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The discovery transforming how we look at prostate cancer

Professor Vanessa Hayes (pictured below, far left), head of the Human Comparative and Prostate Cancer Genomics Laboratory at the Garvan Institute, explains the revolutionary discovery that has the potential to transform the way we look at and ultimately treat prostate cancer. One in four Australian men will be diagnosed with prostate cancer at some stage in their life, but for a disease that’s so common there’s still so much we don’t know about it. Because there is so much we still don’t know, many Australian men are being over-treated, receiving invasive, sometimes life-altering treatments that may not be necessary. Groundbreaking research at the Garvan Institute is transforming the way we look at prostate cancer, giving us a better understanding of this devastating disease. <img width="500" height="333" src="https://oversixtydev.blob.core.windows.net/media/7818328/g_0686_500x333.jpg" alt="G_0686"/> How does prostate cancer affect someone’s life? Prostate cancer can have a profound physical impact on someone’s life, with frequent urination, pelvis pain and a reduced sex drive eventually progressing to advanced symptoms like sudden, unexpected weight loss and fatigue. But what sometimes gets overlooked is the psychological impact. As the Garvan Institute’s Professor Vanessa Hayes argues, prostate cancer is a disease that can do just as much damage to the mind as the body. “Traditionally men don’t want to have to deal with or talk about the side effects of having such a condition and living with it for such a long time. Most men will die with prostate cancer, not from prostate cancer,” says Professor Hayes. “This means having to live 15, 20, 25 years knowing you have this cancer, while not feeling comfortable to talk about it – I think psychologically it’s a very hard cancer to deal with.” What makes prostate cancer so tricky to deal with? Prostate cancer differs from some other cancers in the sense that the factors impacting an individual’s likelihood of getting it are largely out of their hands. Other cancers have “modifiable risk factors” based on your lifestyle choices. For example, the amount of time you spend in the sun could be considered a modifiable risk factor for melanomas, while smoking could be considered a modifiable risk factor for being diagnosed with lung cancer. The problem is the likelihood of getting prostate cancer is affected by factors like ageing, family history and ethnic background. These are not modifiable risk factors, but genetic factors. <iframe width="560" height="315" src="https://www.youtube.com/embed/WlKBiPUwvCI" frameborder="0" allow="autoplay; encrypted-media" allowfullscreen=""></iframe> How could genomic research help? Unfortunately, there’s not a lot we can do about the genetic factors we’re born with. You can’t swallow a pill and change your age, family history or ethnic background. But what researchers at the Garvan Institute are hoping to understand with genomic research is what exactly is happening on a genetic level that is causing the cancer to emerge in certain people. “We need to look at the DNA sequence of this tumour and what is actually happening to cause this prostate cell to become cancerous,” says Professor Hayes. What is it about the Garvan Institute’s research that has been so revolutionary? Driven by revolutionary advances in genetic technology, the Garvan Institute has been able to examine the entire DNA sequence of a cancer cell. Prior to this, scientists were only able to look at a small portion of the human genome, representing roughly two per cent of the bigger picture. But new technology has given the Garvan Institute an opportunity to inspect the instrumental drivers of this unusual cancer, offering hope for a way forward. “Prostate cancer is a disease of the altered genetic code. Genetics provides a definitive answer; it’s a yes/no, there’s a change on, or a change off. And these we can read, so if we can find that on and off button, then we can provide a much better tool to the clinicians to be able to use,” explains Professor Hayes. What would be the next step? If the Garvan Institute can understand the instrumental factors driving the disease on a genomic level, there’s a huge opportunity to tailor treatments according to cases. This would ensure patients who are at highest risk are treated effectively and efficiently, while those at lower risk levels avoid receiving unnecessary and unneeded treatments. “We want to put prostate cancer into treatable buckets. A do nothing bucket. A do very minimal bucket. A get rid of the prostate bucket. And a tailored treatment bucket,” says Professor Hayes. “We want to be able to go even further than the buckets and treat the individual. As each person is unique, so is their cancer and ultimately so is their treatment. Genomics will allow us to make prostate cancer treatment unique.” What can you do to help? Contributing funds to organisations like the Garvan Institute is a good way to start, and you’ll be surprised how far your dollar goes. As Professor Hayes explains, “We always discover something, whether it’s a new technology, a new way to look at something, you’re looking at it differently, you’re approaching your question differently to everyone else, you have to find something.” To contribute to the Garvan Institute’s fight against prostate cancer, visit <a href="https://www.giving.garvan.org.au/donate-today?utm_source=over60&utm_medium=content&utm_campaign=tax2018">garvan.org.au/support-prostate-research</a><a href="#_msocom_1"></a> <div>THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH THE GARVAN INSTITUTE.</div> <div> <div> </div> </div>

