tag:theconversation.com,2011:/africa/topics/antiageing-5417/articlesAntiageing – The Conversation2024-01-05T16:14:27Ztag:theconversation.com,2011:article/2188712024-01-05T16:14:27Z2024-01-05T16:14:27ZThe curious link between animal hibernation and ageing – and what humans could learn from it<figure><img src="https://images.theconversation.com/files/566564/original/file-20231219-23-pbwlq4.jpg?ixlib=rb-1.1.0&rect=0%2C24%2C5355%2C3535&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/woman-being-cold-rubbing-her-hands-2234194923">Nicoleta Ionescu/Shutterstock</a></span></figcaption></figure><p>When the cold and dark winter is setting in, some of us envy animals that can hibernate. This long, deep rest is an example of how nature develops clever solution to difficult problems. In this case, how to survive a long, cold and dark period without much food and water. </p>
<p>But hibernation has closer links to human history than you might expect. </p>
<p>An article in a copy of the British Medical Journal from 1900 describes a strange human dormancy-like hibernation called “<em>lotska</em>” that was <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1117993/">common among farmers</a> in Pskov, Russia. In this area, food was so scarce during the winter that the problem was solved by sleeping through the dark part of the year. </p>
<p>Once a day people woke up to eat a piece of bread and drink a glass of water. After the simple meal, they went back to sleep and family members then took turns keeping the fire alive. You will also find descriptions in <a href="https://pubmed.ncbi.nlm.nih.gov/15881270/">Inuit Greenlandic</a> stories of a prolonged hibernation-like sleep during the long dark winter months. In parts of Greenland it is dark from November to the end of January.</p>
<p>There is a study from 2020 which suggests the ancient ancestors of man, called hominins, may have been able to hibernate 400,000 years ago. Bones discovered in a cave in Spain show seasonal disruption in growth, suggesting that one of man’s predecessors may have used <a href="https://www.researchgate.net/publication/347706305_Hibernation_in_hominins_from_Atapuerca_Spain_half_a_million_years_ago">the same strategy</a> as cave bears to survive long winters.</p>
<h2>Animals and hibernation</h2>
<p>Hibernation is deeper and more complex than usual sleep, including dramatic changes in metabolism. This long resting period combines several conditions linked to longevity, reduced calorie intake, low body temperature and lowered metabolism.</p>
<p>Animals that hibernate <a href="https://royalsocietypublishing.org/doi/10.1098/rspb.2011.0190">usually live longer</a> compared to other species of the same size. Recent studies using epigenetic clocks, which map activity within genes over time, suggest that hibernation slows down <a href="https://www.nature.com/articles/s41559-022-01679-1">ageing in marmots</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/35946154/">bats</a>. So hibernation may hold important clues on how to slow down ageing processes. </p>
<p>There are different forms of ageing – chronological and biological age. </p>
<p>Chronological age is actually only about how many revolutions the earth has circled around the sun since we were born. </p>
<p>It is not time itself that ages us but rather “wear and tear”. <a href="https://pubmed.ncbi.nlm.nih.gov/37635161/">Biological age</a> measures wear and tear. It is a more comprehensive and personal measure of health than chronological age and a better predictor of longevity. A 2023 study established that biological age varies and that a temporary increase, for example during surgery and stress, is reversed <a href="https://pubmed.ncbi.nlm.nih.gov/37086720/">when you have recovered</a>. </p>
<p>Diseases that are <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8331090/">linked to lifestyle</a> and accumulate with age, such as such as cardiovascular disease, obesity, dementia and chronic kidney disease are driven by “wear and tear”. This result in inflammation, altered composition of the gut microbiota and increased <a href="https://www.hindawi.com/journals/omcl/2017/8416763/">oxidative stress</a>. Oxidative stress is when there are too many <a href="https://www.medicalnewstoday.com/articles/318652">free radicals</a> (unstable atoms that damage cells) in your body. </p>
<p>New science based on epigenetic clocks and lessons from hibernating animals could help us to treat patients who have diseases driven by “wear and tear”. We could use drugs that may slow down ageing. </p>
<p>For example, <a href="https://www.nhs.uk/medicines/metformin/">metformin</a> is the main first-line medication for the treatment of type-2 diabetes. It regulates inflammation, insulin-sensitivity and slows down DNA damage caused by oxidative-stress. There is growing evidence it may help manage other “wear and tear” diseases such as <a href="https://cardiab.biomedcentral.com/articles/10.1186/s12933-019-0860-y">cardiovascular disease</a> and long term use of the drug may be associated with <a href="https://www.frontiersin.org/articles/10.3389/fnagi.2021.773797/full">lower cognitive impairment</a>. </p>
<p>Learning more about hibernation may benefit human medicine for the treatment of <a href="https://www.sciencedirect.com/science/article/abs/pii/S0891584901006281?via%3Dihub">traumatic brain injuries</a>, <a href="https://journals.lww.com/shockjournal/fulltext/2018/07000/hibernation_based_approaches_in_the_treatment_of.3.aspx">severe blood loss</a>, preservation of muscle and bone mass and providing better protection during <a href="https://www.liebertpub.com/doi/10.1089/ars.2017.7127">organ transplantation</a>.</p>
<p>A 2018 study found that mimicking hibernation conditions for the storage of renal grafts from deceased donors seemed to improve their preservation. Muscular skeletal degeneration is often determined by genes, but these genes seemed to be deactivated in <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0215489">hibernating bears</a>. </p>
<h2>Animals and longevity</h2>
<p>There are long-lived, non-hibernating animals we can learn from too such as the Greenland shark, naked mole rat, Icelandic clam and Rougheye rockfish. These species have developed superior mechanisms that <a href="https://pubmed.ncbi.nlm.nih.gov/31366472/">protect them against ageing</a>. It seems like protection against inflammation, oxidative stress and modifications of proteins that happen with age are mechanism that in general benefit all long-lived animals. </p>
<p>Genetic studies of rougheye rockfish, which can <a href="https://wdfw.wa.gov/species-habitats/species/sebastes-aleutianus">live for over 200 years</a>, suggest that a food group called flavonoids is related to longevity. Citrus fruits, berries, onions, apples and parsley are high in flavonoids, which have anti-inflammatory properties and protect against organ damage, for example, from chemicals or ageing. </p>
<p>The <a href="https://www.science.org/doi/10.1126/sciadv.add2743">2023 study</a> of rougheye rockfish found that one set of its genes which could be linked to longevity were associated with flavonoid metabolism. So a long-lived fish may have something to teach us about what to eat to live longer. </p>
<p>Lessons from nature and hibernating animals tell us that preserving cells, regulation metabolism and genetic adaptions play key roles in longevity. Our life style and eating habits are our best tools to mimic some of these mechanisms. </p>
<h2>Forty winks</h2>
<p>There is still so much we don’t understand about hibernation but we do know that normal sleep is connected to longevity too. For example, a March 2023 study showed that with <a href="https://www.jacc.org/doi/10.1016/S0735-1097%2823%2902119-8">good quality sleep</a>, you can add five years to the life of men and two and a half years if you are a woman. The researchers defined good quality sleep as getting seven to eight hours of sleep per day, not needing sleep medication and waking up feeling rested at least five days a week. </p>
<p>Animals have huge variations in their sleeping patterns, from bears and marmots hibernating for eight months of the year to <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171903">elephants that get only two hours a day</a>.<br>
How elephants can become so old while sleeping so little is still a mystery to scientists. </p>
<p>Finding out how nature resolved these extremes may help scientists decipher new ways to improve human health.</p><img src="https://counter.theconversation.com/content/218871/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Peter Stenvinkel receives funding from Astra Zeneca, Fresenius, Baxter, Novo Nordisk, Bayer, Invizius, Vifor for lectures and scientific advisory boards</span></em></p>Animals that hibernate live longer, so could hold clues on how to slow down ageing.Peter Stenvinkel, Professor of Nephrology, Karolinska InstitutetLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2110612023-08-15T15:35:26Z2023-08-15T15:35:26ZYour body can be younger than you are – here’s how to understand (and improve) your ‘biological age’<figure><img src="https://images.theconversation.com/files/542812/original/file-20230815-17-dwl420.jpg?ixlib=rb-1.1.0&rect=17%2C0%2C5906%2C3641&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Your chronological age and biological age may not be the same.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/old-young-sportsmen-running-on-road-1266665947">Realstock/ Shutterstock</a></span></figcaption></figure><p>The saying goes that money can’t buy you love. But can it buy you time? This is what <a href="https://www.standard.co.uk/tech/bryan-johnson-tech-millionaire-reverse-ageing-b1083695.html">US billionaire Bryan Johnson</a> is hoping to find out. </p>
<p>The 45-year-old reportedly spends millions each year in an attempt to reverse ageing and regain his 18-year-old body (presumably sans acne). To achieve this, Johnson sticks to a rigid diet and exercise regime, takes multiple supplements, and has frequent tests to analyse the function of his organs. He’s also tried some <a href="https://pubmed.ncbi.nlm.nih.gov/37500974/">novel procedures</a> to rejuvenate his body, such as injecting himself with his 17-year-old son’s <a href="https://www.thetimes.co.uk/article/tech-millionaire-injected-with-sons-blood-in-quest-for-youth-z8bbtm9f8?utm_medium=Social&utm_source=Twitter#Echobox=1684906320">blood plasma</a>.</p>
<p>Not only has Johnson’s quest garnered a lot of attention online, it has also left many wondering to what extent his ultimate goal is achievable – can your body really be younger than your calendar age?</p>
<p>There are two interconnected ways of measuring your age. The first is chronological age, which is the easiest to understand. It’s really nothing more than how long you’ve been alive. The most accurate estimate of that is the date and time on your birth certificate.</p>
<p>But, in circumstances where documentary evidence is lacking (typically, archaeological excavations or forensics), there are several techniques available to estimate chronological age. Arguably, the best method is by looking at teeth – specifically, their annual “<a href="https://pubmed.ncbi.nlm.nih.gov/35088895/">cemental lines</a>”, which are much like growth rings in trees, alongside changes in the dentine (which sits beneath the enamel and supports tooth structure).</p>
<h2>How to measure your ‘true’ age</h2>
<p>Biological age, on the other hand, reflects the exponential increase in an organism’s chances of becoming sick or dying with the passage of time. Basically, this translates to the rate at which your body is losing function. </p>
<p>While <a href="https://pubmed.ncbi.nlm.nih.gov/31449890/">most species age</a>, there are some rare creatures on the planet that are truly non-ageing – such as the <a href="https://genomics.senescence.info/species/entry.php?species=Arctica_islandica">ocean quahog</a>. These have such a low chance of dying that some alive today are old enough that <a href="https://pubmed.ncbi.nlm.nih.gov/24347613/">Henry VIII could have eaten them</a> in a bowl of chowder.</p>
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Read more:
<a href="https://theconversation.com/is-there-a-natural-limit-to-how-long-humans-can-live-66460">Is there a natural limit to how long humans can live?</a>
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<p>Yet, while we all grow older, we don’t all lose functional capacity at identical rates – and the organ systems in our body <a href="https://pubmed.ncbi.nlm.nih.gov/6967883">decline at different speeds</a>. This means that some people’s biological age may be younger or older than the average for their chronological age.</p>
<p>Take the example of the <a href="https://www.runnersworld.com/news/a25593341/70-year-old-marathon-record/">70-year-old US marathon runner</a> who set a world record for his age group in 2018, and contrast it with many of his peers who are in delicate health or long-term care. This shows how biological age can be uncoupled from chronological age. </p>
<p>There are several ways to estimate biological age. Surprisingly, one of the best is incredibly simple: use your eyes. Research shows that age estimates made by <a href="https://pubmed.ncbi.nlm.nih.gov/35650301">looking at someone</a> are just as good as some more complicated techniques of gauging biological age.</p>
<p>Another study found that smokers, people who were obese, and those in poor health were all perceived as <a href="https://pubmed.ncbi.nlm.nih.gov/7100970/">being older</a> than their chronological age by their peers. Given <a href="https://pubmed.ncbi.nlm.nih.gov/19485966/">these factors</a> do indeed <a href="https://pubmed.ncbi.nlm.nih.gov/3226152/">increase biological age</a>, this shows how accurate just looking at someone can be. </p>
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<img alt="A photo of a woman at three different stages in life." src="https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=360&fit=crop&dpr=1 600w, https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=360&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=360&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=453&fit=crop&dpr=1 754w, https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=453&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/542814/original/file-20230815-27-b6u290.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=453&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Our eyes may be one of the best methods for determining biological age.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/aging-process-rejuvenation-antiaging-skin-procedures-436064953">Leszek Glasner/ Shutterstock</a></span>
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<p>Another simple but powerful predictor of biological age is measuring a person’s <a href="https://pubmed.ncbi.nlm.nih.gov/36215867">grip strength</a>, which tends to decrease with age as they lose muscle mass. <a href="https://theconversation.com/how-strong-your-grip-is-says-a-lot-about-your-health-145861">Other factors</a> – such as illness, obesity, and lack of fitness – can also affect this. Low grip strength is one sign that your biological age is probably higher than your calendar age.</p>
<p>Other, more complicated methods of estimating biological age include testing multiple <a href="https://academic.oup.com/biomedgerontology/article/68/6/667/873700">organ function</a> and looking at <a href="https://pubmed.ncbi.nlm.nih.gov/32554926/">sterile inflammation</a>, which measures how many inflammatory molecules are circulating in the body (a high level is not good news). You could also look at <a href="https://pubmed.ncbi.nlm.nih.gov/36206857/">epigentic changes to DNA</a>, the length of <a href="https://theconversation.com/end-of-ageing-and-cancer-scientists-unveil-structure-of-the-immortality-enzyme-telomerase-95591">chromosomal ends</a>, or the <a href="https://www.frontiersin.org/articles/10.3389/fragi.2021.686382/full">number of senescent cells</a> a person has to measure their biological age. However, the latter two methods typically only provide a <a href="https://pubmed.ncbi.nlm.nih.gov/33552142/">rough estimate</a>.</p>
<h2>Staying young</h2>
<p>If you’re hoping to turn back the clock and “reverse ageing”, the best place to start is by focusing on your lifestyle.</p>
<p>Regular exercise, quitting smoking, drinking in moderation, watching your weight and eating plenty of fruit and veg are all simple things that make a huge difference to your biological age. There’s a roughly <a href="https://www.epic-norfolk.org.uk/study-findings">15-year difference</a> in life expectancy between a person who does four of these five things and someone who does none of them. </p>
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<a href="https://theconversation.com/life-extension-the-five-most-promising-methods-so-far-169881">Life extension: the five most promising methods – so far</a>
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<p>There are also treatments in development that could rapidly and significantly reverse ageing, if they translate effectively from rodents to humans. </p>
<p>For example, researchers have demonstrated that the accumulation of senescent cells in tissue is a primary cause of ageing in mice. <a href="https://pubmed.ncbi.nlm.nih.gov/22048312/">Removing them</a> has shown improvements in both their <a href="https://pubmed.ncbi.nlm.nih.gov/26840489/">health and lifespan</a>.</p>
<p>These studies have also compared the effects of removing senescent cells throughout the animal’s life with letting them accumulate, then removing them when the mouse is old. Both interventions improve the health and lifespan of mice – and the latter could justly be described as “reversing ageing”. </p>
<p>Many attempts are ongoing to <a href="https://pubmed.ncbi.nlm.nih.gov/36857968/">duplicate these effects in humans</a>, while a range of <a href="https://www.ukanet.org.uk/">other techniques</a> to improve late-life health are also being studied. Success with any of these could <a href="https://pubmed.ncbi.nlm.nih.gov/37117804/">dramatically reduce healthcare costs</a> and revolutionise how we <a href="https://www.theactuarymagazine.org/breaking-the-dam">spend our later years</a>. </p>
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Read more:
<a href="https://theconversation.com/the-secret-to-staying-young-scientists-boost-lifespan-of-mice-by-deleting-defective-cells-54068">The secret to staying young? Scientists boost lifespan of mice by deleting defective cells</a>
