Sarcopenia predicts 5-year mortality in older adults with intellectual disabilities

Background: People with intellectual disabilities (ID) have a lower life expectancy than their peers without ID. A contributing factor to the lower life expectancy and early mortality could be sarcopenia: low muscle mass and low muscle function. In the general population, sarcopenia strongly predicts early mortality, but this association is unknown in people with ID. Therefore, this study aims to explore the association between sarcopenia and 5-year mortality in older adults with ID. Methods: In the Healthy Ageing and Intellectual Disabilities (HA-ID) study, the prevalence of sarcopenia was measured at baseline among 884 older adults (≥50 years) with ID. All-cause mortality was measured over a 5-year follow-up period. Univariable and multivariable Cox proportional hazard models were applied to determine the association between sarcopenia (no sarcopenia, pre-sarcopenia, sarcopenia, severe sarcopenia) and early mortality, adjusted for age, sex, level of ID, presence of Down syndrome, and co-morbidity (chronic obstructive pulmonary disease, diabetes type 2 and metabolic syndrome). Results: The unadjusted hazard ratio (HR) for sarcopenia was 2.28 [95% confidence interval (CI) 1.48–3.42], P &lt; 0.001), and 2.40 (95% CI 1.40–4.10, P = 0.001) for severe sarcopenia. When adjusted for age, sex, level of ID, and Down syndrome, sarcopenia (HR = 1.72, 95% CI 1.08–2.75, P = 0.022) and severe sarcopenia (HR = 1.86, 95% CI 1.07–3.23, P = 0.028) were significantly associated with early mortality. When additionally adjusted for co-morbidity, the adjusted HR decreased to 1.62 (95% CI 1.02–2.59, P = 0.043) and 1.81 (95% CI 1.04–3.15, P = 0.035) for sarcopenia and severe sarcopenia, respectively. Conclusion: Sarcopenia is an independent risk factor for early mortality in older adults with ID over a 5-year follow-up period. Our results stress the need to delay the incidence and development of sarcopenia in older adults with ID.</p

Macronutrient intake and frailty: the Rotterdam Study.

PURPOSE To investigate the longitudinal association between the macronutrient composition of the diet and frailty. METHODS Data were obtained from 5205 Dutch middle-aged and older adults participating in the Rotterdam Study. Frailty was measured using a frailty index based on the accumulation of 38 health-related deficits, score between 0 and 100, and a higher score indicating more frailty. Frailty was assessed at baseline and 11 years later (range of 23 years). Macronutrient intake was assessed using food-frequency questionnaires. The association between macronutrients and frailty over time was evaluated using multivariable linear regression, adjusted for the frailty index at baseline, energy intake, and other relevant confounders. All analyses were performed in strata of BMI. RESULTS Median frailty index score was 13.8 points (IQR 9.6; 19.1) at baseline and increased by a median of 2.3 points (IQR - 2.0; 7.6) after 11 years. Overall, we found no significant associations between intake of carbohydrates or fat and frailty over time. We did observe a significant positive association between an iso-energetic intake of 10 g protein and frailty over time (β 0.31 (95% CI 0.06; 0.55)) which was mainly driven by animal protein (β 0.31 (95% CI 0.07; 0.56)). It did not depend on whether it was substituted fat or carbohydrates. CONCLUSIONS Our findings suggest that a reduction in the intake of animal protein may improve the overall health status over time in a relatively healthy population. More research is needed on the optimal macronutrient composition of the diet and frailty in more vulnerable populations

Sarcopenia and Sarcopenic Obesity and Mortality Among Older People

Importance: Sarcopenia and obesity are 2 global concerns associated with adverse health outcomes in older people. Evidence on the population-based prevalence of the combination of sarcopenia with obesity (sarcopenic obesity [SO]) and its association with mortality are still limited. Objective: To investigate the prevalence of sarcopenia and SO and their association with all-cause mortality. Design, Setting, and Participants: This large-scale, population-based cohort study assessed participants from the Rotterdam Study from March 1, 2009, to June 1, 2014. Associations of sarcopenia and SO with all-cause mortality were studied using Kaplan-Meier curves, Cox proportional hazards regression, and accelerated failure time models fitted for sex, age, and body mass index (BMI). Data analysis was performed from January 1 to April 1, 2023. Exposures: The prevalence of sarcopenia and SO, measured based on handgrip strength and body composition (BC) (dual-energy x-ray absorptiometry) as recommended by current consensus criteria, with probable sarcopenia defined as having low handgrip strength and confirmed sarcopenia and SO defined as altered BC (high fat percentage and/or low appendicular skeletal muscle index) in addition to low handgrip strength. Main Outcome and Measure: The primary outcome was all-cause mortality, collected using linked mortality data from general practitioners and the central municipal records, until October 2022. Results: In the total population of 5888 participants (mean [SD] age, 69.5 [9.1] years; mean [SD] BMI, 27.5 [4.3]; 3343 [56.8%] female), 653 (11.1%; 95% CI, 10.3%-11.9%) had probable sarcopenia and 127 (2.2%; 95% CI, 1.8%-2.6%) had confirmed sarcopenia. Sarcopenic obesity with 1 altered component of BC was present in 295 participants (5.0%; 95% CI, 4.4%-5.6%) and with 2 altered components in 44 participants (0.8%; 95% CI, 0.6%-1.0%). An increased risk of all-cause mortality was observed in participants with probable sarcopenia (hazard ratio [HR], 1.29; 95% CI, 1.14-1.47) and confirmed sarcopenia (HR, 1.93; 95% CI, 1.53-2.43). Participants with SO plus 1 altered component of BC (HR, 1.94; 95% CI, 1.60-2.33]) or 2 altered components of BC (HR, 2.84; 95% CI, 1.97-4.11) had a higher risk of mortality than those without SO. Similar results for SO were obtained for participants with a BMI of 27 or greater. Conclusions and Relevance: In this study, sarcopenia and SO were found to be prevalent phenotypes in older people and were associated with all-cause mortality. Additional alterations of BC amplified this risk independently of age, sex, and BMI. The use of low muscle strength as a first step of both diagnoses may allow for early identification of individuals at risk for premature mortality.</p