Caring

The radical idea offering hope for millions of Aussies suffering from autoimmune disease

Professor Chris Goodnow, Deputy Director of the Garvan Institute of Medical Research, talks about the radical idea that’s offering hope for millions of Australians currently suffering from autoimmune disease. Autoimmune diseases are on the rise in Australia, and fast becoming a problem for our already-stretched healthcare system. One in 8 people will be affected by an autoimmune disease like arthritis, multiple sclerosis, Type 1 diabetes and coeliac disease at some point in their life. These conditions can have a devastating effect, not just on patients, but on their family members and friends as well. While much about autoimmune disease remains a mystery, early findings from research at the Garvan Institute offers hope, with many believing it it may lead to a cure. What we know about autoimmune disease Most of our understanding of autoimmune disease is restricted to what’s going on in the body. We know autoimmune disease occurs when the body attacks and damages its own tissue, we know the symptoms, we have methods to manage these diseases as best we can, and we know what to expect when someone’s diagnosed. What’s less clear, and what the Garvan Institute’s Hope Research project is trying to answer, is why the immune system is doing this, and whether this is curable. <img width="499" height="555" src="https://oversixtydev.blob.core.windows.net/media/7268400/artwork-2_499x555.jpg" alt="Artwork 2" style="display: block; margin-left: auto; margin-right: auto;"/> How close are we to understanding causes? The encouraging news is we’re closer to an understanding than we’ve ever been, which could one day lead to a cure. The Garvan Institute has been leading the way in autoimmune disease research, thanks largely to work spearheaded by a radical hypothesis from the organisation’s Deputy Director, Professor Chris Goodnow. Over a decade ago, Professor Goodnow theorised that there was a common cause for all autoimmune diseases – disruptions in the immune system’s clever “checkpoint” process causing “rogue clone” cells to spread and replicate. The technology to put this theory to the test didn’t exist previously. But recent advances have given Professor Goodnow and his team the ability to isolate individual disease-causing cells from the blood of patients and target the “rogue clones”. And this has far-reaching implications of the management and treatment of these diseases. “For the last 10 years, we’ve had a pretty good idea as to what might cause autoimmune disease, and we’ve figured out many of the mechanisms that normally stop it. But we haven’t had the tools and the technology to be able to test those ideas,” Professor Goodnow explains. “In the last three years, we’ve acquired the tools and technology here at the Garvan Institute. We are now bringing them together with a fantastic team of medical experts at the major hospitals around Sydney to really focus those tools and know-how on cracking this problem.” Why it’s important to understand the causes of autoimmune disease While many autoimmune diseases can be managed, there’s yet no cure. But the revolutionary research from Professor Goodnow and the team at the Garvan Institute suggests this is about to change. If researchers can pin down the “rogue cells” and what prompted them to go rogue, they could theoretically use existing immunotherapies and drugs to eradicate them from the body, targeting the disease at the source. The Garvan Institute has already made exciting strides through the work of Dr Joanne Reed, who put Professor Goodnow’s theory to the test in a pilot study for Sjögren’s syndrome. The results she recorded were nothing short of spectacular. “Excitingly, our pilot study has already identified disease causing rogue clones in Sjögren’s syndrome,” Dr Reed says. “We’ll now apply this discovery to 36 clinically diverse autoimmune diseases.” <img width="500" height="334" src="https://oversixtydev.blob.core.windows.net/media/7268452/rsz_joanne_reed_with_etienne_masle-farquhar2_500x334.jpg" alt="Rsz _joanne _reed _with _etienne _masle -farquhar2" style="display: block; margin-left: auto; margin-right: auto;"/> The challenges of this revolutionary research? As is often the case, progress in the world of science doesn’t come cheap. The costs associated with the Hope Research project’s revolutionary work are substantial. “To identify the rogue cells in one person costs thousands of dollars; to identify the mutations in those rogue cells costs $5,000-$20,000. It will get cheaper the more we do it, and the more the technology continues to mature,” Professor Goodnow says. “You could say we should just wait 10 years, until the technology has gotten cheaper, but we can’t wait. We want to know the root cause of autoimmune disease now. We’ve got the technology. We know what we need to do. We just need the resources to do it.” How you can help Contributing funds to the Garvan Institute is a good way to start, and you’ll be surprised how far your dollar goes to tackling autoimmune disease. As Professor Goodnow says, “For every dollar you give, we will leverage that many, many times over, in terms of being able to reach a cure for these diseases.” <a href="https://www.garvan.org.au/foundation/give-hope/?utm_source=fairfax&utm_medium=sponsoredcontent&utm_campaign=give_hope" target="_blank">You can contribute</a> to Garvan’s fight against autoimmune disease. Visit <a href="https://www.garvan.org.au/foundation/give-hope/?utm_source=fairfax&utm_medium=sponsoredcontent&utm_campaign=give_hope" target="_blank">garvan.org.au/give-hope</a><a href="#_msocom_1"></a> <div>THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH THE GARVAN INSTITUTE.</div>