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<p>In my view, Johnson’s attempts to reverse ageing are something of a mixed bag of the practical and the hopeful. However, achieving his long-term goal of reaching the age of 200 might be a tad optimistic.</p><img src="https://counter.theconversation.com/content/211061/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Richard Faragher is co-Director of the BLAST Healthy Ageing Network and a co-ordinator of the UK Ageing Research Networks (UKAN). He receives funding from the Biotechnology and Biological Sciences Research Council and the Medical Research Council. He serves on the Scientific Advisory Board of the Longevity Vision Fund and is a member of the Board of Directors of the American Federation for Aging Research. </span></em></p>Many factors such as smoking, how much your exercise and what foods you eat, can affect your biological age.Richard Faragher, Professor of Biogerontology, University of BrightonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1873222022-08-08T15:46:59Z2022-08-08T15:46:59ZSunscreen: here’s why it’s an anti-ageing skincare essential<figure><img src="https://images.theconversation.com/files/478083/original/file-20220808-2624-dua4s0.jpg?ixlib=rb-1.1.0&rect=0%2C8%2C5694%2C3782&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Sunscreens can help reduce the amount of damaging radiation our skin gets.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/attractive-young-black-african-woman-model-2052802880">Ground Picture/ Shutterstock</a></span></figcaption></figure><p>Every month there seems to be a trendy new product to add to your skincare collection. Lately, a commonplace product that many people already use has taken the top spot, with everyone from dermatologists to influencers swearing by it as the number one way to stay looking youthful through the years: sunscreen. </p>
<p>It’s no wonder. It’s thought that solar exposure – also known as “photoageing” – causes up to <a href="https://pubmed.ncbi.nlm.nih.gov/24101874/">80% of skin ageing</a>. So if you’re someone who’s worried about fine lines, wrinkles and uneven pigmentation, limiting the amount of solar radiation you get is one of the most important things you can do.</p>
<p>There are thought to be a number of different triggers for photoageing. Most research has linked it to the expression of a group of proteins called matrix metalloproteinases (MMPs). These proteins are enzymes that break down elastins and collagens in the skin’s deeper layer (called the dermis). Elastins and collagens are responsible for the skin’s structure, strength and stretchiness.</p>
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<img alt="Quarter life, a series by The Conversation" src="https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/451343/original/file-20220310-13-1bj6csd.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<p><em><strong><a href="https://theconversation.com/uk/topics/quarter-life-117947?utm_source=TCUK&utm_medium=linkback&utm_campaign=UK+YP2022&utm_content=InArticleTop">This article is part of Quarter Life</a></strong>, a series about issues affecting those of us in our twenties and thirties. From the challenges of beginning a career and taking care of our mental health, to the excitement of starting a family, adopting a pet or just making friends as an adult. The articles in this series explore the questions and bring answers as we navigate this turbulent period of life.</em></p>
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<p>Expression of these MMP proteins has been linked to both <a href="https://europepmc.org/article/med/18459971">DNA damage</a> in skin cells and the <a href="https://pubmed.ncbi.nlm.nih.gov/19116368/">production</a> of <a href="https://link.springer.com/article/10.1007/BF02505041">reactive oxygen species</a>. Reactive oxygen species are highly reactive chemicals formed from oxygen that can damage other cellular components, such as DNA and proteins. </p>
<p>Both of these factors are caused by too much sun exposure. Over time, this damage accumulates to cause characteristic signs of ageing. This may explains why one study even showed people who tended to avoid the sun had <a href="https://pubmed.ncbi.nlm.nih.gov/24101874/">significantly fewer signs of ageing</a> compared to people who enjoyed spending time in the sun. </p>
<p>But it isn’t always possible to avoid the sun – which is where sunscreens help. These products contain ingredients (such as zinc oxide) which absorb or reflect UV radiation and dissipate it safely before it can damage our skin cells. This also reduces the cumulative dose of radiation received by the skin.</p>
<p>Studies have shown that sunscreens can prevent many signs of photoageing by tackling the triggers, with <a href="https://pubmed.ncbi.nlm.nih.gov/16520862/">numerous studies</a> showing they can prevent the expression of MMPs. A study that compared the effects of <a href="https://pubmed.ncbi.nlm.nih.gov/7490363/">using sunscreen versus a placebo</a> on skin ageing, found that people in the placebo group had higher levels of solar elastosis (a sign of photoageing which causes a loss of elasticity) after two years.</p>
<p><a href="https://pubmed.ncbi.nlm.nih.gov/23732711/">An Australian study</a> compared levels of photoageing in groups assigned to daily sunscreen use versus discretionary sunscreen use. In the daily sunscreen use group, there was no detectable increase in skin ageing over the four-and-a-half year study period compared to the discretionary sunscreen group. <a href="https://pubmed.ncbi.nlm.nih.gov/27749441/">Another study</a> has also shown daily sunscreen use for a year may reverse visible signs of ageing when assessed by a dermatologist.</p>
<h2>Choosing the right product</h2>
<p>While there is plenty of evidence that sunscreens can prevent photoageing, many only block the UV (ultraviolet) range of the solar spectrum. In the case of photoageing, exposure to <a href="https://pubmed.ncbi.nlm.nih.gov/34585779/">visible radiation</a> (particularly <a href="https://www.nature.com/articles/s41598-018-30738-6">blue light</a>) and <a href="https://pubmed.ncbi.nlm.nih.gov/19675547/">infrared</a> have all been shown to contribute to photoageing. Basically, this means that sunscreens can’t protect against photoageing entirely, but can reduce it significantly.</p>
<figure class="align-center ">
<img alt="A young woman stands in the aisle of a store, holding two bottles of sunscreen in each hand. There is a row of shelves beside her filled with sunscreen bottles." src="https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=394&fit=crop&dpr=1 600w, https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=394&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=394&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=495&fit=crop&dpr=1 754w, https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=495&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/478084/original/file-20220808-2583-9n9kdk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=495&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">There’s plenty of products to choose from nowadays.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/smiling-woman-choosing-bottles-sun-protection-1312068065">BearFotos/ Shutterstock</a></span>
</figcaption>
</figure>
<p>Some <a href="https://www.sciencedirect.com/science/article/pii/S1011134421002517">newer solar filters</a> used in sunscreens have been developed which can block some blue light. Other ingredients sometimes added to sunscreens (<a href="https://pubmed.ncbi.nlm.nih.gov/30071261/">such as antioxidants</a>) have also been shown to prevent the production of MMPs and reduce <a href="https://pubmed.ncbi.nlm.nih.gov/34789788/">reactive oxygen species</a> – which will likely help in the fight against photoageing beyond the UV spectrum, too. Antioxidants may also protect against factors such as <a href="https://pubmed.ncbi.nlm.nih.gov/31927691/#:%7E:text=Recent%20findings%3A%20Traffic%2Drelated%20air,effects%20on%20premature%20skin%20aging.">pollution</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/17951030/">smoking</a>, which are both linked to faster ageing.</p>
<p>Photoageing is a cumulative process that occurs over time. Doing anything you can to <a href="https://www.britishskinfoundation.org.uk/how-to-stay-safe-in-the-sun">limit exposure</a> will slow this process – such as covering up with clothing when you go outside. But choosing the right kind of sunscreen may also help somewhat.</p>
<p>The best product to use comes down largely to personal preference. But in general, the higher the SPF, the greater protection you’ll have against photoageing. You should also try to find a sunscreen with five-star UVA protection on the label, which will help protect against the broadest range of UV radiation.</p>
<p>Be sure to regularly use sunscreen or SPF-containing products from spring to autumn. If you’re going to be getting a lot of sun (such as on a beach holiday) it’s best to use a higher SPF product and reapply regularly. Although some people recommend wearing sunscreen even in winter, this is unlikely to be of much benefit to people living in the UK, as UV radiation is lowest this time of year. But if you go on a skiing holiday or live somewhere with lots of snow, sunscreen will still be beneficial as snow reflects solar radiation. </p>
<p>All the evidence suggests that by far the most effective way to prevent photoageing is with the use of sunscreens, as these prevent damage from happening in the first place. Now with more choice than ever and formulations always being improved, it’s just a matter of finding what product works best for you. </p>
<p>But a final word of warning: slathering on sunscreen before sitting out tanning won’t be enough to protect you completely – and this goes beyond photoageing. Too much sun exposure can carry other risks – such as sunburn and skin cancer – which is something to bear in mind during the summer months.</p>
<p><iframe src="https://action.bridged.media/?id=62f190752e78b514b03fffc1&embed=true" width="100%" height="400px" style="border:none; overflow: hidden;"></p></iframe></p><img src="https://counter.theconversation.com/content/187322/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Karl Lawrence has previously received funding from the sunscreen industry.</span></em></p>It’s thought that up to 80% of skin ageing is the result of sun exposure.Karl Lawrence, Post Doctoral Researcher, Photobiology, King's College LondonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1432552020-08-11T06:53:21Z2020-08-11T06:53:21ZCan ageing really be ‘treated’ or ‘cured’? An evolutionary biologist explains<figure><img src="https://images.theconversation.com/files/352143/original/file-20200811-14-1qjonhd.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Shutterstock</span></span></figcaption></figure><p>As time passes, our fertility declines and our bodies start to fail. These natural changes are what we call ageing.</p>
<p>In recent decades, we’ve come leaps and bounds in treating and preventing some of the world’s <a href="https://www.aihw.gov.au/reports/life-expectancy-death/deaths-in-australia/contents/summary">leading age-related diseases</a>, such as coronary heart disease, dementia and Alzheimer’s disease.</p>
<p>But some research takes an entirely unique view on the role of science in easing the burden of ageing, focusing instead on trying to prevent it, or drastically slow it down. This may seem like an idea reserved mainly for cranks and science fiction writers, but it’s not.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=389&fit=crop&dpr=1 600w, https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=389&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=389&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=488&fit=crop&dpr=1 754w, https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=488&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/350145/original/file-20200729-31-101lw1i.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=488&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The Fountain of Youth, a 1546 painting by Lucas Cranach the Elder. The famous fountain is a mythical spring that supposedly regenerates anyone who bathes in or drinks its waters. Stories of its power have circulated for thousands of years.</span>
<span class="attribution"><span class="source">Wikimedia Commons</span></span>
</figcaption>
</figure>
<h2>The futurist’s quest</h2>
<p>There have been myriad scientific research efforts focused on stopping or slowing the effects of ageing. </p>
<p>Last year, scientists studying the
<a href="https://www.wormatlas.org/aging/introduction/mainframe.htm">nematode</a> worm <em>Caenorhabditis elegans</em> (a common model organism for ageing-related research) managed to <a href="https://www.sciencedirect.com/science/article/pii/S2211124719308587?via%3Dihub">manipulate its biochemical pathways</a>. The resulting worms lived five times longer than their typical lifespan of 20 days.</p>
<p>The length of the <a href="https://learn.genetics.utah.edu/content/basics/telomeres/">telomere</a> has also received a lot of interest. This is a tiny structure within a cell that protects chromosomes from deterioration. One <a href="https://www.pnas.org/content/pnas/116/30/15122.full.pdf">study</a> found a faster rate of telomere shortening resulted in a shorter lifespan in many species, including humans. </p>
<p>This suggests if we can protect these structures, we could greatly increase our lifespan. However, <a href="https://link.springer.com/article/10.1007/s10522-018-9748-6#Sec2">telomere maintenance</a> is complex. Also, telomeres can vary in how quickly they shorten, depending on where they are in the body. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/want-to-live-longer-consider-the-ethics-101301">Want to live longer? Consider the ethics</a>
</strong>
</em>
</p>
<hr>
<p>The drug <a href="http://www.wch.sa.gov.au/services/az/divisions/paedm/endodiab/documents/metformin_information_sheet.pdf">metformin</a>, usually prescribed to manage type 2 diabetes, has also been touted as a way to delay the onset of a range of age-related diseases, thus increasing “health-span” (how long we remain healthy).</p>
<p>Nir Barzilai, director of the Institute for Ageing Research at the Albert Einstein College of Medicine is seeking approval from the US Food and Drug Administration for the <a href="https://www.afar.org/tame-trial">first clinical trial</a> of metformin to treat ageing.</p>
<p>But other researchers are <a href="https://www.karger.com/Article/FullText/502257">concerned</a>, as metformin intake has been associated with a higher risk of <a href="https://www.healthdirect.gov.au/vitamin-b">B vitamin</a> deficiencies. <a href="https://pubmed.ncbi.nlm.nih.gov/31119857/">Some studies</a> suggest this can result in <a href="https://academic.oup.com/jcem/article-abstract/104/10/4837/5421021?redirectedFrom=fulltext">cognitive dysfunction</a>.</p>
<p>One 2018 study found metformin can reduce aerobic capacity and quash the benefits of <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/acel.12880">excercise</a> – something we know to help fight the effects of <a href="https://link.springer.com/article/10.1007/s10522-017-9719-3">old age</a>.</p>
<p>Metformin also shows mixed results in its effects on ageing depending on which model organism is used (such as rats, flies or worms). This raises doubts about whether its supposed anti-ageing capabilities would apply to humans.</p>
<p>Another <a href="https://blogs.scientificamerican.com/guest-blog/beyond-resveratrol-the-anti-aging-nad-fad/">compound of interest</a> is nicotinamide adenine dinucleotide (NAD). This naturally occurring substance is vital to energy metabolism in most animals including humans, plants, bacteria and even <a href="https://onlinelibrary.wiley.com/doi/pdf/10.1002/(SICI)1097-0134(199705)28:1%3C29::AID-PROT3%3E3.0.CO;2-E?casa_token=C73Z5lTPgsQAAAAA:D3RUbNbpUVWp0B27r_x7aZsp0inBSSY7VJbv-prNzC_yJNTRd8OoEZ85srBuvr8Ifiql2C23FTVQEXv8Vg">yeast</a>. In mice and humans, <a href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(16)30244-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413116302443%3Fshowall%3Dtrue">NAD levels appear to decline</a> as we age.</p>
<p>NAD and compounds like resveratrol (a chemical isolated from wine) have been <a href="https://www.sciencedirect.com/science/article/pii/S0092867413015213?via%3Dihub#!">shown to</a> work together to maintain the function of our <a href="https://www.nature.com/scitable/topicpage/mitochondria-14053590/">mitochondria</a> – the structures that produce energy inside our cells – and thus fight off ageing in mice. But this research lacks much-needed human trials.</p>
<h2>The immortal jellyfish</h2>
<p>Evolutionary biologists know ageing is a highly “plastic” process influenced by many factors including diet, climate, genetics and even the age at which our grandparents <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000556">conceived our parents</a>. But, we don’t know why some species age more slowly than others.</p>
<p><a href="https://www.nature.com/articles/nature12789#:%7E:text=A%20genotype%20moulds%20its%20phenotype's,across%20the%20tree%20of%20life.">Research</a> has shown several species appear not to age. For example, the “immortal” jellyfish <em>Turritopsis dohrnii</em> can revert to a juvenile stage of life and seemingly escape the process of ageing.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/352118/original/file-20200811-19-bpcm9w.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Turritopsis dohrnii, famously known as the ‘immortal jellyfish’, can transform its existing cells into a younger state when suffering starvation, physical damage or other afflictions.</span>
<span class="attribution"><span class="source">Shutterstock</span></span>
</figcaption>
</figure>
<p>To figure out why some species age better than humans, we have to understand so-called “<a href="https://www.nature.com/articles/s41580-019-0204-5">epigenetic changes</a>” which alter our DNA expression throughout the ageing process.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/ageing-how-our-epigenetic-clocks-slow-down-as-we-get-older-129345">Ageing: how our 'epigenetic clocks' slow down as we get older</a>
</strong>
</em>
</p>
<hr>
<p><a href="https://press.princeton.edu/books/hardcover/9780691157672/extended-heredity">Epigenetic changes</a> are mechanisms that can determine which genes are turned on or off in offspring. They have a huge influence on the course of a species’ evolution. </p>
<p>Understanding these mechanisms could also help us understand why humans and other animals evolved to age in the first place. </p>
<h2>The culture of DIY biology</h2>
<p>When it comes to research on ageing, immense interest from the public and large companies has created an environment where it’s difficult to separate unfounded claims from science. In this grey area, biohackers emerge.</p>
