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seven - Understanding immunesenescence
- Edited by Alan Walker, The University of Sheffield
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- Book:
- The New Dynamics of Ageing Volume 2
- Published by:
- Bristol University Press
- Published online:
- 13 April 2022
- Print publication:
- 25 July 2018, pp 107-130
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Summary
Introduction
With the ageing of the population, hip fractures are a growing issue in the UK (Dennison et al, 2006). At least half of older adults who have suffered a hip fracture never regain their previous function (Stevens and Olson, 2000), with mortality at one year after the fracture recorded as high as 33 per cent (Roche et al, 2005). The factors influencing recovery from hip fracture are poorly understood. These include depression, a common co-morbidity in these patients (Nightingale et al, 2001).
The prevalence rate for depression in people who have had a hip fracture across eight US and UK studies ranged from 9 to 47 per cent (Holmes and House, 2000). Importantly, depression in people who have suffered a hip fracture has been associated with increased risk of infections and poor survival (Nightingale et al, 2001), impaired recovery and a reduced ability to regain pre-fracture levels of physical functioning (Mossey et al, 1990).
It is well documented that ageing is accompanied by poor functioning of the body's immune system (Dorshkind et al, 2009; Panda et al, 2009). This is called immunesenescence, or immune ageing, and contributes to the increased risk of infection in old age (Gavazzi and Krause, 2002). Particular aspects of immune ageing can be observed in specific important immune system cells. For example, neutrophils are key cells in the immune system that are responsible for providing protection against bacteria such as those that cause hospital-acquired infections and pneumonia. Ageing is accompanied by a decline in neutrophil ability to ingest such bacteria (Butcher et al, 2001), and their ability to kill the bacteria once ingested (Tortorella et al, 2000). Similar reductions in efficacy have been shown in other immune cells, such as monocytes, with advancing age (Shaw et al, 2011).
An additional important component of the immune system are natural killer (NK) cells, which are capable of destroying cancer cells and cells infected with viruses (Farag et al, 2003). Older adults have an age-related decrease in NK cell function (Hazeldine et al, 2012), which may explain why they are more susceptible to cancer and virus infections such as influenza.
four - Maintaining health and well-being: overcoming barriers to healthy ageing
- Edited by Alan Walker, The University of Sheffield
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- Book:
- The New Science of Ageing
- Published by:
- Bristol University Press
- Published online:
- 04 March 2022
- Print publication:
- 29 August 2014, pp 113-154
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Summary
This chapter concentrates on health and well-being, drawing on 11 New Dynamics of Ageing (NDA) projects covering the whole range, from basic biology to the arts and humanities. Our main purpose is to employ the findings from our projects to examine the barriers to healthy ageing and how to overcome them. By way of introduction to this discussion of healthy ageing we first consider some key concepts in this field: ageing and ill health, older age, quality of life and subjective well-being. We begin with an overview of the main demographic changes that underline the importance of research on healthy ageing.
Key concepts for healthy ageing
Demographic changes
Major demographic shifts are currently under way in countries of the developed world such as the UK. In the 25-year period from 1985 to 2010 the number of adults aged over 65 in the UK increased by 1.7 million, and the number of those aged over 85 almost doubled to 1.4 million (ONS, 2011a). This is partly due to improvements in mortality leading to higher numbers in old age. Life expectancy is increasing at a rate of two years per decade in developed societies. However, there are sharply divergent views about how trends in life expectancy may develop during this century. For example, Christensen et al (2009, p 1196) pointed out, ‘if the pace of increase in life expectancy in developed countries over the past two centuries continues through the 21st century, most babies born since 2000 … [in] countries with long life expectancies will celebrate their 100th birthdays … research suggests that ageing processes are modifiable and that people are living longer without severe disability.’ On the other hand, Olshansky et al (2005, p 1142) stated, ‘as a result of the substantial rise in the prevalence of obesity and its life-shortening complications such as diabetes, life expectancy at birth and at older ages could level off or even decline within the first half of this century’.