Caring

The deadly cancer with a survival rate of less than 8%

With a five-year survival rate of just 7.7 per cent, pancreatic cancer is the fifth most common cause of cancer-related deaths in Australia – but awareness of the disease is at an alarmingly low 15 per cent, <a href="https://www.garvan.org.au/pancreatic-cancer/" target="_blank">research from the Garvan Institute</a> of Medical Research has found. As a result, research into pancreatic cancer isn’t receiving the funds it desperately needs to find a potential breakthrough. It’s not just the cancer that people aren’t aware of, however. A staggering 83 per cent of Australians aren’t even sure of the organ’s function – to secrete digestion-aiding enzymes and produce hormones that help regulate the metabolism of sugar. Furthermore, 77 per cent of people have an incorrect view of the signs and symptoms of pancreatic cancer. Unfortunately, correct symptoms of the disease, such as upper abdominal pain, jaundice, loss of appetite, weight loss, depression and blood clots, may not present themselves until the cancer is at such an advanced stage that surgical intervention is no longer possible. We asked members of the Over60 community affected by this insidious disease to share their experiences, and were absolutely overwhelmed by the responses. “I was diagnosed in 2012,” Over60 member Noreen Wheatley recalls. “I had a Whipple’s [pancreaticoduodenectomy] done. I was one of the lucky ones to survive. I have joined the over-5-year survival group and they are studying our DNA to see if there is a common denominator. Hopefully they can and then be able to diagnose precursors in family genetics and treat it early, and survival rates increase.” Most, however, are not as fortunate. “I lost dad in 1994 to pancreatic cancer. He had been unwell but ok for several months. He was diagnosed in December and was able to stay at home and live his life, but he lost half his body weight in a couple of months and became frail. I nursed him 24 hours a day, slept in his room for the weeks before he died. He died surrounded by his wonderful family. He was 65 years old.” So, a recent breakthrough from Australian and UK scientists couldn’t have come at a better time. Associate Professor Paul Timpson, Head of Invasion and Metastasis at the Garvan Institute, and Professor Kurt Anderson of the Beatson Institute for Cancer Research, UK, have created a “biosensor mouse” which allows them to track the disease’s progression – and perhaps even stop it in its tracks. To find out more about this incredible innovation, Over60 spoke to Associate Professor Paul Timpson. “We’ve made a green glow-in-the-dark mouse that can show a pancreatic cancer tumour getting ready to break apart and spread throughout the body before it even occurs,” he explains. “For a tumour to spread, it has to lose its contact with adjacent cells, with which it’s zipped together, just like a common zip on a piece of clothing. With this mouse, we can actually watch the process of those cells unzipping (or spreading) in real-time. So, we can say, ‘This tumour has not yet spread, it’s not yet broken apart, it’s just weaker’. And then what we do is give it drugs that we know can control that zip, and kind of re-zip it before it moves.” Associate Professor Timpson adds, “For pancreatic cancer, which is highly invasive and spreading, when metastasis occurs we do not have a cure. So, if you can increase the number of cases in which that tumour stays in the same place, then the surgeons can go in and take it out.” In addition to the biosensor mouse, Associate Professor Timpson and his team have created another mouse which could be the key to fine-tuning chemotherapy, increasing drug effectiveness and minimising nasty side-effects. “The second mouse we’ve got is called a FRET (fluorescence resonant energy transfer) mouse. Using the green and red fluorescent proteins found in glow-in-the-dark jellyfish, we’ve created a mouse that’s basically like a traffic light. Before, drugs were administered with a one-size-fits-all approach to the amount of treatment and length it was given. What we’re trying to do now is fine-tune treatment, so you can watch the cancer-causing molecule switch on and off like a traffic light, indicating whether the chemotherapy is working (the mouse glows amber) or not (the mouse glows red and green). By doing that, we can determine how long to give the drugs, where to give the drugs, and when. This way you maximise the drug response while minimising side-effects.” Just how does it work, then? Associate Professor Timpson explains: “The behaviour in the solid middle of a tumour is very different to the behaviour out at the edges, when it’s about to spread. What you find is that drugs work way better on the outside of the tumour than they do deep inside because it’s really hard to penetrate. So we can now see not only is the drug working for how long, but how deep it’s penetrating into the tumour.” “Now imagine the tumour – it’s covered in a meshwork, kind of like collagen (the protein which makes up the shape of your lips and your organs, for example). What happens with pancreatic cancer is that you get a massive deposition of too much collagen all around the tumour. Because it’s covered in this meshwork, any drug you give just cannot get into the tumour – it’s protected.” “So, what we can do is give a very low dose of a drug that can break up that mesh, we can make it softer, and easier to penetrate so the cancer drug can get in. You can then fine-tune that to get the tumour soft enough to allow the drug in, while still being hard enough to allow the pancreas to still function.” Garvan is also an expert in patient-derived xenografts, which are tumour samples taken direct from the patients. “We’ve got the largest cohort in the world, with over 400 samples,” Associate Professor Timpson explains. “With these, we can say patients 1 through 15 are going to respond to the treatment, 15 to 200 we have no cure for these people, and then from 200 to 400 they’ve got a different molecular signature that we know we can attack.” “Using these samples, we can replicate each individual’s tumour in mice and test treatments, fine-tune it and then take it to the human. That’s called personalised therapy.” But it’s not just one cancer that will benefit from these new breakthroughs, Associate Professor Timpson says. “If this can work for pancreatic cancer, it could also help breast cancer, prostate cancer, colon cancer and even skin cancer. It may even be applicable in diabetes and neuroscience research – it’s always bigger than you ever imagine.” To find out more about pancreatic cancer and how you can help Associate Professor Paul Timpson and his team at the Garvan Institute continue their research to find a cure, visit <a href="http://www.garvan.org.au/pancreatic-cancer" target="_blank">garvan.org.au/pancreatic-cancer</a>. THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH <a href="https://www.garvan.org.au/" target="_blank">GARVAN</a>.