<p><a href="https://www.vox.com/future-perfect/2019/6/25/18682583/biohacking-transhumanism-human-augmentation-genetic-engineering-crispr">“Biohacking”</a> refers to actions that supposedly let you “hack” your brain and body to optimise their performance, without traditional medicine. </p>
<p>Its proponents often peddle claims exaggerated by cherry-picked evidence. One example is <a href="https://www.healthline.com/health/food-nutrition/alkaline-water-benefits-risks">alkaline water</a>, <a href="https://www.tyentusa.com/blog/a-wrinkle-in-time-slow-down-the-aging-process-with-a-water-ionizer-part-2/">claimed</a> to slow ageing by reducing <a href="https://www.healthline.com/health/oxidative-stress">oxidative stress</a>. </p>
<p>Two studies highlight alkaline water’s positive effects for <a href="https://jissn.biomedcentral.com/articles/10.1186/1550-2783-7-29">acid-base balance</a> in the bloodstream, and <a href="https://jissn.biomedcentral.com/articles/10.1186/s12970-016-0153-8#auth-1">increasing hydration status</a> during exercise. But both of these studies were funded by companies selling alkaline water. </p>
<p>A <a href="https://bmjopen.bmj.com/content/6/6/e010438.full">systematic review</a> of the literature shows there is no research to support or disprove beliefs about alkaline water being a genuine biohack. </p>
<p>There are also bogus “young blood transfusions”, in which an older person is injected with a younger person’s blood to “cure” ageing. This is a <a href="https://static.insider.com/young-blood-transfusions-ambrosia-shut-down-2019-6">very real and exploitative</a> part of the <a href="https://www.washingtonpost.com/outlook/2019/03/27/egalitarian-dreams-that-fueled-quest-young-blood-treatments/">anti-ageing industry</a>.</p>
<h2>Even if we could, should we?</h2>
<p>The concept of fighting ageing has <a href="https://www.nationalgeographic.com/history/archaeology/fountain-of-youth/">long been woven</a> into the human narrative.</p>
<p>But forcefully extending the human lifespan by even one decade would present difficult social realities, and we have little insight into what this would mean for us.</p>
<p>Would a “cure” for ageing be abused by the wealthy? Would knowing we had longer to live decrease our motivation in life? </p>
<p>Perhaps it’s a good thing we won’t be diving into the fountain of youth any time soon – if ever.</p>
<hr>
<p><em>Correction: this article was updated to reflect the Albert Einstein College of Medicine is no longer affiliated with Yeshiva University.</em></p><img src="https://counter.theconversation.com/content/143255/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Zachariah Wylde does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>As modern medicine improves, so too does our ability to stave off disease. But can we overcome the most inescapable of afflictions - old age? Researchers around the world are trying to find out.Zachariah Wylde, Postdoctoral Researcher in Evolutionary Biology, UNSW SydneyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1102142019-11-05T11:47:22Z2019-11-05T11:47:22ZHow to stay fit into your 60s and beyond<figure><img src="https://images.theconversation.com/files/300136/original/file-20191104-88387-y1b8de.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/323449430?size=medium_jpg">Alex Brylov/Shutterstock</a></span></figcaption></figure><p>Ageing is inevitable and is influenced by many things – but keeping active can <a href="https://www.nature.com/articles/s41586-019-1365-2">slow ageing and increase life expectancy</a>. Evidence <a href="https://www.ukactive.com/wp-content/uploads/2018/09/Reimagining_Ageing.pdf">shows</a> that ageing alone is not a cause of major problems until you are in your mid-90s. And strength, power and muscle mass <a href="https://www.ncbi.nlm.nih.gov/pubmed/24030238">can be increased</a>, even at this advanced age. </p>
<p>So here are my top exercise tips for people in their 60s and older, at different levels of fitness.</p>
<h2>For lifetime fitness fanatics</h2>
<p>If you fall into this group, you are in the minority. You are <a href="https://academic.oup.com/ageing/article/43/1/10/24207">robust</a>, likely to be a “super-ager” and you are doing wonderfully. You are certainly <a href="https://www.ncbi.nlm.nih.gov/pubmed/3299702">optimising your chance of living longer and ageing successfully</a>. </p>
<p>Generally, this is when you reap your reward from a lifetime of keeping active. With your <a href="https://bjsm.bmj.com/content/53/14/856">healthier metabolic, skeletal, cardiovascular and immune systems</a> you can <a href="https://www.who.int/ageing/healthy-ageing/en/">probably outperform people decades younger</a>.</p>
<p>Keep up the kettlebells, spin classes, rowing, triathlons or manual work such as gardening – whatever you like to do. You can keep challenging yourself physically. Mix your routine up – a combination of aerobic and resistance work as well as an activity to challenge your balance is ideal.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/five-brain-boosting-reasons-to-take-up-martial-arts-at-any-age-95263">Five brain-boosting reasons to take up martial arts – at any age</a>
</strong>
</em>
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<p>Maximise health benefits by swimming outdoors and as part of a community. You might want to <a href="https://www.ncbi.nlm.nih.gov/pubmed/31610442">try sea swimming</a> – although it’s not for everybody.</p>
<p>But watch out for chronic overloading, that is, diversify your exercise programme by incorporating cross-training. For example, if you are a runner, incorporate cycling or swimming to avoid overloading any part of your body.</p>
<p>Recovery after strenuous exercise is <a href="https://link.springer.com/article/10.1007/BF01075989">slower as you age</a> and <a href="https://link.springer.com/article/10.1007/BF00839156">can take up to five days</a>. So exercise smart.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/300226/original/file-20191105-88378-1rg3nyg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Make use of the great outdoors.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/1206075718?size=medium_jpg">Rawpixel/Shutterstock</a></span>
</figcaption>
</figure>
<h2>For the averagely fit</h2>
<p>You are doing well, so keep going. Long-term consistency is the key for benefits. You don’t necessarily have to join a gym, just keep building meaningful physical activity into your day. For example, walk briskly to the shops to get your groceries, keep up gardening and be active around your house. Even repeating simple stair climbing is a great exercise.</p>
<p>If you are suffering from hip or knee pain, walking may be painful, so try cycling or water-based exercise instead.</p>
<p>Coupling <a href="https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-017-0584-3">physical activity with social engagement</a> can optimise its benefits, so try yoga or a dance class. Incorporate some <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/ggi.12895">outdoor exercise</a> for an <a href="https://www.ncbi.nlm.nih.gov/pubmed/21291246">added mental health boost</a>.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/what-science-tells-us-about-successful-ageing-77342">What science tells us about successful ageing</a>
</strong>
</em>
</p>
<hr>
<p>The main thing is to avoid long periods of sitting. Also, ideally, continue to do the exercise you enjoy. Try to steadily build up your level of aerobic exercise at a level where you <a href="https://health.gov/paguidelines/second-edition/pdf/Physical_Activity_Guidelines_2nd_edition.pdf">build up a sweat and feel slightly out of breath</a>.</p>
<p>Often strengthening and flexibility exercises are neglected, so try to include these type of exercises where possible. </p>
<h2>For the unfit or unwell</h2>
<p>You may be managing complex chronic conditions, which make it more difficult to exercise. Or it may be that exercise is not a habit for you. If you have several chronic conditions, you may need clearance from a doctor to exercise and specialised exercise advice from a physiotherapist or other exercise professional. </p>
<p>If you are experiencing three or more of the following: unplanned weight loss, exhaustion, slowness, weakness of grip and physical inactivity you may be considered <a href="https://jamanetwork.com/journals/jama/fullarticle/204046">frail</a>, which will leave you vulnerable to even minor health stresses. But it is never too late to build more physical activity into your daily life. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/cancer-and-exercise-do-mix-66315">Cancer and exercise do mix</a>
</strong>
</em>
</p>
<hr>
<p>Even reducing time spent sitting and doing a little exercise will have major health benefits, doing any type of activity at all is <a href="https://health.gov/paguidelines/second-edition/pdf/Physical_Activity_Guidelines_2nd_edition.pdf">better than none</a>. Even chair-based exercises or practising sit-to-stand can be a great start.</p>
<p>Feeling a bit out of breath with exercise is normal and some initial aches and joint pain are fine. But if you ever feel chest pain or severe discomfort, you need to see a doctor straight away.</p>
<p>If you have a set-back such as a chest infection or fall which results in a hospital admission, get up and moving as soon as is safely possible. Even a few days of bed rest can result in <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=19548502">major decreases in strength and fitness</a>.</p>
<p>If you have surgery scheduled, being as active as possible before being admitted to hospital and start moving as soon as possible afterwards will help your recovery. It may also <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1111/anae.14508">prevent complications</a> that could prolong your hospital stay.</p>
<p>If you are diagnosed with cancer, keep active, even <a href="https://insights.ovid.com/crossref?an=00005768-201911000-00023">during treatment</a>, such as chemotherapy and radiotherapy, and <a href="https://link.springer.com/article/10.1007%2Fs00520-013-2064-4">during recovery</a>.
If you have other common chronic conditions, such as heart or lung disease, <a href="https://health.gov/paguidelines/second-edition/pdf/Physical_Activity_Guidelines_2nd_edition.pdf">keep as active as your condition allows</a>.</p>
<p>Just remember, whatever your state of health, it’s never too late to reap the benefits of being more physically active.</p><img src="https://counter.theconversation.com/content/110214/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Julie Broderick does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>A guide to physical activity for those over 60, from the lifetime physically active to the late starter.Julie Broderick, Assistant Professor, Physiotherapy, Trinity College DublinLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1012142018-08-10T12:02:14Z2018-08-10T12:02:14ZAgeing in human cells successfully reversed in the lab<figure><img src="https://images.theconversation.com/files/231081/original/file-20180808-7141-g2mxvh.jpg?ixlib=rb-1.1.0&rect=11%2C0%2C3882%2C2598&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/294290969?src=eMJ-U37JxuiHMiz-Q5Ip_Q-1-42&size=huge_jpg">perfectlab/Shutterstock</a></span></figcaption></figure><p>The ability to reverse ageing is something many people would hope to see in their lifetime. This is still a long way from reality, but in our latest experiment, we have <a href="https://www.ncbi.nlm.nih.gov/pubmed/30026406">reversed the ageing of human cells</a>, which could provide the basis for future anti-degeneration drugs.</p>
<p>Ageing can be viewed as the progressive decline in bodily function and is linked with most of the common chronic diseases that humans suffer from, such as cancer, diabetes and dementia. There are many reasons why our cells and tissues stop functioning, but a new focus in the biology of ageing is the <a href="https://www.ncbi.nlm.nih.gov/pubmed/28781767">accumulation of “senescent” cells</a> in the tissues and organs. </p>
<p>Senescent cells are older deteriorated cells that do not function as they should, but also compromise the function of cells around them. Removal of these old dysfunctional cells has been <a href="https://www.ncbi.nlm.nih.gov/pubmed/22048312">shown to improve</a> many features of ageing in animals such as the delayed onset of cataracts.</p>
<p>We still don’t fully understand why cells become senescent as we age, but damage to DNA, exposure to inflammation and damage to the protective molecules at the end of the chromosomes – the <a href="https://www.ncbi.nlm.nih.gov/pubmed/9454332">telomeres</a> – have all been suggested. </p>
<p>More recently, people have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5531163/">suggested</a> that one driver of senescence may be loss of our ability to turn genes on and off at the right time and in the right place.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=576&fit=crop&dpr=1 600w, https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=576&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=576&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=724&fit=crop&dpr=1 754w, https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=724&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/230917/original/file-20180807-191019-17mfsso.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=724&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">A senescent cell.</span>
<span class="attribution"><span class="source">Eva Latorre</span>, <span class="license">Author provided</span></span>
</figcaption>
</figure>
<h2>One gene, many messages</h2>
<p>As we age, we lose our ability to control how our genes are regulated. Each cell in the body contains all the information needed for life, but not all genes are switched on in all tissues or under all conditions. This is one of the ways that a heart cell is different from a kidney cell, despite the fact they contain the same genes. </p>
<p>When a gene is activated by signals from inside or outside the cell, it makes a molecular message (called an RNA) that contains all the information needed to make whatever that gene makes. We <a href="https://www.nature.com/articles/ng.259">now know</a> that over 95% of our genes can actually make several different types of messages, depending on the needs of the cell.</p>
<p>A good way to think about this is to consider each gene as a recipe. You could make either a vanilla sponge, or a chocolate cake, depending on whether you include the chocolate. Our genes can work like this. The decision as to which type of message is produced at any given time is made by a group of about 300 proteins called “splicing factors”. </p>
<p>As we age, the amount of splicing factors we are able to make declines. This means that aged cells are less able to switch genes on and off to respond to changes in their environment. We and others have shown that the levels of these important regulators <a href="https://www.ncbi.nlm.nih.gov/pubmed/21668623">decline</a> in blood samples from elderly humans, and also in <a href="https://www.ncbi.nlm.nih.gov/pubmed/23747814">isolated human senescent cells</a> of different tissue types.</p>
<h2>Rejuvenating old cells</h2>
<p>We have been looking for ways to turn the splicing factors back on. In our <a href="https://www.ncbi.nlm.nih.gov/pubmed/30026406">new work</a>, we showed that by treating old cells with a chemical that releases small amounts of hydrogen sulphide, we were able to increase levels of some splicing factors, and to rejuvenate old human cells. </p>
<p>Hydrogen sulphide is a molecule that is found naturally in our bodies and has been shown to <a href="https://www.ncbi.nlm.nih.gov/pubmed/29717417">improve several features</a> of age-related disease in <a href="https://www.ncbi.nlm.nih.gov/pubmed/24964843">animals</a>. But it can be toxic in large amounts, so we needed to find a way to deliver it directly to the part of the cell where it is needed. </p>
<p>By using a “molecular postcode” we have been able to deliver the molecule <a href="https://www.ncbi.nlm.nih.gov/pubmed/25960429">directly to the mitochondria</a>, the structures that produce energy in cells, where we think it acts, allowing us to use tiny doses, which are less likely to cause side effects. </p>
<p>We are hopeful that in using molecular tools such as this, we will be able to eventually remove senescent cells in living people, which may allow us to target multiple age-related diseases at once. This is some way in the future yet, but it’s an exciting start.</p><img src="https://counter.theconversation.com/content/101214/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lorna Harries is a trustee for the British Society for Research on Ageing and receives funding from the Dunhill Medical Trust. LWH has intellectual property (patent) on chemical modifiers of splicing factor expression as senolytic or senostatic therapeutics.</span></em></p><p class="fine-print"><em><span>Matt Whiteman (MW) has intellectual property (patents) on mitochondria-targeted, and other, slow release hydrogen sulfide releasing molecules for therapeutic and agricultural use. MW receives funding from the Medical Research Council (UK) and the Royal Society (UK).</span></em></p>New research on reversing ageing in human cells could be the first step to new anti-degenerative drugs.Lorna Harries, Associate Professor in Molecular Genetics, University of ExeterMW, Professor of Experimental Therapeutics, University of ExeterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/760782017-04-24T05:54:54Z2017-04-24T05:54:54ZResearch Check: are Aussie women ageing up to 20 years faster than US women?<figure><img src="https://images.theconversation.com/files/166043/original/file-20170420-2426-1by24ce.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">There's more to ageing than wrinkles and crow's feet.</span> <span class="attribution"><span class="source">from shutterstock.com</span></span></figcaption></figure><p>Across the developed world, looking older than your chronological age is considered a drawback. Western societies value physical beauty and vitality while science is actively trying to find a <a href="https://theconversation.com/the-search-to-extend-lifespan-is-gaining-ground-but-can-we-truly-reverse-the-biology-of-ageing-75127">way to reverse the ageing process</a> altogether.</p>
<p>This is probably why a study published in the latest issue of <a href="http://onlinelibrary.wiley.com/doi/10.1111/ajd.12637/abstract">The Australasian Journal of Dermatology</a>, that concluded Australian women report more severe signs of facial ageing sooner than other women, received a <a href="https://news.google.com/news/story?ncl=dwL1pRkK3Ut25EM6GZL7v8C_U2hRM&q=ageing+australian+women+us+women&lr=English&hl=en&sa=X&ved=0ahUKEwi8yrbcr7LTAhUCtJQKHWvuBCIQqgIIIjAA">fair amount of media coverage</a>.</p>
