Suchergebnisse

The past century has witnessed a revolution. Less than a hundred years ago, the average Western life expectancy was 40; now it is 80. And there is no end in sight: the first person who will reach 135 has already been born. It's the most radical change in our society since industrialisation, and naturally it raises many questions. What do longer life spans mean for the way we organise our societies? How can people best prepare themselves for living considerably longer? Does it help to eat less, or to take hormones, vitamins, or minerals? And what can we learn from old people who remain full

Nie zuvor sind die Menschen so alt geworden wie heute. Und ein Ende ist nicht in Sicht: Jede Woche fügen wir ein Wochenende zu unserer Lebenszeit hinzu, ohne dass die kranke Zeit im Alter zunimmt. 75 ist das neue 65. Aber haben wir auf das lange Leben schon die richtigen Antworten? Kann man mit 75 noch ein neues Leben anfangen? Der prominente niederländische Altersmediziner Rudi Westendorp erklärt, wie es dazu kam, dass "Älter werden" und "Alt sein" nicht mehr dasselbe sind, und wie wir mit der Explosion unserer Lebenserwartung umgehen können. Wie kaum jemand vor ihm beleuchtet er das Phänomen

n/a

The COVID-19 pandemic has presented us with a unique opportunity to examine how societies manage urgent biological risk. While evaluating the available evidence is an important aspect of risk analysis, the resultant political decisions may contain certain biases and blind spots; thus, when they are experienced in everyday life, public-health measures may not consider the lived experience of those whom the decisions affect. As such, the pandemic has also provided us with an opportunity to learn how people experience risk-adverse public-health measures, and how they manage uncertainty. In Denmark, for example, the government's response included a risk-adverse approach that labelled people age 65+ as one of the population groups most 'at risk' for infection. But what are older people's (phenomenological) experiences of being categorised in a 'high-risk' group? This paper is based on telephone interviews with 32 people across Denmark, including 14 people (eight women and six men) between the ages of 65 and 83, which were conducted to gain insight into how the pandemic and the first months of the societal lockdown in Denmark affected their mental health, everyday behaviour, and social lives (both in person and on the internet/social media). We describe how, in response to unclear biopolitical discourses and decisions being made for 'their own good,' older people reclaimed their agency by evaluating their individual circumstances to determine their own situated risk and to manage this existential uncertainty on their own terms. Our reflections focus on the consequences of the current pandemic on older lives, and particularly how governments – when faced with future public-health crises – can implement fairer preventative measures that consider the societal value and capabilities of older people.

Background: While the field of rehabilitation has determined a common definition of professional practice, legislators and healthcare professionals in various Western countries have struggled to reach consensus about how the newer offer of 'reablement' should be organised, operationalised, and understood as a health service for older adults. International research indicates that there is confusion, ambiguity, and disagreement about the terminology and the structure of these programmes, and they may not be adequately supporting older people's self-identified goals. Could an analysis of the concept's genealogy illuminate how reablement can be more effective and beneficial in theory and in practice? Methods: We conducted a qualitative and quantitative scoping review to determine how reablement has developed through time and space. Eligible articles (n=86) had to focus on any of the defined features of current reablement programmes; there were no restrictions on study designs or publication dates. In articles published from 1947–2019, we identified themes and patterns, commonalities, and differences in how various countries described and defined reablement. We also performed an analysis using computer software to construct and visualise term maps based on significant words extracted from the article abstracts. Results: The fundamental principles of reablement have a long history. However, these programmes have undergone a widespread expansion since the mid-2000s with an intention to reduce costs related to providing long-term care services and in-home assistance to growing older populations. Despite theoretical aspirations to offer person-centred and goal-directed reablement, few countries have been able to implement programmes that adequately promote older people's goals, social involvement, or participation in their local community in a safe, culturally sensitive and adaptable way. Conclusions: Reablement is meant to support older people in attaining their self-defined goals to be both more physically independent at home and socially involved in their communities. However, until legislators, health professionals, and older people can collectively reach consensus about how person-centred reablement can be more effectively implemented and supported in professional homecare practice, it will be difficult to determine a conceptual description of reablement as a service that is unique, separate, and distinct from standard rehabilitation.

AbstractThrough its ability to induce the enhanced release and production of cytokines, amyloid-β is responsible for the chronic inflammatory response that contributes to Alzheimer's disease (AD). Determining whether the response of monocytes to amyloid-β stimulation is under genetic control may help understand the basis of why some people are more prone to develop neuronal degeneration than others. In the current study we investigated the heritability of the cytokine (IL-10, IL-6, IL-1β, IL-1ra, TNF-[.alpha]) production capacity upon ex vivo stimulation with amyloid-β in whole blood samples of 222 twins and 85 singleton siblings from 139 extended twin families. It was found that individual differences in amyloid-β-induced cytokine production capacity are to a large extent of genetic origin, with heritability estimates ranging from 55% (IL-1β) to 68% (IL-6). We conclude that genes influencing amyloid-β-induced cytokine response may provide clues to the progression of AD pathology.

BACKGROUND: Road traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution. METHODS: Twenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (Lden [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM2.5 and PM10], nitrogen dioxide [NO2], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of Lden preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government's maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential Lden thresholds. RESULTS: Of 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of Lden and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98-1.14) per 10 dB, which attenuated to 1.01 (0.93-1.09) and 1.00 (0.91-1.09) in models further adjusted for PM2.5 or NO2, respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between Lden and stroke. CONCLUSIONS: Long-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air pollution.

BACKGROUND: Road traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution. METHODS: Twenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (L(den) [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM(2.5) and PM(10)], nitrogen dioxide [NO(2)], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of L(den) preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government's maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential L(den) thresholds. RESULTS: Of 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of L(den) and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98–1.14) per 10 dB, which attenuated to 1.01 (0.93–1.09) and 1.00 (0.91–1.09) in models further adjusted for PM(2.5) or NO(2), respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between L(den) and stroke. CONCLUSIONS: Long-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air ...

Background: Road traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution. Methods: Twenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (L den [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM 2.5 and PM 10 ], nitrogen dioxide [NO 2 ], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of L den preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government's maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential L den thresholds. Results: Of 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of L den and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98–1.14) per 10 dB, which attenuated to 1.01 (0.93–1.09) and 1.00 (0.91–1.09) in models further adjusted for PM 2.5 or NO 2 , respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between L den and stroke. Conclusions: Long-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air pollution.

It has been postulated that aging is the consequence of an accelerated accumulation of somatic DNA mutations and that subsequent errors in the primary structure of proteins ultimately reach levels sufficient to affect organismal functions. The technical limitations of detecting somatic changes and the lack of insight about the minimum level of erroneous proteins to cause an error catastrophe hampered any firm conclusions on these theories. In this study, we sequenced the whole genome of DNA in whole blood of two pairs of monozygotic (MZ) twins, 40 and 100 years old, by two independent next-generation sequencing (NGS) platforms (Illumina and Complete Genomics). Potentially discordant single-base substitutions supported by both platforms were validated extensively by Sanger, Roche 454, and Ion Torrent sequencing. We demonstrate that the genomes of the two twin pairs are germ-line identical between co-twins, and that the genomes of the 100-year-old MZ twins are discerned by eight confirmed somatic single-base substitutions, five of which are within introns. Putative somatic variation between the 40-year-old twins was not confirmed in the validation phase. We conclude from this systematic effort that by using two independent NGS platforms, somatic single nucleotide substitutions can be detected, and that a century of life did not result in a large number of detectable somatic mutations in blood. The low number of somatic variants observed by using two NGS platforms might provide a framework for detecting disease-related somatic variants in phenotypically discordant MZ twins.