Body

This silent disease affects millions of Australians

Osteoporosis, a disease that makes bones brittle and fragile, affects 1.2 million Australians. According to Osteoporosis Australia, a further 6.3 million Australians have low bone density, putting them at risk of osteoporosis. Known as the “silent disease” as osteoporosis generally has no signs or symptoms, an estimated four out of five people in Australia don’t know they are at risk of breaking a bone. Most people don’t find out they have osteoporosis until a fracture happens. Your risk of osteoporosis increases with age As we start losing bone from our skeleton from around 30 years of age, our risk of osteoporosis increases as we get older. When bones become thinner, we’re vulnerable to “minimal trauma” fractures, where a minor fall or bump can cause serious fractures. Think falling from standing height or stumbling on steps – basically, any event that would not normally result in a fracture if the bone was healthy. Professor Peter Croucher is the Head of the Bone Biology Division at the Garvan Institute of Medical Research, an international leader in <a rel="noopener" href="https://www.garvan.org.au/foundation/diseases-we-research/osteoporosis/" target="_blank">osteoporosis research</a>. He says one of their biggest challenges is getting the public to take their bone health seriously before they have their first fracture. “There are estimates that 155,000 fractures will occur in Australia due to poor bone health. There’s probably two-thirds of Australians over 50 who have osteopenia – which is low bone mass – and this places them at risk of having a fracture in the future,” says Professor Croucher. The “cascade effect” of fractures Anybody who has suffered a fracture, especially in older age, knows it’s a serious matter. What is most concerning with osteoporotic fractures is that once you have your first one, your risk of further fractures significantly rises. About half of the people who experience an osteoporotic fracture will have another fracture within the year – and the risk greatly increases with each new fracture. “You don't necessarily know you've got problems with your skeleton until you have that first fracture and the challenge then is once you've had one fracture you're more likely to have others,” says Professor Croucher, adding, “It's a signal you've already lost bone from your skeleton and you're susceptible to having future fractures.” Falls and fractures are not an inevitable part of growing old. However, at the moment the majority of older women and men who suffer a first fracture don’t get optimal treatment to reduce the risk of further broken bones. Unfortunately, osteoporosis is still a severely undertreated disease and often the underlying cause of the fracture won’t be investigated. Osteoporosis Australia advises that if you are 50 and over and experience a fracture following a minor bump or fall, talk to your doctor about osteoporosis. Osteoporotic fractures are a serious condition that can lead to chronic pain, disability, a loss of independence and even death, especially from hip and spine fractures. “Our studies have led to the discovery that if you have fractures, this is associated with a poor outcome and an increased risk of dying prematurely,” says Professor Croucher. “If you’re 50 years and older and you have a fracture, you have a greater risk of dying from that than you do of breast cancer.” He adds, “People are completely unaware of the mortality associated with osteoporotic fractures.” The gender effect Osteoporosis has commonly been viewed as a women’s disease as it was believed to predominantly affect women, but research from <a rel="noopener" href="https://www.garvan.org.au/news-events/news/media_release.2007-06-27.8075708161" target="_blank">Garvan scientists has found that it’s a misconceived view.