<p>It generated alarming <a href="http://www.smh.com.au/lifestyle/health-and-wellbeing/wellbeing/why-aussie-women-are-ageing-up-to-20-years-faster-than-us-women-20170410-gvho9k.html">headlines such as</a>:</p>
<blockquote>
<p>Why Aussie women are ageing up to 20 years faster than US women</p>
</blockquote>
<p>Like the research paper itself, these articles focused on photoageing – the damage done to our skin by exposure to high UV levels. But there is quite a bit more to the ageing process than wrinkles and crow’s feet. And the “20 years faster” claim also deserves scrutiny.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=831&fit=crop&dpr=1 600w, https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=831&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=831&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1045&fit=crop&dpr=1 754w, https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1045&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/166388/original/file-20170424-12658-19cxur.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1045&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"></span>
<span class="attribution"><span class="source">The Conversation</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<h2>How was the study done?</h2>
<p>The paper was published in a reputable, peer-reviewed outlet – the official journal of the Australasian College of Dermatologists and the New Zealand Dermatological Society.</p>
<p>The sample was 1,472 women aged 18-75 (averaging late 40s) from Australia, the UK, Canada and the US. They were recruited between December 2013 and February 2014 from an internet-based polling panel. </p>
<p>The women were asked to use a mirror to compare their own facial features to photographs illustrating increasing signs of ageing (from none to severe) for eight different characteristics.</p>
<p>These were static forehead lines, crow’s feet, glabellar (frown) lines, tear troughs (groove between lower eyelid and cheek), mid-face volume loss, nasolabial folds (the two skin folds that run from the nose to the corner of the mouth), oral commissures (the corners of the mouth) and perioral lines (wrinkles around the lips). </p>
<p>They were asked to choose one image – out of four to six (depending on the feature) – that most represented their current facial features in the absence of facial expression.</p>
<p>People were excluded if they had significant facial trauma or burns, or if they’d had any form of plastic surgery, including Botox, fillers or laser treatments. </p>
<p>Skin colour can be categorised by its typical response to UV light: from type one, which is very fair skin that always burns and never tans, to type six, which is dark brown skin that never burns and always tans. In this study, only women with skin types one to three were included. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=506&fit=crop&dpr=1 600w, https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=506&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=506&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=636&fit=crop&dpr=1 754w, https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=636&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/166046/original/file-20170420-2418-kilq9x.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=636&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The women were asked to use a mirror to compare their own facial features to photographs illustrating increasing signs of ageing.</span>
<span class="attribution"><a class="source" href="http://onlinelibrary.wiley.com/doi/10.1111/ajd.12637/full">Screenshot/Australasian Journal of Dermatology</a></span>
</figcaption>
</figure>
<h2>What were the results?</h2>
<p>Australian women reported more severe facial lines and higher rates of facial change with age than women from the other countries, particularly those from the US. Though, interestingly, for women in their 70s, the average severity of facial lines was generally similar from country to country.</p>
<p>The researchers then looked at the 30% or more of women who reported moderate or severe ageing for all features. They found that in Australia, this occurred:</p>
<blockquote>
<p>from the ages of 30-59 years […] but this proportion of US women did not report this level of severity until the ages of 40–69 years. </p>
</blockquote>
<p>This seems to be the crux of the paper, and the finding that underpins the conclusion that we’re ageing 20 years faster than we should be.</p>
<p>The study has many strengths. It is elegantly written and some aspects of the methodology are robust. For example, Asian women experience skin wrinkling later than Caucasian women, and smoking is associated with more skin ageing. So the researchers made sure these factors were not responsible for the results by adjusting their analyses for age, race and smoking status. </p>
<p>The results are certainly plausible and consistent with other studies. People living in Australia are exposed to higher levels of UV radiation, which is responsible for most age-associated cosmetic skin problems in fair-skinned people. </p>
<p>A <a href="https://www.ncbi.nlm.nih.gov/pubmed/21196710">study</a> of 1,400 randomly selected residents of a Queensland community used casts of the back of the hand and dermatological assessment to show that premature ageing of the skin was associated with high sun exposure during leisure or work.</p>
<h2>What is the problem?</h2>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/166434/original/file-20170424-12640-1wrfeks.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">People living in Australia are exposed to higher levels of UV radiation.</span>
<span class="attribution"><span class="source">from shutterstock.com</span></span>
</figcaption>
</figure>
<p>There are two main limitations of the study. First, the differences in self-reported facial lines may be statistically significant across countries, but this does not mean they are clinically significant. </p>
<p>Figures in the research plot the average severity of each line against age, with different colours representing each of the four countries. </p>
<p>Participants had up to six photographs to choose from, so the severity scale could range from 0 to 6. In the figures, the colours follow very similar trajectories and often overlap. Even the biggest gap between the countries looks like it represents a difference of 0.3 or 0.5. This is relatively small and may not be something anyone could observe.</p>
<p>Second, it is not clear why the researchers decided to focus on the 30% or more of women who reported moderate or severe ageing for all features. No other studies have used this cut-off.</p>
<p>The authors said that:</p>
<blockquote>
<p>this cut-off was chosen to yield the best sensitivity in detecting differences in facial ageing severity among countries.</p>
</blockquote>
<p>This suggests fewer differences were found than if another cut-off was considered. For example, would there have been significant differences when 20% of women rated each feature as having moderate or severe signs of ageing? Or 50%? Or 90%? Choosing a cut-off which is not based on a clinically meaningful or validated proportion raises questions about the true significance of the reported changes.</p>
<h2>What else should we consider?</h2>
<p>The title of the study is an accurate reflection of its content, stating that it is a comparison of self-reported signs of facial ageing. But the accompanying media coverage implies Australian women are ageing prematurely.</p>
<p>There is no evidence this is true. Robust studies of many tens of thousands of women show Australians are very similar to women in Europe and North America, through middle age to the extremes of old age. The <a href="http://www.alswh.org.au/">Australian Longitudinal Study on Women’s Health</a> provides a wealth of data in this field.</p>
<p>More important markers of health status in older people – disability, self-rated health, depression and anxiety, dementia – are all comparable. Life expectancy at birth (84.4 years for women) is slightly <a href="http://www.aihw.gov.au/deaths/life-expectancy/">higher in Australia</a> than in the other countries studied in this paper. </p>
<h2>What is the take-home message?</h2>
<p>Despite the methodological limitations of the study, in some ways it is good for it to be widely publicised. </p>
<p>Just like public health campaigns about premature ageing were used to decrease smoking rates in women (and thus reduced multiple smoking-related disease), the message Aussies may be looking older because of UV radiation may encourage us to limit our sun exposure. This would then reduce melanoma and other skin cancers. </p>
<p>As a type one redhead living in Brisbane, I shall certainly continue to wear my hat. <strong>– Ruth Hubbard</strong></p>
<hr>
<h2>Peer Review</h2>
<p>This Research Check fairly outlines the strengths (number of participants, accounting for age and other factors like smoking) and limitations (self-reporting and limitations in adjusting for confounding variables).</p>
<p>It also addresses the issue that caused the alarmist headlines – the graph showing when more than 30% of women rated a facial feature as reflecting moderate or severe signs of ageing. The author correctly points out there is no justification in choosing the 30% cutoff, that no other study uses it and that it is unlikely to be of any clinical significance.</p>
<p>More importantly, the Research Check analyses the figure that presents data for women across the various age groups. It points out most of the curves overlap, and that differences between groups of women are actually hard to see.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=508&fit=crop&dpr=1 600w, https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=508&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=508&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=639&fit=crop&dpr=1 754w, https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=639&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/166422/original/file-20170424-27254-4s22ze.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=639&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">It’s difficult to see the variations between countries in the graphs.</span>
<span class="attribution"><a class="source" href="http://onlinelibrary.wiley.com/doi/10.1111/ajd.12637/full">Screenshot/Australasian Journal of Dermatology</a></span>
</figcaption>
</figure>
<p>I would go even further and say that while the 95% confidence interval - an important estimate of variation - is presented in the tables, it is not applied to the graphs. If you show the 95% confidence intervals reported in the tables to the graphs, you would see most of the values for the women in other countries would not be significantly different to those in Australia. </p>
<p>For example, in the graph showing nasolabial folds, women in the light-poor UK have the same (age 18-29, 40-49) or marginally worse (age 70-79) nasolabial folds than in Australia. </p>
<p>This Research Check gives a clear, detailed and easily understandable background to the paper made visible by somewhat frenetic media reports. <strong>– Ian Musgrave</strong></p><img src="https://counter.theconversation.com/content/76078/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ian Musgrave receives funding from the National Health and Medical Research Council to study adverse reactions to herbal medicines and has previously been funded by the Australian Research Council to study potential natural product treatments for Alzheimer's disease. He is co-investigator of a grant to explore the metabolism of rodenticides. He lectures in biostatistics and the toxicology of retinoids, which have been used in "anti-aging" creams</span></em></p><p class="fine-print"><em><span>Ruth Hubbard does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>A recent study suggests Australian women are ageing 20 years earlier than their US counterparts. But this claim deserves some close scrutiny.Ruth Hubbard, Associate Professor, Centre for Research in Geriatric Medicine, The University of QueenslandLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/673082016-10-20T19:15:53Z2016-10-20T19:15:53ZIs the red wine compound resveratrol a miracle drug for infertility and ageing?<figure><img src="https://images.theconversation.com/files/142445/original/image-20161020-5009-1npr55r.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Resveratrol is found at only trace levels in red wine.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/fitzchev/15251314332/in/photolist-peGYpo-6Ujusr-azdEM4-7PFZA1-7uFYiM-84vwYj-fm9mAq-ojZfp-7TKquV-4af16x-9ad82M-6oQEM8-5yQTGe-7i4rdY-9GMxPb-8HAVK9-qgH4JR-9tuGB4-5cnxH3-7zXgtF-6ugZ4-djjuS1-5Diavg-2C1dVt-7GpoNz-ewWBU1-7qvC6y-rnVrzw-5MhNbh-ofTM8X-g3oJU-61Keie-5Twc6L-a4S5mF-dXkC43-e4gTXq-4oqP1t-6Y1hBw-5H49Dy-7WN9vQ-kS6SS-aUSjeB-5E3jEy-3bWTn4-buwxtD-7zpig5-7NETQv-8ku5N1-acTaYC-5SEotn">Cyril Hanquez/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span></figcaption></figure><p>“A glass of red wine a day could keep polycystic ovaries at bay,” <a href="http://www.dailymail.co.uk/health/article-3848452/A-glass-red-wine-day-polycystic-ovaries-bay-Compound-grapes-nuts-corrects-hormone-imbalance-women-PCOS.html">said a news headline this week</a>. This and <a href="http://www.tv3.ie/xpose/article/fitness-and-wellbeing/220449/Antioxidant-found-in-red-wine-lowers-chance-of-polycystic-ovaries">similar reports</a> were based on research from a team in Poland and California that showed high daily doses – 1,500 mg – of a natural compound found in red wine, called resveratrol, could lower steroid hormone levels in <a href="http://press.endocrine.org/doi/10.1210/jc.2016-1858">women suffering from polycystic ovarian syndrome</a> (PCOS). This, in effect, should lower symptoms of PCOS including weight gain, excess hair, infertility and abnormal menstrual cycles.</p>
<p>This is not the first time resveratrol has been linked to health benefits. Back in 2006, <a href="http://www.nytimes.com/2006/11/01/science/02winecnd.html">headlines announced</a> a “natural substance found in red wine” could extend lifespan in mice. The internet soon became flooded with <a href="http://www.ebay.com/sch/i.html?_from=R40&_trksid=p2050601.m570.l1313.TR0.TRC0.H0.TRS0&_nkw=resveratrol&_sacat=0">online sellers</a> of resveratrol supplements ranging from highly pure, to pills containing mashed up grape skins with very little resveratrol. </p>
<p>The fact resveratrol is naturally found in the skin of red grapes then led to the happy idea that drinking lots of red wine can make you live longer. But unfortunately, resveratrol is found at only <a href="http://www.ajevonline.org/content/43/1/49">trace levels</a> in red wine - so you would need to drink over a thousand bottles per day to obtain the amount of resveratrol found in two 250 mg pills.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=402&fit=crop&dpr=1 600w, https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=402&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=402&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=505&fit=crop&dpr=1 754w, https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=505&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/142455/original/image-20161020-15094-2x04fx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=505&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Resveratrol is naturally found in the skin of red grapes.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/mynameisharsha/3596243364/in/photolist-6tMFRW-bwpyGC-73unWw-pWcx7-iuRtWL-b694Yp-d3nYTS-9k5qNd-8dVNzh-4mVb8E-d33AjL-gBz2xt-bvJU9y-76MeHq-a7KK33-5dgo9C-5XMkRM-5nSwQG-6Brg7c-9dagin-eCnugf-c7gK27-APMUiX-aqq92y-83zNeD-9VCuPx-d33AiQ-9yNNQ9-85iu3F-6rp3HC-91kt5u-v3tW2-efTaX2-85iukt-owjtYv-85mDiw-xxKy9D-85mDmj-tLXVjd-vzz8VE-vdm3XE-62F7Uz-ncrvi5-cDWQtY-jKpcKS-4C7hsn-swgMCF-pNciGd-qrF5Z-7p84hw">Harsha K R/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>The 2006 reports - based on a paper <a href="http://www.nature.com/nature/journal/v444/n7117/abs/nature05354.html">published in the esteemed journal Nature</a> – were exciting for science though. Resveratrol <a href="https://www.ncbi.nlm.nih.gov/pubmed/12939617">turns on an enzyme called SIRT1</a>, which is thought to enhance the age-delaying benefits of diet and exercise. The Nature study showed resveratrol extended lifespan in a mouse, an animal far more complex than the simple organisms the compound had previously been tested on, such as <a href="https://www.ncbi.nlm.nih.gov/pubmed/12939617">yeast</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/15254550">worms and flies</a>.</p>
<p>Other studies of resveratrol in mice then showed benefits to <a href="http://www.nature.com/nature/journal/v444/n7117/abs/nature05354.html">lifespan</a>, diseases such as <a href="https://www.ncbi.nlm.nih.gov/pubmed/8985016">cancer</a> and <a href="http://www.nature.com/nature/journal/v450/n7170/full/nature06261.html">diabetes</a>, and <a href="http://www.ncbi.nlm.nih.gov/pubmed/15013856">inflammation</a>. So why has resveratrol not been made into a drug yet?</p>
<p>When it is taken as a pill, the liver <a href="https://www.ncbi.nlm.nih.gov/pubmed/15779070">quickly degrades the majority of resveratrol</a> before it can make it into the rest of the body. This means only a very small amount actually gets to other tissues where it could have an effect. So it would have to be given at very high doses. </p>
<p>But at doses where it can have an effect, resveratrol can <a href="https://www.ncbi.nlm.nih.gov/pubmed/20935227">cause gut problems</a> such as diarrhoea. Despite this, small <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3782695/">clinical trials using resveratrol</a> in humans have shown some benefits to their <a href="https://www.ncbi.nlm.nih.gov/pubmed/21385509">metabolism</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/22520621">markers of inflammation</a>, and <a href="https://www.ncbi.nlm.nih.gov/pubmed/26362286">Alzheimer’s disease</a>. </p>
<p>There has also been controversy as to how resveratrol actually works; in particular whether it activates SIRT1, the enzyme thought to delay the ageing process. </p>
<p>David Sinclair, an Australian based at Harvard Medical School, first showed resveratrol could “turn on” SIRT1 in 2003. With a series of papers in quick succession, Sinclair showed resveratrol extended lifespan in <a href="https://www.ncbi.nlm.nih.gov/pubmed/12939617">yeast</a>, <a href="https://www.ncbi.nlm.nih.gov/pubmed/15254550">worms, flies</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/16461283">fish</a>, and <a href="http://www.nature.com/nature/journal/v444/n7117/abs/nature05354.html">mice</a>. </p>