The magnitude and implications of population ageing depend heavily on the magnitude of mortality improvement in decades to come. At present, overall age-standardised mortality rates (both sexes combined) are improving at about 2.5 per cent per annum in the UK (based on ONS, 2012a), but current trends are heavily influenced by patterns at ages where deaths are concentrated.
two - Understanding ageing: biological and social perspectives
- Edited by Alan Walker, The University of Sheffield
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- Book:
- The New Science of Ageing
- Published by:
- Bristol University Press
- Published online:
- 04 March 2022
- Print publication:
- 29 August 2014, pp 25-76
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Summary
Introduction
In this chapter, we discuss how social and biological studies of ageing can converge to provide a meaningful framework for progress in both understanding ageing and dealing with it in a positive manner. We start by discussing the meaning of the term ‘ageing’ and how it is in part defined by social context, and then, how psychosocial factors have an impact on both perception and the biological reality of ageing. From a theoretical perspective, we assess how ageing might have evolved, and how it is measured. The biological impacts of ageing are then described, moving from individual cells through tissues to major organ systems (immune, cardiovascular and nervous systems) (see Figure 2.1). What causes individual cells of the body to age is dealt with at both a cellular and molecular level, and we further discuss how studies of both extremely long-lived and short-lived humans have contributed significantly not only to our understanding of the biological processes of ageing, but also to the possibility of developing therapies to deal with the problems that cause greatest loss of quality of life in older age. We end by assessing the ethical case for intervening in those biological processes underpinning the development of those illnesses that so undermine health in later life.
Given the enormous scope and breadth of material that is covered, and the wide differences in perspectives and language used by the diverse disciplines that contribute to this chapter, we have tried to avoid jargon terms wherever possible, and provide simple definitions of unavoidable terminology as notes at the end of the chapter to assist the reader not specialist in that particular field.
Not ‘what’ is ageing, but ‘how’?
In order to study ageing in any meaningful way, we need to understand how the term ‘ageing’ is being used. To biologists, it can mean damage to molecules of the cell, and to cells of the tissue; to the physiologist, alterations in organ function; to the clinician, increased frailty and accumulation of diverse diseases. For the older person, ageing is felt and experienced, with changes in physical abilities and social activities and status having both positive and negative effects on the quality of their later life. Ageing is thus not so much a thing, but rather multi-dimensional, underpinned by complex social and biological processes, made up of many different mechanisms.
Contributors
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- By Carolin Biewer, Charles Boberg, Sean Bowerman, John Corbett, Felicity Cox, Hubert Devonish, Elizabeth Gordon, Ulrike Gut, Raymond Hickey, William A. Kretzschmar, Manfred Krug, Claudia Lange, Lisa Lim, Charles F. Meyer, Sallyanne Palethorpe, Anna Rosen, Josef Schmied, Daniel Schreier, Jane Stuart-Smith, Ewart A. C. Thomas, Ingrid Tieken-Boon van Ostade, Clive Upton
- Edited by Raymond Hickey, Universität Duisburg–Essen
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- Book:
- Standards of English
- Published online:
- 05 January 2013
- Print publication:
- 06 December 2012, pp xiv-xx
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The influence of selenium-enriched milk proteins and selenium yeast on plasma selenium levels and rectal selenoprotein gene expression in human subjects
- Ying Hu, Graeme H. McIntosh, Richard K. Le Leu, Jane M. Upton, Richard J. Woodman, Graeme P. Young
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- Journal:
- British Journal of Nutrition / Volume 106 / Issue 4 / 28 August 2011
- Published online by Cambridge University Press:
- 30 March 2011, pp. 572-582
- Print publication:
- 28 August 2011
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Certain forms of dietary Se may have advantages for improving human Se status and regulating the risk for disease, such as cancers, including colorectal cancer (CRC). The present study compared the effects of a Se-enriched milk protein (dairy-Se) with a Se-rich yeast (yeast-Se) on plasma Se levels and rectal selenoprotein gene expression since we reasoned that if these genes were not regulated, there was little potential for regulating the risk for CRC in this organ. A total of twenty-three healthy volunteers with plasma Se in the lower half of the population range were supplemented with dairy-Se (150 μg/d) or yeast-Se (150 μg/d) for 6 weeks, followed by 6 weeks of washout period. Blood was sampled every 2 weeks, and rectal biopsies were obtained before and after Se supplementation and after the washout period. Plasma Se levels and glutathione peroxidase (GPx) activity, and rectal mRNA of selenoprotein P (SeP), cytosolic GPx-1 (GPx-1), gastrointestinal GPx-2 (GPx-2) and thioredoxin reductase-1 (TrxR-1) were measured. Plasma Se levels increased rapidly in both Se groups (P < 0·001); plasma GPx activity was not significantly changed. Rectal SeP mRNA increased at 6 weeks compared with baseline in both Se groups (P < 0·05); only dairy-Se resulted in a sustained elevation of SeP after the washout period (P < 0·05). Rectal GPx-1 and GPx-2 mRNA were higher with dairy-Se (P < 0·05) than with yeast-Se at 6 weeks. In conclusion, three rectal selenoprotein mRNA were differentially regulated by dairy-Se and yeast-Se. Changes in rectal selenoproteins are not predicted by changes in plasma Se; dairy-Se effectively regulates the expression of several rectal selenoproteins of relevance to the risk for CRC.