. presented precise information on the relationship. Each component of a meta-analysis should be added for stable estimation....
Show MoreWe thank Professor Kawada for his interest in our study.(1) We agree that the three recent papers he quotes are interesting studies that make important contributions. We do not agree with his expression of concerns about our study as they seem to reflect an assumption that different reporting to the papers he quoted were the concerns; these studies are not comparable to ours.
Oppewal et al. studied only elderly people,(2) whilst our study was of adults aged 16 years and over; their study included people using three care providers, whilst ours was population based. Oppewal et al. gathered cause of death information from medical case-files, and acknowledged, amongst other limitations, that information on cause of death in these files was sometimes limited which was beyond their control. Indeed they reported immediate and primary (underlying) cause of death, but not contributing causes of death, raising the question of whether it was possible for them to distinguish underlying and contributing causes of death from the case-files. We found the most common underlying causes of death for the adults with Down syndrome were dementia (35.1%), then other infection (12.3%); but when considering all contributing causes of death (not just the underlying cause), we found the most common after Down syndrome to be dementia (42.1%), and respiratory infection (38.6%) (reported in our table 5).
In a study published in the same month as ours, De Campos Gomes et al. reported hig...
Show MoreVery nice work by the authors. Perhaps they could provide additional details about the methods used here to test particle filtration.
Aslam et al. conducted a prospective study to assess the association between milk/total dairy consumption and major osteoporotic fracture (MOF) in women (1). The authors handled women aged ≥50 years, and MOFs (hip, forearm, clinical spine and proximal humerus) were confirmed radiologically. Consuming >500 mL/d of milk was not significantly associated with increased HR for MOF. In addition, adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of Non-milk drinkers against drinkers consuming <250 mL/d of milk and consumption of ≥800 g/d total dairy against 200-399 g/d of total dairy for MOF were 1.56 (0.99 to 2.46) and 1.70 (0.99 to 2.93), respectively. They concluded that there was a trend for increased MOF in women with zero milk and higher total dairy consumption. I want to present results from recent meta-analyses.
Malmir et al. summarized the association of milk and dairy intake with risk of osteoporosis and hip fracture (2). There was an inverse relationship of milk and dairy intake with risk of osteoporosis and hip fracture in cross-sectional and case-control studies. By meta-regression analysis, every additional 200-gram intake of dairy and milk were associated with a 22% and 37% reduced risk of osteoporosis, respectively. In addition, milk consumption was associated with a 25% reduced risk of hip fracture. In contrast, the significance disappeared in cohort studies, and a greater intake of milk and dairy products did not reduce the risk of osteo...
Show MoreCooper et al. investigated clinical predictors of mortality in adults with intellectual disabilities (1). Standardized mortality ratios (SMRs) (95% confidence interval [CI]) in Down syndrome adults and adults without Down syndrome were 5.28 (3.98, 6.57) and 1.93 (1.68, 2.18), respectively. In addition, SMRs in males and females were 1.69 (1.42, 1.95) and 3.48 (2.90, 4.06), respectively. Aspiration/reflux/choking and respiratory infection were the most common causes of mortality in adults without Down syndrome, and dementia was the most common causes of mortality in Down syndrome adults. Mortality risk related to percutaneous endoscopic gastrostomy/tube fed, Down syndrome, diabetes, lower respiratory tract infection at cohort-entry, smoking, epilepsy, hearing impairment, increasing number of prescribed drugs, increasing age were related to mortality in adults with intellectual disabilities. I have some concerns about their study.
First, Oppewal et al. also reported the cause-specific mortality of older Down syndrome adults with intellectual disability (2). The common cause of mortality was respiratory disease (51.1%), followed by dementia (22.2%), and this information was not consistent with data by Cooper et al. Methodological difference of survey, including definition, might contribute to the statistical information.
Second, de Campos Gomes et al. analyzed mortality and related factors in individuals with Down syndrome in Brazil (3). They concluded that ethn...
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