<p>Controversy struck when it was <a href="https://www.ncbi.nlm.nih.gov/pubmed/20061378">suggested</a> resveratrol was working through “off target” effects, meaning it was interacting with enzymes other than SIRT1. As a small molecule with a simple structure, it is likely resveratrol has non-specific interactions throughout the body, especially at higher doses. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=448&fit=crop&dpr=1 600w, https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=448&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=448&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=563&fit=crop&dpr=1 754w, https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=563&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/142456/original/image-20161020-15081-1a8bx7z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=563&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Products containing resveratrol range from being highly pure, to pills containing mashed up grape skins with very little resveratrol.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/streamishmc/5547704360/in/photolist-qHpaYN-61HftU-fxFESK-5x3fQ1-bo2BFc-rsHUc-6zSN93-66kzUa-8HoMuq-7t6ZoF-akvYHo-69XFwT-nxgqkc-61mnoc-az1gPm-9sereb-8eRWdx-BWQB1S-v9gasS">Jason Tester Guerrilla Futures/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>But then in 2012, these doubts were assuaged, when mice genetically engineered to be missing the SIRT1 gene were found to be <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3545644/">immune to the effects of resveratrol</a>. In 2013, it was found resveratrol <a href="https://www.ncbi.nlm.nih.gov/pubmed/23471411">binds to and activates SIRT1</a> in a very intricate manner. So that part is clear.</p>
<p>There are still uncertainties as to how specific it is; such as with the recent study involving women with PCOS. PCOS is a <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/polycystic-ovarian-syndrome-pcos">common endocrine condition</a> that occurs when follicles in the ovary, which contain egg cells, swell up and the egg cell itself does not mature properly. The eggs contained in these cysts fail to be released at ovulation, which can cause infertility in women. </p>
<p>PCOS is thought to be caused by high levels of male steroid hormones known as androgens. Key risk factors for PCOS are metabolic problems such as high insulin levels, obesity, insulin resistance, and type II diabetes. Body weight reductions can therefore reduce PCOS risk.</p>
<p>Women suffering from PCOS experience irregular or no menstrual cycle, acne, hair growth and elevated levels of the male steroid hormone testosterone. In the recent study, resveratrol treatment lowered levels of testosterone, and its precursor DHEAS – two key steroid hormonal markers of PCOS. </p>
<p>But it’s actually not clear whether the testosterone reduction was due to a direct effect on the release of the hormone itself. This is because insulin, which at high levels can cause metabolic disease, was also reduced. As with other studies, it may be that resveratrol is actually improving metabolism, with reduced PCOS severity as a secondary side-effect. So there is still a lot we don’t know about the compound.</p>
<p>Should people want to go online and buy resveratrol, be aware it has not yet been approved as a drug by regulatory authorities. Also, plant-based resveratrol extracts such as Japanese knotweed contain a crude cocktail of compounds, some of which may be harmful, with only a small amount of resveratrol. Meanwhile, red grape skin pills are likely to contain vanishingly small quantities. </p>
<p>Stay tuned though: efforts to formulate resveratrol so greater proportions actually reach the rest of the body are underway.</p><img src="https://counter.theconversation.com/content/67308/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lindsay Wu's lab receives funding from Cancer Institute NSW, the National Helath and Medical Research Council (NHMRC) of Australia, and MetroBiotech NSW Pty Ltd. He is a director of Metro Biotech NSW, Intravital Pty Ltd, and Liberty Biosecurity Pty Ltd, and is a shareholder in Intravital, EdenRoc Sciences, and Hydra Capital. </span></em></p>You would need to drink over a thousand bottles of red wine per day to get the amount of resveratrol - the compound said to have many health benefits - needed to even have an effect.Lindsay Wu, Senior Lecturer, School of Medical Sciences, UNSW SydneyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/668522016-10-12T05:31:18Z2016-10-12T05:31:18ZIf we were like mice we could live to 400 – but we’re not, so we don’t<figure><img src="https://images.theconversation.com/files/141351/original/image-20161012-8418-1x6rscg.jpg?ixlib=rb-1.1.0&rect=8%2C116%2C2959%2C2241&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Mice can slow the wheel of ageing almost at will. Humans, not so much.</span> <span class="attribution"><span class="source">Ron and Joe/Shutterstock.com</span></span></figcaption></figure><p>You may have seen the news that the human lifespan <a href="https://theconversation.com/is-there-a-natural-limit-to-how-long-humans-can-live-66460">cannot be extended beyond about 115 years</a>, as shown by a <a href="http://www.nature.com/nature/journal/vaop/ncurrent/full/nature19793.html">demographic analysis</a> confirming that the steady improvements in lifespan seen for many populations over recent decades has stalled since the 1990s.</p>
<p>The researchers’ conclusion that “the maximum lifespan of humans is fixed and subject to natural constraints” is sobering reading for those who dream that human ageing can one day be successfully hacked. But for evolutionary ecologists, it should not come as a surprise.</p>
<p>As well as striking a note of biological realism, this research also highlights how research on human ageing often neglects the insights available from evolutionary theory – and particularly from a research field called “comparative life-history ecology”. </p>
<p>This genre of research explains why mice and humans grow old at such different rates (more on why this is a problem for ageing research later). It aims to bring us closer to understanding the “ultimate” reasons why we age – which in turn can tell us whether the hundreds of millions of dollars poured into ageing research are actually a good investment. </p>
<p>Strive as we might, an evolutionary perspective tells us that maximum lifespans will not be extended by simply solving one symptom of ageing after another.</p>
<h2>Growing old – the ‘why’ as well as the ‘how’</h2>
<p>Ageing – or “senescence”, to use the biological term – is defined as a decline in physiological condition with age. You might wonder why natural selection allows this to happen at all. The answer is that senescence happens in a “selection shadow” – that is, after organisms have already reproduced and passed on their genes. There is no real evolutionary penalty for failing to ward off the ravages of old age, because in animal populations relatively few individuals make it into their geriatric years anyway, thanks to predators, disease, hardship or bad luck.</p>
<p>Natural selection reaches a crescendo at sexual maturity, when most individuals in a population are alive and striving to produce viable offspring. This is the age at which the genetic baton is passed to the next generation. Unfortunately for those of us over 40, it’s all downhill from here in terms of the evolutionary pressure to maintain a healthy body.</p>
<p>This knowledge – that selection pressure changes with age in a way that depends not just on the expected lifespan but also on the timing of reproductive effort – is fundamental to evolutionary theories of ageing. It is also fundamental to how we design and interpret the research that aims to help us prolong our own maximum lifespans.</p>
<p>Many of the species most frequently studied by biologists – such as mice, flies and worms – are chosen precisely because their short lifespans and fast generational turnover make them quicker and easier to work with. But their short lives and adaptable reproductive strategies actually make them unsuitable models for testing drugs or other anti-ageing interventions aimed at slowing human ageing.</p>
<p>Short-lived species seem to be able to “trade in” their investment in growth and sexual reproduction in return for slowing down the ageing process – <a href="http://rspb.royalsocietypublishing.org/content/282/1806/20150209">switching to a physiological state</a> in which they instead invest in maintenance of body condition and warding off senescence. </p>
<p>This strategy makes sense for species whose brief lives can be subject to wide variability in environmental conditions. For a small rodent, having a litter of pups would be rather pointless if food is too scarce for them to grow and survive to adulthood. Hamsters, for example, can instead enter a torpid state that actually <a href="http://rsbl.royalsocietypublishing.org/content/8/2/304">protects their cells from ageing</a> over winter.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/141349/original/image-20161012-8401-tvejbw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">For mice, having babies really can age you faster.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File%3ABabymouse.jpg">ShwSie/Wikimedia Commons</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
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<p>In contrast, species with long expected natural lifespans (which have reduced their mortality risk by evolving to a large size, or being able to fly or hibernate, or having a large brain) have already invested strongly, and perhaps maximally, in protecting their cells from ageing. This suggests there is no “anti-ageing switch” available to flick for a species such as ourselves. Whether or not we have children, it seems we’re already naturally geared to live as long as we possibly can.</p>
<p>This might sound weird, but it’s supported by a <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0012019">simple comparative analysis</a> that a colleague and I published back in 2010, in which we compared the <em>average expected</em> lifespan with the <em>maximum recorded</em> lifespan for various mammals. From this we can calculate a simple ratio of average to maximum lifespan, which tells you, for a given species, how much it is theoretically possible to expand lifespan.</p>
<p>If we take the ratio of a short-lived species like a mouse and apply it to humans, we would predict a maximum lifespan of about 400 years! But despite all of our efforts to push the boundaries through medicine and nutrition, humans (along with elephants and other highly durable animals) don’t come close to these biblical lifespans.</p>
<p>So if mice find it much easier to slow down the ageing process than we do, what does that mean for anti-ageing studies using mice? Sadly, the implication is that most tactics shown to prolong lifespan in mice – such as calorie restriction – will be <a href="http://www.nature.com/nature/journal/v489/n7415/full/nature11432.html">far less effective in humans</a>. </p>
<p>If we are to break the evolutionary constraints on maximum lifespan in humans, we need to better take account of life-history ecology. This theory tells us that the causes of ageing are to be found not at the end of our lives, but at the beginning. </p>
<p>How our maximum lifespan is ultimately limited will be understood by research that seeks to answer why the pace of life varies so much among different animals. For me, this is the take-home message from this recent excellent research.</p><img src="https://counter.theconversation.com/content/66852/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Christopher Turbill's research has been funded by a Discovery Early Career Researcher Award (DECRA) from the Australian Government.</span></em></p>Anti-ageing research often uses short-lived model species such as mice. But these species age in a very different way to us, so they may not tell us all that much about boosting our own lifespans.Christopher Turbill, Senior Lecturer in Animal Ecology, Western Sydney UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/580242016-04-20T05:42:55Z2016-04-20T05:42:55ZQueen Elizabeth II at 90: does old age affect a monarch’s ability to reign?<figure><img src="https://images.theconversation.com/files/119326/original/image-20160419-13905-pwqx78.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption"></span> </figcaption></figure><p>Modern British monarchs may have it easier than their forebears – but strength, intelligence and a hearty constitution are just as necessary today as they were in the Middle Ages. This may seem surprising. After all, as a constitutional monarch, Elizabeth II reigns but does not rule. She may have been given the Sword of State at her Coronation “for the terror and punishment of evildoers” but she isn’t expected to swing it herself. </p>
<p>By contrast, Richard the Lionheart (1157-1199) did so enthusiastically until a crossbowman eventually shot him. However Lionheart wasn’t expected to <a href="http://www.telegraph.co.uk/news/uknews/queen-elizabeth-II/12077343/Queen-carries-out-more-engagements-than-William-Kate-and-Harry-combined.html">attend about 400 engagements a year</a>, give out the <a href="https://www.royal.uk/">Queen’s Award for Enterprise</a> or chat to loyal subjects. Although separated by almost a millennium, both monarchs have had to manage Royal Estates as part of the job. The Queen seems the better of the two at this. Lionheart once said he would sell London if he could find a buyer.</p>
<p>So how well can a nonagenarian do the job of being a monarch – or, to be slightly more egalitarian, discharge the role of a constitutional head of state? </p>
<h2>Fit for the job</h2>
<p>Looking at her diary it seems to be a slow day when Elizabeth II doesn’t have <a href="https://www.royal.uk/search/her-majesty-the-queen">some official duties to perform</a>. There’s a lot of travel and standing around involved, so she need to be physically fit. She’ll need to stay mentally alert for all those constitutional briefings and regular meetings with the prime minister. And, if she’s to survive all those visits to hospitals, Elizabeth II needs a reasonable immune system. </p>
<p>Therefore, in social gerontology terms, the Queen needs to have the appropriate level of “<a href="http://www.ncbi.nlm.nih.gov/pubmed/21052807">work ability</a>”. In essence this is a proper balance between the capacities of the individual and the work he or she does. Work ability subsumes a wide range of factors including the right values, attitude, knowledge and skills to discharge the job (compared to most of us the Queen has the benefits of extensive prior training and considerable work experience). However health is a major determinant of work ability in general and the royal role in particular. So just how healthy are Britain’s very old people?</p>
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<p>At first sight the data is not encouraging. The <a href="http://www.bmj.com/content/339/bmj.b4904.long">Newcastle 85+ study</a> of about 1,000 men and women which is roughly representative of the population of the UK found that about 90% of participants had at least three distinct clincial conditions (out of a possible score of 18). Women were between six and ten times more likely than men to have rheumatoid arthritis, osteoporosis and thyroid problems and overall had significantly higher levels of disability. </p>
<p>Many of the problems reported by 20-40% of this cohort could compromise the discharge of royal duties including incontinence, falling and visual impairment. Given that listening to politicians is an important part of the role, readers may wish to decide for themselves if advancing age has conferred an advantage or a disadvantage on the two-thirds of the cohort who report hearing difficulties.</p>
<h2>High-class health</h2>
<p>Thus, if she wishes to continue working, it might seem that Elizabeth II has the odds stacked against her. However she does have three potential advantages. Firstly she has blue blood, and in the general population there is an (approximately) <a href="http://www.ncbi.nlm.nih.gov/pubmed/20383164">linear relationship between healthy life expectancy and social class</a>. </p>
<p>Women from social class I (doctors, chartered accountants, professionally qualified engineers, etc) can expect to live about 80 years in a fairly good state of health. In contrast, healthy life expectancy at birth for unskilled women is only about 69 years. Thus Elizabeth II has a good chance of being healthier than one of her average subjects.</p>
<p>Secondly, data from the 85+ study indicate there is a good chance that she feels positive about her health in general (and indeed the same study shows she is less likely than a man of the same age to develop atherosclerosis or cancer). Thus, palace coup d'état being a thing of the past, she may feel she can continue working.</p>
<p>Lastly, unlike those of her ancestors who continued to reign into old age such as Edward I (who died at 68) or Elizabeth I (who died at 70), Elizabeth II lives in the era of science. We now know that ageing occurs because the fundamental mechanisms which keep us in good health start to fail. Enough is <a href="http://www.ncbi.nlm.nih.gov/pubmed/25540326">already known</a> about these to use that knowledge to improve vaccination responses in the elderly using a selective inhibitor of the TOR protein which may also be beneficial for <a href="http://www.ncbi.nlm.nih.gov/pubmed/25481271">cognitive impairment</a>. A <a href="http://healthspancampaign.org/2015/04/28/dr-nir-barzilai-on-the-tame-study/">major study</a> aimed at improving late life health using a cheap and simple drug – metformin – is also planned. </p>
<p>While an enhanced immune system is certainly a bonus to a older monarch who spends a lot of time opening hospital wards, it is equally valuable to those of us who would rather avoid them. Indeed if the full potential of the new science of ageing can be translated into clinical practice, then a time in which inclination, rather than ill health, is the primary determinant of remaining in work may be nearer than you think. </p>