Sarcopenic obesity research perspectives outlined by the sarcopenic obesity global leadership initiative (SOGLI) – Proceedings from the SOGLI consortium meeting in rome November 2022

The European Society for Clinical Nutrition and Metabolism (ESPEN) and the European Association for the Study of Obesity (EASO) launched the Sarcopenic Obesity Global Leadership Initiative (SOGLI) to reach expert consensus on a definition and diagnostic criteria for Sarcopenic Obesity (SO). The present paper describes the proceeding of the Sarcopenic Obesity Global Leadership Initiative (SOGLI) meeting that was held on November 25th and 26th, 2022 in Rome, Italy. This consortium involved the participation of 50 researchers from different geographic regions and countries. The document outlines an agenda advocated by the SOGLI expert panel regarding the pathophysiology, screening, diagnosis, staging and treatment of SO that needs to be prioritized for future research in the field

Risk thresholds for alcohol consumption : combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies

Background Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease. Methods We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies. Findings In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1.14, 95% CI, 1.10-1.17), coronary disease excluding myocardial infarction (1.06, 1.00-1.11), heart failure (1.09, 1.03-1.15), fatal hypertensive disease (1.24, 1.15-1.33); and fatal aortic aneurysm (1.15, 1.03-1.28). By contrast, increased alcohol consumption was loglinearly associated with a lower risk of myocardial infarction (HR 0.94, 0.91-0.97). In comparison to those who reported drinking >0-100-200-350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively. Interpretation In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines. Copyright (C) The Author(s). Published by Elsevier Ltd.Peer reviewe

Dietary Protein, Exercise, and Frailty Domains

Increasing awareness of the impact of frailty on elderly people resulted in research focusing on factors that contribute to the development and persistence of frailty including nutrition and physical activity. Most effort so far has been spent on understanding the association between protein intake and the physical domain of frailty. Far less is known for other domains of frailty: cognition, mood, social health and comorbidity. Therefore, in the present narrative review, we elaborate on the evidence currently known on the association between protein and exercise as well as the broader concept of frailty. Most, but not all, identified studies concluded that low protein intake is associated with a higher prevalence and incidence of physical frailty. Far less is known on the broader concept of frailty. The few studies that do look into this association find a clear beneficial effect of physical activity but no conclusions regarding protein intake can be made yet. Similar, for other important aspects of frailty including mood, cognition, and comorbidity, the number of studies are limited and results are inconclusive. Future studies need to focus on the relation between dietary protein and the broader concept of frailty and should also consider the protein source, amount and timing

Dietary Patterns and Healthy Aging

The increased life expectancy in the last two centuries has led to a shift in age distribution. However, the additional life years are not always healthy life years, as aging is often accompanied by chronic diseases, cognitive decline, increased dependency, and frailty. Because these age-related conditions heavily influence individuals' quality of life and pose a large burden on society, healthy aging has become a major public health challenge. One of the key modifiable factors that influence healthy aging is nutrition. Traditionally, research on nutrition has focused on the effects of single foods or nutrients on health outcomes. Nevertheless, foods are combined into meals and meals constitute a dietary pattern. Studies on dietary patterns take into account quantities and combinations of foods, food groups, and nutrients, allowing for possible interaction effects. In this chapter we summarize what is known about the effects of dietary patterns on healthy aging. First, the current evidence on the association between dietary patterns and age-related diseases is summarized. Then, the associations of dietary patterns with comprehensive healthy aging indicators, including sarcopenia, inflammation, and frailty, are discussed.</p

Development and validation of a shortened and practical frailty index for people with intellectual disabilities

Background: There is no widely used instrument to detect frailty in people with intellectual disabilities (IDs). We aimed to develop and validate a shorter and more practical version of a published frailty index for people with IDs. Method: This study was part of the longitudinal ‘Healthy Ageing and Intellectual Disability’ study. We included 982 people with IDs aged 50 years and over. The previously developed and validated ID-Frailty Index consisting of 51 deficits was used as the basis for the shortened version, the ID-FI Short Form. Content of the ID-FI Short Form was based on statistics and clinical and practical feasibility. We evaluated the precision and validity of the ID-FI Short Form using the internal consistency, the correlation between the ID-FI Short Form and the original ID-Frailty Index, the agreement in dividing participants in the categories non-frail, pre-frail and frail, and the association with survival. Results: Seventeen deficits from the original ID-Frailty Index were selected for inclusion in the ID-FI Short Form. All deficits of the ID-FI Short Form are clinically and practically feasible to assess for caregivers and therapists supporting people with ID. We showed acceptable internal consistency with Cronbach's alpha of 0.75. The Pearson correlation between the ID-Frailty Index and the ID-FI Short Form was excellent (r = 0.94, P < 0.001). We observed a good agreement between the full and short forms in dividing the participants in the frailty categories, with a kappa statistic of 0.63. The ID-FI Short Form was associated with survival; with every 1/100 increase on the ID-FI Short Form, the mortality probability increased by 7% (hazard ratio 1.07, P < 0.001). Conclusion: The first validation of the ID-FI Short Form shows it to be a promising, practical tool to assess the frailty status of people with ID