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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">Front. Ag. Neurosci.</journal-id>
<journal-title>Frontiers in Aging Neuroscience</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Ag. Neurosci.</abbrev-journal-title>
<issn pub-type="epub">1663-4365</issn>
<publisher>
<publisher-name>Frontiers Research Foundation</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.3389/fnagi.2011.00003</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Neuroscience</subject>
<subj-group>
<subject>Opinion Article</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Healthy Aging as Disease?</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name><surname>Nieuwenhuis-Mark</surname> <given-names>Ruth Elaine</given-names></name>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
<xref ref-type="author-notes" rid="fn001">&#x0002A;</xref>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup><institution>Department of Medical Psychology and Neuropsychology, Tilburg University</institution> <country>Tilburg, Netherlands</country></aff>
<author-notes>
<fn fn-type="corresp" id="fn001"><p>&#x0002A;Correspondence: <email>r.e.mark&#x00040;uvt.nl</email></p></fn>
</author-notes>
<pub-date pub-type="epub">
<day>22</day>
<month>02</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="collection">
<year>2011</year>
</pub-date>
<volume>3</volume>
<elocation-id>3</elocation-id>
<history>
<date date-type="received">
<day>02</day>
<month>08</month>
<year>2010</year>
</date>
<date date-type="accepted">
<day>11</day>
<month>02</month>
<year>2011</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#x000A9; 2011 Nieuwenhuis-Mark.</copyright-statement>
<copyright-year>2011</copyright-year>
<license license-type="open-access" xlink:href="http://www.frontiersin.org/licenseagreement"><p>This is an open-access article subject to an exclusive license agreement between the authors and Frontiers Media SA, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.</p></license>
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<ref-count count="9"/>
<page-count count="1"/>
<word-count count="1063"/>
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</front>
<body>
<p>In the scientific and popular literature recently there has been a widespread call for classifying normal aging as a disease, a condition that can be &#x0201C;manipulated, treated, and delayed&#x0201D; (Gems, <xref ref-type="bibr" rid="B4">2010</xref>; Kelland, <xref ref-type="bibr" rid="B5">2010</xref>). The main argument given by supporters of this suggestion is that grant-awarding bodies would be more likely to fund research into how, when, and why we age, and that doctors would become duty-bound to treat it (Kelland, <xref ref-type="bibr" rid="B5">2010</xref>). However, it has recently been suggested that there is actually a chronic underinvestment in Alzheimer&#x00027;s disease research (Cassels, <xref ref-type="bibr" rid="B2">2010</xref>). Why then, would relabeling normal old age a disease suddenly increase funding in fundamental aging research when money is hard enough to come by for research into AD? A recent study investigated the genetic profiles of centenarians and claimed evidence for &#x0201C;Methuselah genes&#x0201D; which enable certain people to live to 100 and beyond (Sebastiani et al., <xref ref-type="bibr" rid="B7">2010</xref>). Predictions suggest that tests for these gene-driven traits will be commercially available in 2&#x02013;5 years (Rogers, <xref ref-type="bibr" rid="B6">2010</xref>). There is therefore a move among geneticists and gerontologists toward treating normal old age as a health issue, and, as Dr. David Gems, a biogerontologist at UCL, suggests &#x0201C;We need to reclassify it [aging] as a disease rather than as a benign, natural process&#x0201D; (Gems, <xref ref-type="bibr" rid="B4">2010</xref>). Indeed, many of the most devastating of the world&#x00027;s diseases, namely diabetes, heart disease, cancer, and dementia all have aging as a common mechanism in the sense that they tend to become more problematic and thus costly as sufferers age.</p>
<p>The word &#x0201C;disease&#x0201D; has of course more negative connotations than positive. In most dictionary definitions words like &#x0201C;pathology&#x0201D; and &#x0201C;impairment&#x0201D; are used. The main problem of adopting the aging-as-disease viewpoint is that it surely strengthens the already negative stereotype which hangs around aging: that of the depressed, lonely elder who can only look forward to increasing health problems as the years go by (Sneed and Whitbourne, <xref ref-type="bibr" rid="B8">2005</xref>). Instead of aging being seen as a normal process we all must go through (unless we die young) disease supporters want us to view it as something which can and must be prevented. Yet, the truth is that many elderly people live fulfilling lives and successful aging is more the norm than the exception, while at the same time individual differences in coping style, personality, cognitive functioning, and motivation are widespread. And therein lies the rub: if normal aging is classified as a disease process will it not make aging more feared and reviled than it already is?</p>
<p>A popular theory in the aging literature since the early 1990s is the socioemotional selectivity theory (SST; Carstensen, <xref ref-type="bibr" rid="B1">1992</xref>). SST was put forward as an attempt to explain the so-called &#x0201C;paradox of aging&#x0201D; which refers to the finding that while physical health tends to decline as we age subjective well-being may be maintained or even improve (Diener and Suh, <xref ref-type="bibr" rid="B3">1998</xref>). At the heart of SST is time perspective, with elderly people said to be present- rather than future-focused, and that they are motivated to maximize positive experiences, minimize the negative, and spend quality-time with loved ones in smaller social networks. Focusing on normal aging as a disease could therefore be seen as a step-back for aging research rather than a move forward. Aging-as-disease proponents would argue however that their focus is on improving quality of life in our final years, not on increasing our lifespans <italic>per se</italic>.</p>
<p>Alzheimer&#x00027;s dementia is set to become the number one concern of health professionals and carers as populations worldwide age due to its direct link with advancing age (Kelland, <xref ref-type="bibr" rid="B5">2010</xref>). Whether we can make the jump from AD to all aging as disease is however, at the very least, questionable, and indeed, worrisome. Do we really need to feed the already negative stereotypes which exist of the elderly in society? Should we not be celebrating how much the old bring to the world and have still to offer not only to close family and friends but also to society at large? Indeed, author Strauch (<xref ref-type="bibr" rid="B9">2010</xref>) suggests in her recent book that people underestimate the many talents of the mature brain and that it reaches its peak performance between the ages of 40 and 68. There are also calls for raising the pension age across Europe in recognition of the fact that people are not &#x0201C;finished&#x0201D; when they hit 65, that they can still be productive, worthwhile. Labeling aging as a disease may or may not help research funding but it can only hurt public opinion of what it means to age.</p>
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<ref-list>
<title>References</title>
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