<p>Which may or may not be good news for the Prince of Wales.</p><img src="https://counter.theconversation.com/content/58024/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Richard Faragher is affiliated with the British Society for Research on Ageing, the American Aging Association and the American Federation for Aging Research.</span></em></p>It’s a demanding job, but all indicators suggest that the Queen is still up to it.Richard Faragher, Professor of Biogerontology, University of BrightonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/514192015-12-08T14:42:49Z2015-12-08T14:42:49ZKeep calm – it’s the secret to ageing well<figure><img src="https://images.theconversation.com/files/104461/original/image-20151204-29720-osoc88.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Get your chill on</span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/cat.mhtml?lang=en&language=en&ref_site=photo&search_source=search_form&version=llv1&anyorall=all&safesearch=1&use_local_boost=1&autocomplete_id=&searchterm=old%20person%20meditating&show_color_wheel=1&orient=&commercial_ok=&media_type=images&search_cat=&searchtermx=&photographer_name=&people_gender=&people_age=&people_ethnicity=&people_number=&color=&page=1&inline=160899158">www.shutterstock.com</a></span></figcaption></figure><p>As we get older our physical and mental abilities decline, but it doesn’t have to be that way. <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Nutrition%2C+Exercise%2C+and+Healthy+Aging+WILLIAM+J+EVANS%2C+PhD%2C+DEANNA+CYR-CAMPBELL">Research suggests</a> that the way we live our lives – our diets, our exercise regimes – can have a big impact on how we age. And it’s not just about the things we do to age well, it’s also about the things we avoid.</p>
<p>There is a large field of <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Health+habits+and+risk+of+cognitive+impairment+and+dementia+in+old+age%3A+A+prospective+study+on+the+effects+of+exercise%2C+smoking+and+alcohol+consumption">research</a> that seeks to understand the factors that cause different rates of age-related decline. In particular, scientists look at how these factors change our ability to remember and pay attention to things in everyday life. We call such changes “cognitive ageing”. </p>
<p>Earlier <a href="http://www.ncbi.nlm.nih.gov/pubmed/19876740">work</a> has looked at how diet or doing physical or mental exercise (sudoku, crosswords) affects ageing. However, the amount of stress we experience over a lifetime and the impact it has on cognitive ageing has remained an under-researched area, until recently. </p>
<h2>A lifetime of stress</h2>
<p>Work from our lab and from <a href="http://www.ncbi.nlm.nih.gov/pubmed/21370277">others</a> has found that many of the negative aspects of cognitive ageing seen in older people appear to be linked to the amount of stress they have experienced in their life. We began by measuring the number of stressful events experienced over the lifetime. We looked at a number of factors ranging from experiencing a major illness or losing a loved one, to changing one’s social habits or moving home. Old people who have experienced a lot of stress tend to perform worse on cognitive tasks than those who experienced less stress.</p>
<p>Crucially, old people who haven’t experienced much stress in their life perform just as well on cognitive tasks as young people. This suggests that stress has a big impact on mental ability and that the effect of this only appears in old age. Indeed, young people did not differ from each other in their performance of cognitive tests whatever their life experience of stress had been.</p>
<p>Not only that but the patterns of brain activity of the people taking part in <a href="http://www.researchgate.net/publication/273836703_The_Effects_of_Long-Term_Stress_Exposure_on_Aging_Cognition_A_Behavioral__EEG_Investigation">our study</a> reflect the same effect: older people (aged 60 to 80) who have experienced less stress have brain activity similar to that of younger people. However, when it comes to the brain activity of those elderly people who have led stressful lives, we find something very different going on. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=375&fit=crop&dpr=1 600w, https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=375&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=375&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=471&fit=crop&dpr=1 754w, https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=471&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/104645/original/image-20151207-9050-zqxdbt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=471&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">EEG reveals different patterns of brain activity.</span>
<span class="attribution"><a class="source" href="http://www.shutterstock.com/cat.mhtml?lang=en&language=en&ref_site=photo&search_source=search_form&version=llv1&anyorall=all&safesearch=1&use_local_boost=1&autocomplete_id=&search_tracking_id=QqHsH5jN56rsNZpwObrPIg&searchterm=EEG&show_color_wheel=1&orient=&commercial_ok=&media_type=images&search_cat=&searchtermx=&photographer_name=&people_gender=&people_age=&people_ethnicity=&people_number=&color=&page=1&inline=187437812">www.shutterstock.com</a></span>
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<p>This brain activity may give us some clues as to what’s going wrong and where in the brain it is happening. For instance, depending on the task involved, we can see that a significant amount of stress in a person’s lifetime can affect their ability to hold items in their short-term memory and can also reduce their ability to stop irrelevant thoughts from interfering with this process. </p>
<p>In particular, stress appears to affect an area of the brain essential for the formation of new memories (<a href="https://www.researchgate.net/publication/281516717_The_Impact_of_Experienced_Stress_on_Aged_Spatial_Discrimination_Cortical_Overreliance_as_a_Result_of_Hippocampal_Impairment">the hippocampus</a>). </p>
<p>But the long-term effects of stress are not only apparent in memory: recently it has been shown for the first time that brain processes and behaviour associated with our control of <a href="https://www.researchgate.net/publication/283543908_Experienced_Stress_Produces_Inhibitory_Deficits_in_Elderlies'_Flanker_Task_Performance_First_Evidence_for_Lifetime_Stress_Effects_Beyond_Memory">attention and movement</a> are also impaired. This may relate to brain activity you use trying to stop a physical movement (such as moving your arm) that you have already initiated or activity linked to controlling where your attention is focused.</p>
<h2>Do something about it</h2>
<p>So what can we do about it? Most of us know when we are feeling stressed. For those of us who don’t, <a href="https://theconversation.com/dont-call-the-doctor-your-phone-can-now-tell-when-you-are-stressed-27254">smart devices</a> can be used to alert us to the presence of potential dangers. By being aware of stress and its long-term consequences, we can begin to tackle it and to find ways to lessen its consequences. </p>
<p>The paths to de-stressing are numerous. Some people find meditation and <a href="http://www.ncbi.nlm.nih.gov/pubmed/25818837">mindfulness</a> to be useful, for others the same techniques could be fruitless or even <a href="https://www.newscientist.com/article/mg22630210-500-panic-depression-and-stress-the-case-against-meditation/">dangerous</a>. Each person needs to find what works for them. It may take a bit of experimenting, but the pay-off will be worth it. Just don’t expect it to do anything for your wrinkles.</p><img src="https://counter.theconversation.com/content/51419/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>New research shows that the effects of stress accumulate over a lifetime.Nicholas Robert Cooper, Academic Director of the Centre for Brain Science, University of EssexAmanda Claire Marshall, PhD Researcher, University of EssexNicolas Geeraert, University of EssexLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/487552015-10-16T00:38:35Z2015-10-16T00:38:35ZOn eternal life: why an anti-ageing pill might sour the pleasures of existence<figure><img src="https://images.theconversation.com/files/98350/original/image-20151014-876-hcer97.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Would finding the fountain of youth really be such a great thing?</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/quatar/8720503800/in/photolist-ehARXN-6sv9iT-4RgEXC-dgXi32-2ydon8-a5kcXL-Hms1i-JTMZD-9zZ4zM-79cqMv-gh7kVg-gh6Yim-85gy6c-6hXbhj-dSJ9i4-6njXHm-bUf3vL-6nfPSB-eGNMBP-3xaMKg-9UvB6B-4F5V8g-gh6C5U-diJNHv-4F5Vmt-7K56j6-gh6TJa-gh6SN2-tFRnhX-fgZFNH-aLGLWp-faYCmE-6tnQeM-cD3QR3-nEqb7R-84qfbs-6gMtku-4MsGno-6sDobz-7RtQcF-NsN6h-5b4on2-6iaHAJ-K3hs8-7QLXv4-7QQeFb-9Fo3bx-7QQfqA-7BqUfC-7Vkat8">Nicola Sapiens De Mitri/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span></figcaption></figure><p>Centuries ago, Spanish explorer Ponce de Leon searched for the Fountain of Youth, a spring that restores youth to whoever drinks from, or bathes in it. Today, some scientists are keeping the dream alive.</p>
<p>These thinkers believe genetic engineering, or the discovery of anti-ageing drugs, could extend human life far beyond its natural course. </p>
<p>Indeed, Australian geneticist David Sinclair believes such a pill could be as close as <a href="http://www.abc.net.au/7.30/content/2014/s4014272.htm">ten years away</a>. Cambridge researcher <a href="http://www.theguardian.com/science/2015/jan/11/-sp-live-forever-extend-life-calico-google-longevity">Aubrey de Grey thinks</a> there is no reason humans cannot live for at least 1,000 years.</p>
<p>It’s certainly an enticing prospect, which has investors jumping on board. In 2013, <a href="http://www.theguardian.com/science/2015/jan/11/-sp-live-forever-extend-life-calico-google-longevity">Google started Calico</a>, short for the California Life Company. Employing scientists from the fields of medicine, genetics, drug development and molecular biology, <a href="http://www.calicolabs.com">Calico’s aim is to</a> “devise interventions that slow ageing and counteract age-related diseases”. </p>
<p>Those who fear death and want to live as long as possible would welcome this kind of research. But many philosophers and ethicists are sceptical about the implications of longer lifespans, both for the individual and society. Their doubts recall the old saying: be careful what you wish for.</p>
<h2>Individual discontents</h2>
<p>For some, the idea of living longer is a no-brainer. <a href="http://www.livescience.com/10465-ethical-dilemmas-immortality.html">According to bioethicist John Harris</a>, the commitment to extending life indefinitely is justified by the same reasoning that commits us to saving lives. He believes scientists have a moral obligation to do so. </p>
<p>But Leon Kass, a former US presidential advisor on bioethics, takes the concept of eternal life deeper than simply “life is good and death is bad”. He asks whether, if the human lifespan were increased, its pleasures would also increase proportionally.</p>
<blockquote>
<p>Would professional tennis players really enjoy playing 25% more games of tennis? Would the Don Juans of our world feel better for having seduced 1,250 women rather than 1,000?</p>
</blockquote>
<p>He wonders if life would <a href="http://faculty.utpa.edu/jmmartinez/general/genbiocloning.pdf">be as serious</a> or meaningful without mortality’s limit. Kass believes an end point encourages us to make the most of our time, to live it passionately and struggle to achieve our goals in the short time that we have. In other words, “mortality makes life matter”.</p>
<p>Philosopher Larry Temkin is similarly concerned about whether anything would strike him as new, exciting or bewitching if he lived forever. He echoes <a href="http://www.cappe.edu.au/media/docs/TemkinExtendingLifespans.pdf">a worry many philosophers have</a> about the prospect of immortality: all activities and experiences that make our lives interesting would become boring and meaningless after thousands of repetitions.</p>
<h2>Loss of self</h2>
<p>Temkin expresses <a href="http://www.cappe.edu.au/media/docs/TemkinExtendingLifespans.pdf">another philosophical worry</a> about a vastly extended human life. Our ability to remember is probably limited. As we age we tend to forget many things that happened earlier in our lives. Perhaps people who live for 1,000 years or more will forget altogether what happened in the earlier parts of their existence. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/98576/original/image-20151015-30707-rmr222.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">As we age, we tend to forget many things from our earlier life.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/portier/3969225787/in/photolist-73Kjxn-8RjXUy-BirMH-7GvnBw-8f5seR-6dgu39-hHWij-dPLpCG-dXo477-7LxZxW-7MpxBH-4QUPVq-7BGmyS-6XC9s5-fQXwBq-71DGAb-uDUSGN-pxXNqp-6uhura-bQacm6-nHTtX-iPFZcJ-avX6xh-7zAqJA-581U3T-9GXG7v-3efDCx-mfEZiH-a5WcCj-8TgVJq-ZWQuz-jt3Cqw-5GB7bn-r9bwNR-8ocjm4-46j3WW-8J3RR2-kS58D-6hwoZY-2H3Uvf-yUXUZA-9Q9yv2-95m8AC-dNW7J1-8NbpsP-7vNvqK-rsmuM3-c1Unry-e89eR-6k3h9f">Daniel/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
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<p>Even if their early lives were on record, they might have a hard time recognising these recorded experiences as belonging to them. Temkin says were he to live long enough, he might become so distanced from his first set of children that he would no longer care for, or even remember, them. </p>
<p>Echoing this, philosopher Bernard Williams <a href="http://stoa.org.uk/topics/death/the-makropulos-case-reflections-on-the-tedium-of-immortality-bernard-williams.pdf">thinks an extended life</a> would be destructive of identity. As memories are lost and people change their characters and interests during the course of a very long life, they would lose contact with the person they used to be. </p>
<p>Williams thinks attempting to prolong our existence is self-defeating. The self that we want to preserve would, after a time, no longer exist.</p>
<p>But defenders of anti-ageing research, such as Harris, <a href="http://www.livescience.com/10465-ethical-dilemmas-immortality.html">think long-living people</a> would adjust to their new condition and find new ways of valuing and enjoying life. </p>
<p>Even so, social and ethical concerns raised by critics of longevity are not so easy to set aside.</p>
<h2>Social discontents</h2>
<p>Many <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652797/">critics fear</a> life-prolonging treatments aren’t likely to be available to everyone. Wealthy people, including powerful autocrats in poor countries, will be able to afford them. The poor will not.</p>
<p>The prospect of a 1,000-year-reign for the likes of Kim Jong Un, North Korea’s leader, is not appealing.</p>
<p>But let’s say most people would be able to extend their lives. If they continued to have children, then the world would be even more overpopulated than today. And the prospects for younger people won’t be bright if older people, with their wealth of experience, continue to fill available jobs and retain their hold on power.</p>
<p>If children are to flower, says Kass, then we must go to seed. The flourishing of the young is important not only for their own sake. Young people are often the source of innovation and social progress.</p>
<p><a href="http://www.livescience.com/10465-ethical-dilemmas-immortality.html">Harris thinks</a> if we were to overpopulate like this, some form of “generational cleansing” might be necessary. This would mean authorities deciding the length reasonable for a generation to live and ensuring individuals died once they reached the end of their term. Once they have had a “fair go”, the old should be prepared to leave the world to the young.</p>
<p>It would be ironic, however, if a cure for death meant that people had to be forced to die.</p>
<p>But the issues described above are unlikely to be a deterrent. If we truly get a chance to sip from the Fountain of Youth, many are likely to take it. </p>
<p>Just in case the possibility comes about, <a href="http://www.cappe.edu.au/media/docs/TemkinExtendingLifespans.pdf">Temkin thinks</a> now is a good time to reflect on why life is valuable. “If your life isn’t meaningful at 70 years, it’s not going to be meaningful just because it’s a lot longer,” he says.</p><img src="https://counter.theconversation.com/content/48755/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Janna Thompson does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Some scientists claim a pill that would have us living healthier lives for longer is less than a generation away. But many philosophers argue extended life may not be as good as it sounds.Janna Thompson, Professor of Philosophy, La Trobe UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/449492015-07-28T10:20:51Z2015-07-28T10:20:51ZDespite research breakthroughs, an anti-aging pill is still a long way off<figure><img src="https://images.theconversation.com/files/89692/original/image-20150724-8442-yze1r8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-141946222/stock-photo-pill-labeled-with-anti-aging.html?src=pp-same_artist-115097248-3&ws=1">Pills via www.shutterstock.com.</a></span></figcaption></figure><p>A team of doctors and scientists <a href="http://www.nature.com/news/anti-ageing-pill-pushed-as-bona-fide-drug-1.17769">made the case</a> to regulators at the Food and Drug Administration (FDA) in 2015 to consider approving anti-aging drugs as a new pharmaceutical class. Such a designation would treat aging as disease rather than a natural process, potentially opening the door to government funding for anti-aging drug trials. </p>
<p>To some, such a drug may seem impossible. Yet, the physiologic basis for it exists. In fact, some candidate drugs, such as metformin, used to treat diabetes, are already being safely used for treating other conditions. Many scientists <a href="http://dx.doi.org/10.1038/nature11861">believe</a> that designing an anti-aging medication is a matter of “when,” not “if.”</p>
<p>Yet the very idea of a quick-fix pill for stopping, and perhaps even reversing, nature’s intricate biologic clock thus far has proven to be a hubristic notion. There is much we need to learn about how the aging process works. And while some drugs have shown promise as anti-aging treatments in the lab, we don’t know how well, or even if, they will work in humans.</p>
<h2>What actually happens to us when we age?</h2>
<p>Aging remains a mystery. While the visible changes of gray hair and wrinkles are unmistakable, what goes on inside your body is less clear. According to <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995895/">leading theories</a>, aging is an accumulation of damage inside your cells, the building blocks of your tissues.</p>
<p>Cells continually receive cues from your body and the environment that can accelerate age-driving processes such as oxidative damage and inflammation. These processes are interdependent – woven in a complex maze that is perplexing and daunting for researchers.</p>
<p>Rather than trying to extend life by individually targeting prevention and treatment of common age-related diseases such as heart disease, stroke and cancer, scientists are looking for a “<a href="http://dx.doi.org/10.1111/acel.12338">master control switch</a>” that can regulate the divergent and overlapping pathways that contribute to aging itself. </p>
<p>Since aging is the biggest risk factor for developing such diseases, an anti-aging medication that can flip this switch would theoretically not only slow or stop aging but would also defer many diseases associated with aging.</p>
<p>And that is what some of the drugs scientists are investigating may be able to do.</p>
<h2>A drug from dirt: rapamcyin</h2>
<p>Discovered more than 30 years ago in soil samples from the Polynesian island of Rapa Nui, <a href="http://blogs.discovermagazine.com/notrocketscience/2009/07/08/rapamycin-the-easter-island-drug-that-extends-lifespan-of-old-mice/">rapamcyin</a> is perhaps the leading contender in the race for the first anti-aging drug. </p>
<p>It is already FDA-approved for use as an immune suppressant that reduces organ rejection in kidney transplants. It is also used to treat certain cancers, since it can stop cells from growing.</p>
<p>In 2009, researchers made another <a href="http://dx.doi.org/10.1038/nature08221">observation</a> about this versatile drug: when fed to mice at the equivalent age in humans of 60 years, it gave them a boost in life expectancy – an impressive 38% in female mice and 28% in male mice. It has also been proven to extend lifespan in yeast, worms and fruit flies.</p>
<p>Rapamycin’s ability to extend life in these animals comes from its ability to block a cell’s mTOR pathway – which gets its name for being the “mammalian target of rapamycin.” mTOR controls many <a href="http://dx.doi.org/10.1038/nature08221">diverse processes</a> that affect how a cell grows and proliferates. It is one of the master switches researchers have been hoping to find – a unifying pathway in all of our cells that can control the rate of aging as well as the risk of diseases such as heart disease, cancer and Alzheimer’s dementia. </p>
<p>mTOR gets its cues from hormones as well as nutrients. When food is abundant, mTOR signals cells to absorb nutrients and grow. The very process of growing and metabolizing food, however, creates byproducts that stress and age cells. </p>
<p>Restrict calories and mTOR signals cells to stop growing – and hence slows aging. What makes rapamycin attractive as an anti-aging drug is that it can block the mTOR pathway without the need for restricting calories.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=412&fit=crop&dpr=1 600w, https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=412&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=412&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=517&fit=crop&dpr=1 754w, https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=517&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/89741/original/image-20150726-8474-dtoh5c.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=517&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">We don’t know much about how resveratrol affects humans.</span>
<span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-94748437/stock-photo-purple-red-grapes-with-green-leaves-on-the-vine-fresh-fruits.html?src=bLV8gH8pKtu-FSpRCdsdOg-1-37">Grapes via www.shutterstock.com.</a></span>
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</figure>
<h2>Grapes, nuts and resveratrol</h2>
<p>Finding a drug that can mimic calorie restriction – which otherwise may not be practical or sustainable – has become a focal point for anti-aging research.</p>
<p>Mostly an experimental tool, calorie-restricted diets are ones that reduce calorie consumption by 30%–40% while still including all needed nutrients. </p>
<p>It was discovered as a way to extend lifespan in the 1930s when Clive McCay, a nutritionist at Cornell University, <a href="http://jn.nutrition.org/content/140/7/1205.full.pdf+html?sid=95388266-03db-44fe-a990-9044e2c0aa55">incidentally observed</a> that rats that were on calorie-restricted diets were living considerably longer than their litter mates. Since then, calorie restriction has been proven to extend life in yeast, worms, flies, certain strains of mice and some nonhuman primates. </p>
<p>Exactly how calorie restriction extends longevity isn’t known, but is likely to involve reducing stress inside cells caused by harmful byproducts, called free radicals, that are produced in the process of breaking down food.</p>
<p>Blocking the mTOR pathway is one way to mimic calorie restriction a la rapamycin. David Sinclair, an Australian researcher now based at Harvard, has been studying another pathway: a group of genes called sirtuins. Similar to mTOR, one of these genes, SIRT1, may be a unifying pathway, or master regulator, with the potential to extend lifespan and prevent a slew of age-related diseases.</p>
<p>SIRT1 is switched on by calorie restriction. In 2003, Sinclair and his colleagues made the discovery that resveratrol, a natural compound found in grapes, red wine and certain nuts, <a href="http://dx.doi.org/10.1038/nature01960">can also turn on SIRT1</a> – and extend lifespan in yeast by 70%. </p>
<p>Subsequently given to mice on a high-fat diet, resveratrol-fed mice <a href="http://dx.doi.org/10.1038/nature05354">lived longer</a> than their non-resveratrol-fed counterparts. </p>
<p>However, given to mice on a regular diet, resveratrol did not show the same impressive life-extending results. This, along with other studies, has raised questions about resveratrol’s anti-aging benefit. </p>
<p>Although preliminary human studies on the anti-aging benefit of resveratrol are promising, resveratrol thus far has mostly been extensively studied in laboratory and animal studies. There have been over 4,000 studies on resveratrol, but <a href="http://dx.doi.org/10.1002/mnfr.201100143">only a handful</a> have been done in humans, so it is too early to know if resveratrol will have an anti-aging and disease preventing benefit for us.</p>
<p>While research continues on resveratrol, <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/">over a hundred other drugs</a> have been studied that can activate sirtuin genes – with the <a href="http://www.sciencedaily.com/releases/2013/03/130308111312.htm">leading three</a> currently being studied in human trials. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/89742/original/image-20150726-8439-ucko5l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Some drugs might target telomeres.</span>
<span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-286464095/stock-photo-a-telomere-is-a-region-of-the-dna-sequence-at-the-end-of-a-chromosome-their-function-is-to-protect.html?src=1Jel9O1Yp1EvV9RuJsuYNA-1-14">Telomeres via www.shutterstock.com.</a></span>
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</figure>
<h2>Genetically engineering longevity</h2>
<p>Searching for drugs that can flip a master-switch longevity gene is one approach to extending lifespan. Researchers are also looking at other ways of manipulating genes.</p>
<p>Telomeres, caps at the end of chromosomes that shorten every time a cell divides, are one potential target. When telomeres are dwindled down, a cell can no longer divide, and dies.</p>
<p>Ronald DePinho and his group at the Dana-Farber Cancer Institute in Boston <a href="http://dx.doi.org/10.1038/nature09603">have been studying</a> how manipulating telomerase, an enzyme that can preserve these tips, affects mice.</p>
<p>Other researchers are looking for a drug that could ramp up telomerase, in particular as a potential treatment for people with <a href="http://www.ncbi.nlm.nih.gov/pubmed/10591218/">rare disorders that cause premature aging</a>. But there is a caveat to this approach: ramping up telomeres could potentially encourage cells to divide indefinitely and become tumor cells.</p>
<p>Another longevity gene that is being explored is the Klotho gene. Klotho is an aging suppressor gene. Researchers have <a href="http://www.ncbi.nlm.nih.gov/pubmed/12362891">discovered</a> that mice without Klotho age faster and are more prone to age-related diseases. It’s much too early to know if manipulating Klotho will affect human longevity.</p>
<h2>Of mice and men</h2>
<p>These drugs are all amazing and groundbreaking, yes – but not in humans. The role of mTOR, sirtuins, telomerase and Klotho in human aging is more nuanced and complex than in lab animal studies. Making the leap from mice to men – and realizing the futuristic vision of communities full of active, healthy, independent centenarians – will require overcoming many hurdles.</p>
<p>Rapamycin’s life-extending ability in invertebrates and mice is encouraging but it remains to be seen whether it will have the same longevity benefit in humans. Rapamycin is also not without <a href="http://dx.doi.org/10.1038/nature11861">side effects</a>. It can raise cholesterol and blood sugar. </p>
<p>And, <a href="http://dx.doi.org/10.1111/j.1474-9726.2012.00832.x">a 2012 study</a> of long-term rapamycin treatment in mice reported increased incidence of cataracts and testicular degeneration – not very sexy for a longevity drug. </p>
<p>Another unresolved question is whether rapamycin would suppress the immune system of healthy people, which may slow aging while making people susceptible to otherwise innocuous bacteria and viruses.</p>
<p>Despite widespread acceptance, scientists do not yet know if long-term calorie restriction is nutritionally safe or effective in humans. Although encouraging in lab animal models, calorie restriction doesn’t seem to have the same life extending benefit in non-lab, or wild, mice. Studies in nonhuman primates and humans are under way, but it will be years until we know the results.</p>
<p>While the race to find the first true anti-aging pill – and our obsession with eternal youth – continues, it is easy to overlook that we already have a proven “breakthrough” for slowing aging and delaying or preventing age-related diseases: following a balanced diet full of fruits, vegetables and whole grains and getting regular physical activity. And, all the side effects, I promise, are ones you will enjoy.</p><img src="https://counter.theconversation.com/content/44949/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sharon Horesh Bergquist does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The very idea of a quick-fix pill for stopping, and perhaps even reversing, nature’s intricate biologic clock thus far has proven to be a hubristic notion.Sharon Horesh Bergquist, Physician, teacher, researcher in preventive medicine and healthy aging, Emory UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/164062013-07-26T05:33:09Z2013-07-26T05:33:09ZThe worm that died in a blaze of blue glory<figure><img src="https://images.theconversation.com/files/28083/original/8qymx9s9-1374753486.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">C. Elegans alive (left) and dead (right).</span> <span class="attribution"><span class="source">Wellcome Trust</span></span></figcaption></figure><p>Never has “feeling blue” carried such a sense of finality. A new study has revealed the simple worm (<em>Caenorhabditis elegans</em>) meets its death in a flash of azure. And, according to researchers, the blue light shows that dying may be a coordinated process that could probably be delayed.</p>
<p>Scientists have known for many years that cells can die in two ways. Necrosis occurs when either the cell’s machinery breaks down with age, or exposure to trauma damages the cell beyond repair. Apoptosis is a programmed process triggered on demand, by which even healthy cells can undergo a series of changes resulting in an orderly death.</p>
<p>But when it comes to multicellular organisms dying, such as humans, defining the exact mechanisms becomes more complicated. It cannot simply be explained by a bunch of cells dying independently. How do you define the precise moment when an animal stops being alive and what is the sequence of events leading to death?</p>
<p>To answer that question, David Gems of University College London, who led the study published in the journal <a href="http://dx.doi.org/10.1371/journal.pbio.1001613">PLOS Biology</a>, looked at a simple worm (<em>Caenorhabditis elegans</em>) dying under his microscope. This model organism is easy to study because it is tiny, completely transparent, has a relatively short life and its genes have been studied inside-out.</p>
<p>What Gems and his colleagues found was that under ultraviolet light, the intestine of <em>C. elegans</em> would emit a blue fluorescent light as the worm was about to die. The light, termed “death fluorescence” by the researchers, got more and more intense as the worm’s cells became necrotic. The light reached its maximum intensity at the exact moment the worm died and then quickly faded away.</p>
<p>The finding is remarkable because the blue light was observed both for worms dying from natural causes and for stress-related death, such as under extreme heat or cold. Starting from one end of the worm, the blue light wave would propagate along its intestine until it was dead. This ordered propagation suggested that, among multicellular organisms, death may happen through a series of coordinated “self-destruct” signals.</p>
<p>Gems found that the blue light was caused by the activation of a biological pathway related to calcium signalling, ultimately triggering the fluorescence of small molecules called anthranilic acids (AAs). They found that the spark of blue light was not due to the sudden production of AAs, but because of their release from acidic cellular compartments when the membranes keeping them trapped broke open upon necrosis.</p>
<p>When the team blocked the calcium signalling pathway, the burst could be delayed if a stress was the cause of death. However, no delay could be obtained if it was a case of age-related death. This suggests that age-related death involves more than just calcium signalling.</p>
<p>The work casts doubt on the idea that age-related death is simply a consequences of accumulated damage at the cellular level. It may well be that a coordinated action decides when threshold is met. But the fact that death can now be caught in action under a microscope will help us develop and understand methods to delay it. In which case, seeing the light might be a good thing in the end.</p>
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<p class="fine-print"><em><span>Luc Henry does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Never has “feeling blue” carried such a sense of finality. A new study has revealed the simple worm (Caenorhabditis elegans) meets its death in a flash of azure. And, according to researchers, the blue…Luc Henry, Postdoctoral Fellow, EPFL – École Polytechnique Fédérale de Lausanne – Swiss Federal Institute of Technology in LausanneLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/149112013-06-03T13:41:28Z2013-06-03T13:41:28ZLust for life: breaking the 120-year barrier in human ageing<figure><img src="https://images.theconversation.com/files/24954/original/5yvrs63c-1370265555.jpg?ixlib=rb-1.1.0&rect=331%2C101%2C1545%2C1045&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">I'm 110 and still going strong.</span> <span class="attribution"><span class="source">Nuno Cruz</span></span></figcaption></figure><p>In rich countries, more than 80% of the population today will survive past the age of 70. About 150 years ago, <a href="https://theconversation.com/if-you-want-to-live-longer-do-nothing-14134">only 20% did</a>. In all this while, though, only one person lived beyond the age of 120. This has led experts to believe that there may be a limit to how long humans can live.</p>
<p>Animals display an astounding variety of maximum lifespan ranging from mayflies and gastrotrichs, which live for 2 to 3 days, to giant tortoises and bowhead whales, which can live to 200 years. The record for the <a href="http://news.nationalgeographic.co.uk/news/2007/10/071029-oldest-clam.html">longest living animal</a> belongs to the quahog clam, which can live for more than 400 years.</p>
<p>If we look beyond the animal kingdom, among plants the giant sequoia lives past <a href="http://www.nps.gov/yose/planyourvisit/mg.htm">3000 years</a>, and bristlecone pines reach <a href="http://www.nps.gov/grba/planyourvisit/identifying-bristlecone-pines.htm">5000 years</a>. The record for the longest living plant belongs to the Mediterranean tapeweed, which has been found in a flourishing colony estimated at <a href="http://www.newscientist.com/article/dn21433-patch-of-seagrass-is-worlds-oldest-living-organism.html">100,000 years</a> old.</p>
<figure class="align-left ">
<img alt="" src="https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=397&fit=crop&dpr=1 600w, https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=397&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=397&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=499&fit=crop&dpr=1 754w, https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=499&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/24953/original/kxb48k2p-1370265221.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=499&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">This jellyfish never dies.</span>
<span class="attribution"><span class="source">Michael W. May</span></span>
</figcaption>
</figure>
<p>Some animals like the <a href="http://www.biochem.uci.edu/Steele/PDFs/Hydra_senescence_paper.pdf">hydra</a> and a species of <a href="http://9e.devbio.com/preview_article.php?ch=2&id=6">jellyfish</a> may have found ways to cheat death, but further research is needed to validate this. </p>
<p>The natural laws of physics may dictate that most things must die. But that does not mean we cannot use nature’s templates to extend healthy human lifespan beyond 120 years.</p>
<h2>Putting a lid on the can</h2>
<p>Gerontologist Leonard Hayflick at the University of California thinks that humans have a definite expiry date. In 1961, he showed that human skin cells grown under laboratory conditions tend to divide approximately 50 times before becoming senescent, which means no longer able to divide. This phenomenon that any cell can multiply only a limited number of times is called the <a href="http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60908-2/fulltext">Hayflick limit</a>.</p>
<p>Since then, Hayflick and others have successfully documented the Hayflick limits of cells from animals with varied life spans, including the long-lived Galapagos turtle (200 years) and the relatively short-lived laboratory mouse (3 years). The cells of a Galapagos turtle divide approximately 110 times before senescing, whereas mice cells become senescent within 15 divisions.</p>
<p>The Hayflick limit gained more support when Elizabeth Blackburn and colleagues <a href="http://www.nobelprize.org/nobel_prizes/medicine/laureates/2009/">discovered</a> the ticking clock of the cell in the form of telomeres. Telomeres are repetitive DNA sequence at the end of chromosomes which protects the chromosomes from degrading. With every cell division, it seemed these telomeres get shorter. The result of each shortening was that these cells were more likely to become senescent.</p>
<p>Other scientists used census data and complex modelling methods to come to the <a href="http://link.springer.com/article/10.1007/s10522-008-9156-4/fulltext.html#CR12">same conclusion</a>: that maximum human lifespan may be around 120 years. But no one has yet determined whether we can change the human Hayflick limit to become more like long-lived organisms such as the bowhead whales or the giant tortoise.</p>
<p>What gives more hope is that no one has actually proved that the Hayflick limit actually limits the lifespan of an organism. Correlation is not causation. For instance, despite having a very small Hayflick limit, mouse cells typically divide indefinitely when grown in standard laboratory conditions. They behave as if they have no Hayflick limit at all when grown in the concentration of oxygen that they experience in the living animal (3-5% versus 20%). They <a href="http://www.nature.com/ncb/journal/v5/n8/full/ncb1024.html">make enough telomerase</a>, an enzyme that replaces degraded telomeres with new ones. So it might be that currently the Hayflick “limit” is more the Hayflick “clock”, giving readout of the age of the cell rather than driving the cell to death.</p>
<h2>The trouble with limits</h2>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=181&fit=crop&dpr=1 600w, https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=181&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=181&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=228&fit=crop&dpr=1 754w, https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=228&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/24955/original/wtsgyyhh-1370265976.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=228&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Happy last few days? It doesn’t have to end this way.</span>
<span class="attribution"><span class="source">ptimat</span></span>
</figcaption>
</figure>
<p>The Hayflick limit may represent an organism’s maximal lifespan, but what is it that actually kills us in the end? To test the Hayflick limit’s ability to predict our mortality we can take cell samples from young and old people and grow them in the lab. If the Hayflick limit is the culprit, a 60-year-old person’s cells should divide far fewer times than a 20-year-old’s cells.</p>
<p>But this experiment fails time after time. The 60-year-old’s skin cells still divide approximately 50 times - just as many as the young person’s cells. But what about the telomeres: aren’t they the inbuilt biological clock? Well, it’s <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0045166">complicated</a>.</p>
<p>When cells are grown in a lab their telomeres do indeed shorten with every cell division and can be used to find the cell’s “expiry date”. Unfortunately, this does not seem to relate to actual health of the cells.</p>
<p>It is true that as we get older our telomeres shorten, but only for certain cells and only during certain time. Most importantly, trusty lab mice have telomeres that are five times longer than ours but their lives are 40 times shorter. That is why the relationship between telomere length and lifespan is unclear.</p>
<p>Apparently using the Hayflick limit and telomere length to judge maximum human lifespan is akin to understanding the demise of the Roman empire by studying the material properties of the Colosseum. Rome did not fall because the Colosseum degraded; quite the opposite in fact, the Colosseum degraded because the Roman Empire fell.</p>
<p>Within the human body, most cells do not simply senesce. They are repaired, cleaned or replaced by stem cells. Your skin degrades as you age because your body cannot carry out its normal functions of repair and regeneration.</p>
<h2>To infinity and beyond</h2>
<p>If we could maintain our body’s ability to repair and regenerate itself, could we substantially increase our lifespans? This question is, unfortunately, vastly <a href="http://www.scientificamerican.com/article.cfm?id=researchers-disagree-about-how-to-extend-human-lifespan">under-researched</a> for us to be able to answer confidently. Most institutes on ageing promote research that delays onset of the diseases of ageing and not research that targets human life extension.</p>
<p>Those that look at extension study how diets like calorie restriction affect human health or the health impacts of molecules like resveratrol derived from red wine. Other research tries to understand the mechanisms underlying the beneficial effects of certain diets and foods with hopes of synthesising drugs that do the same. The tacit understanding in the field of gerontology seems to be that, if we can keep a person healthy longer, we may be able to modestly improve lifespan.</p>
<p>Living long and having good health are not mutually exclusive. On the contrary, you cannot have a long life without good health. Currently most ageing research is concentrated on improving “health”, not lifespan. If we are going to live substantially longer, we need to engineer our way out of the current 120-year-barrier.</p><img src="https://counter.theconversation.com/content/14911/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Avi Roy does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>In rich countries, more than 80% of the population today will survive past the age of 70. About 150 years ago, only 20% did. In all this while, though, only one person lived beyond the age of 120. This…Avi Roy, PhD student, University of BuckinghamLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/141342013-05-15T23:06:15Z2013-05-15T23:06:15ZIf you want to live longer, do nothing<figure><img src="https://images.theconversation.com/files/23527/original/qxgq3jtn-1368279301.jpg?ixlib=rb-1.1.0&rect=7%2C446%2C794%2C480&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Worrying about ageing is a waste of your time.</span> <span class="attribution"><span class="source">Faith K Lefever</span></span></figcaption></figure><p>I want to live longer and help others do the same. I assumed the most effective way to do that is by understanding the science of ageing and then engineering solutions to extend human lifespan. That is why I became a biomedical researcher and over the past several years I have pursued this goal almost single-mindedly.</p>
<p>When a <a href="http://www.pnas.org/content/101/15/5524">2004 study</a> showed that reducing the calorie intake in mice extended their life by 42%, I enthusiastically embraced the results and even put myself on a calorie restricted diet. But, subsequently, a <a href="http://www.nature.com/news/calorie-restriction-falters-in-the-long-run-1.11297">2012 study</a> showed that long-term calorie restriction may not have the promised benefits. On the contrary, fewer calories without the required nutrients might actually cause harm.</p>
<p>Calorie restriction is not the first such “promising” route that eventually did not live up to the promise, and it will not be the last. Antioxidants showed promise in <a href="https://www.sciencedirect.com/science/article/pii/0098299794900051?np=y">holding back</a> diseases caused by ageing, but now we know that antioxidant supplements are more likely to <a href="http://summaries.cochrane.org/CD007176/antioxidant-supplements-for-prevention-of-mortality-in-healthy-participants-and-patients-with-various-diseases">shorten</a> your life.</p>
<p>Earlier in May, researchers showed that reducing a protein called NF-kB in mouse brains modestly <a href="http://phenomena.nationalgeographic.com/2013/05/01/almond-sized-brain-region-is-control-centre-for-ageing/">improved their lifespan</a>. I am not holding out for this result either. Before too long, I’m sure there will be reports of severe <a href="http://www.nature.com/ni/journal/v7/n9/full/ni0906-901.html">side effects</a> of manipulating levels of NF-kB.</p>
<h2>Take it easy</h2>
<p>Looking at the data I have come to the conclusion that “doing nothing” may be the best option in most cases. This may not be as pessimistic as it sounds and it is definitely not to say that research in fighting ageing must not be carried out.</p>
<p>When I say “do nothing”, I am assuming that you <a href="http://www.bmj.com/content/328/7455/1519">do not smoke</a> or <a href="http://www.bmj.com/content/318/7200/1725">drink too much</a> alcohol, and have access to medical care in case of injury. Such measures are bound to increase your lifespan.</p>
<p>But currently, not intervening in the ageing process is more likely to help you live longer than trying any of the methods I’ve mentioned, not by a few months but by many years. Trying any of those interventions may actually cause harm, and will do so for the foreseeable future.</p>
<h2>Lesson from the past</h2>
<p>The chart below shows the survival rates – the percentage of the population that lives to a certain age – for men in England and Wales <a href="http://www.mortality.org/cgi-bin/hmd/country.php?cntr=GBRTENW&amp;level=1">from 1860 to 2010</a>.</p>
<p><img src="https://images.theconversation.com/files/23184/original/kdbcsyjq-1367672364.jpg?auto=format&q=45&w=668" alt=""></p>
<p>In the 1860s, more than 20% of children died at birth or soon after. On average, men’s health started to decline around the age of 30, and only about 20% of the population survived for more than 70 years.</p>
<p>By 1910, child mortality decreased, thanks to improvements in hygiene and better medical care. This meant more men lived past the age of 50. Circle A shows this reduction in childhood mortality between 1860 and 2010. But, as can be seen from Circle D, the gain towards the end was not significant. This is because only 30% of males passed the age of 70.</p>
<p>Fifty years later, after the discovery of penicillin and invention of more vaccines, 90% of English and Welsh men lived until 50, and more than half survived to 70. Arrow B marks this trend.</p>
<p>Today almost 80% of men live to the age of 70. Four times as many men reach 70 now than in 1860.</p>
<p>What accounts for the change? Between 1860 and 1960, the significant increase in survival rate was due to medical intervention. Since 1960, the survival curve has improved mainly due to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC27446/">reduction</a> in smoking.</p>
<p>This trend is similar in many rich countries, including the US. Druin Burch, a physician and writer, says in his book Taking the Medicine, that eliminating smoking would provide more benefits than being able to cure people of every possible type of cancer.</p>
<h2>Age gracefully</h2>
<p>Many experts believe that human lifespan might actually have an upper limit of <a href="http://www.nature.com/nature/journal/v408/n6809/full/408267a0.html#B4">125 years</a>. The average may not increase much <a href="http://dx.doi.org/10.1016/S0140-6736(11)60908-2/">beyond 90</a>. If we are to agree with them, this leaves little room for improvement.</p>
<p>But we have never concentrated on maximising human lifespan before. Most people believe human lifespan is finite, so all drugs being manufactured today are targeted towards certain age-related diseases such as diabetes and hypertension. They are not designed to extend human lifespan.</p>
<p>If this bleak outlook is indeed true, we should not practise naive interventionism because it is unlikely to help. As Nassim Nicholas Taleb describes in his book Antifragile, naive interventionism occurs when we try to fix a single thing, but end up disturbing a complex system.</p>
<p>In case of extending human lifespan, those naive interventions would include calorie restriction, antioxidant supplements or manipulating the protein NF-kB, as mentioned earlier. They also include the current obsession with <a href="http://www.guardian.co.uk/business/2012/jun/11/why-our-food-is-making-us-fat">replacing fat</a> in foods <a href="http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?pagewanted=all&amp;_r=0">with sugar</a>, the <a href="http://www.sciencemag.org/content/339/6124/1156.full">health benefits of drinking red wine</a>, or the use of<a href="https://theconversation.com/old-but-not-wise-our-growing-anti-ageing-industry-11863">surgery or supplements</a> to “fight” ageing. This latter industry has grown in the past decade from being non-existent to an estimated worth of $88 billion today.</p>
<p>If intervening in the ageing process with current biomedical science has any positive effect at all, it will be far too small to worry about. It’s far more likely to harm us.</p>
<p>That is why I have decided to do nothing and follow a simple rule: unless I meet with an accident, or suffer from a terminal disease, I will not add anything to my life with the explicit purpose of extending it. To do anything else would most likely do more harm than good.</p><img src="https://counter.theconversation.com/content/14134/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Avi Roy does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>I want to live longer and help others do the same. I assumed the most effective way to do that is by understanding the science of ageing and then engineering solutions to extend human lifespan. That is…Avi Roy, PhD student, University of BuckinghamLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/118632013-05-03T04:31:17Z2013-05-03T04:31:17ZOld but not wise? Our growing anti-ageing industry<figure><img src="https://images.theconversation.com/files/23115/original/qdwqcrrx-1367391310.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Growing old may not be desirable, but it is inevitable.</span> <span class="attribution"><span class="source">kroszk@/Flickr</span></span></figcaption></figure><p>Growing old is generally viewed in negative terms in our society. And our individualistic and consumerist approach to health care leads us to believe that it’s within our power to alter the “biological clock” — if we are willing and able to pay. </p>
<p>But while lifespans may be increasing (largely due to improvements in living standards), there’s no evidence that medicine can alter the process of human biological ageing.</p>
<p>Still, numerous so-called anti-ageing treatments are currently advertised and available for purchase via the internet. These cover a broad spectrum, including cosmetic treatments, hormone replacement therapies, implants, prosthetic devices and stem cell treatments. <a href="http://www.gcmta.com.au/anti-ageing.html">Some providers</a> even offer the treatments as part of a packaged holiday, offering surgery alongside sand and sunshine.</p>
<p>In Australia, <a href="http://www.nitai.com.au/anti-ageing-treatments-melbourne/?utm_medium=cpc&gclid=CMPBrKyg77YCFW45pgodcUMAYw">some common treatments</a> include non-surgical facelifts, anti-wrinkle injections and “dermal fillers”, permanent hair removal and laser treatments. </p>
<p>Consumer organisation, Choice, has <a href="http://www.choice.com.au/reviews-and-tests/food-and-health/beauty-and-personal-care/cosmetics/anti-ageing%20treatments.aspx">questioned some of the claims</a> of those advertising anti-ageing treatments. In a review of such treatments, Choice notes, for instance, that there’s “no such thing as a ‘non-surgical’ face-lift”, and that such procedures “won’t last as long as a surgical face-lift.”</p>
<p>Despite the advertising of questionable claims, the anti-ageing industry is difficult to regulate. </p>
<p>One of the greatest challenges for regulating a market like this is that many treatments are advertised directly to consumers over the internet. If not available in Australia, treatments can almost certainly be purchased overseas. Clever advertising techniques give the impression that there’s an effective treatment for almost any age-related “condition”.</p>
<p>Another challenge for regulators is that the term “anti-ageing” is difficult to pin down. Treatments that were long part of complementary and alternative medicine have been relabelled as “anti-ageing”. These include using antioxidants, vitamins and homeopathic products. </p>
<p>Some treatments that have actually undergone clinical trials and are used for treating conditions such as sexual dysfunction and heart disease have been relabelled to join the anti-ageing marketplace. And there are newer, clinically unproven treatments such as stem cell therapies, that are mostly only available for purchase overseas.</p>
<p>Clearly, many groups have a stake in the “anti-ageing industry”. Chief among these are the biotechnology and pharmaceutical companies that stand to profit from the sale of new pills, potions, prosthetic devices, and implants. And then there are numerous clinics and private hospitals that profit from providing the treatments.</p>
<p>The “anti-ageing industry” <a href="http://www.arleneweintraub.com/Anti-Aging_Book.html">has grown</a> from a low base to reach a net worth of $88 billion in just ten years. <a href="http://www.a4m.com/assets/pdf/medical-news/medical-news-spring-2011.pdf">An industry newsletter</a> predicts that it will be worth nearly $300 billion by 2015. </p>
<p>If these predictions are to be believed, many consumers will, in coming years, be submitting themselves to many treatments that are clinically unproven and potentially harmful. At minimum, these treatments may be ineffective. There’s also the risk that people may be financially exploited. </p>
<p>The irony is, by making ageing a disease, the anti-ageing industry may in fact <em>create</em> illnesses.</p>
<p>There have been some reported increased rates of adverse events, including death, among healthy elderly people resulting from the <a href="http://www.ncbi.nlm.nih.gov/pubmed/17227934">use of human growth hormones</a>. Adverse effects have also been associated with the use of <a href="http://www.scientificamerican.com/article.cfm?id=stem-cell-cosmetics">stem cell-based cosmetics</a>. </p>
<p><a href="http://www.gao.gov/new.items/d011129.pdf">Older people</a> are at greater risk because they may be taking multiple prescription drugs and may suffer harm from the interaction of supplements and drugs. Despite these potential multiple risks, there has been relatively little public debate about the pros and cons of the anti-ageing treatment market. </p>
<p>Growing old may not be desirable, but it is inevitable. In the end, it is better to live healthy, active lives for as long as possible with minimal medical intervention. </p><img src="https://counter.theconversation.com/content/11863/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Alan Petersen receives funding from the Australian Research Council and the Department of Industry, Innovation, Science, Research and Tertiary Education.</span></em></p>Growing old is generally viewed in negative terms in our society. And our individualistic and consumerist approach to health care leads us to believe that it’s within our power to alter the “biological…Alan Petersen, Professor, Monash UniversityLicensed as Creative Commons – attribution, no derivatives.