</a> As women generally have smaller bones than men and experience loss of bone at a faster rate due to menopause, women are initially twice as likely as men to have a fracture. But once men over the age of 60 suffer one fracture, around one in three will have another broken bone within a few years. “The protective effects of being male disappear once you have that first fracture,” notes Professor Croucher. “Men don't have as many fractures initially as women, and that probably explains why it's seen to be less of a problem, but once they’ve had that first fracture, they do as badly as women, and subsequently catch up with women and have just as many fractures.” How well do you know your bones? As we get older, we’re very good at looking after our health. We make sure we’re getting regular check-ups for cancer, work out our brains, ensure our heart is in healthy shape – but our skeleton is often neglected. Bone health is not a health issue that’s at the front of our mind but osteoporosis can be seriously disabling and even fatal so it’s imperative all over-60s be informed. Last year, Garvan and Osteoporosis Australia developed and launched <a rel="noopener" href="http://www.knowyourbones.org.au/" target="_blank">Know Your Bones</a>, a free online tool which helps people assess their risk of bone fractures. The assessment is easy to do and once completed, you will be provided with a personalised estimate of your bone fracture risk, as well as a report which you can share with your GP. Depending on your level of risk, your doctor may recommend you take a bone density test and prescribe treatment. Good treatment is available Although there’s currently no cure for osteoporosis, as there’s not yet a way to put bone back into our skeletons, there are good treatments available for osteoporosis that can halve the likelihood of further fractures. In fact, researchers from Garvan discovered an <a rel="noopener" href="https://www.garvan.org.au/news-events/news/an-extra-5-years-of-life-an-unexpected-benefit-of-osteoporosis-treatment" target="_blank">unexpected benefit of osteoporosis treatment was an extra five years of life.</a> People taking bisphosphonates (osteoporosis treatment) are not only surviving well, they seem to be adding an extra five years to their life. It’s why it’s so important that all over-60s take the first step to understanding their bone health and what they can do about it. “People just don't think about their skeleton – and our big challenge is to get people to think about it and to get them to think about it early enough so they can do things to stop future bone loss and prevent fractures,” says Professor Croucher. As Professor Croucher sums up: “You only have one skeleton. And you’ve got to look after it.” For more information or to support Garvan’s research into osteoporosis, please visit: <a rel="noopener" href="https://tracking.cirrusinsight.com/ab7adc91-1a8b-41bb-834d-2f5131ae1f76/urldefense-proofpoint-com-v2-url8" target="_blank">garvan.org.au/osteoporosis</a> THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH <a rel="noopener" href="https://www.garvan.org.au" target="_blank">GARVAN INSTITUTE</a>.

Body

The key to understanding healthy ageing

The genes of thousands of older Australians who have no history of disease are undergoing sequencing at the Garvan Institute to contribute to the Medical Genome Reference Bank. The database is expected to be finished early next year and will be opened to researchers around the globe as a resource to discover the genetic factors that contribute to healthy ageing. A genome refers to all the genetic information of an individual that is inherited from their parents and it is encoded within DNA. This genome bank is the largest in the world and unlike many other genome banks, which store data on people with health concerns, this bank will analyse healthy genomes so scientists can understand what healthy ageing looks like. To get a better idea of how beneficial this new bank of genome data will be, Over60 spoke to the project co-leader, Associate Professor Marcel Dinger, about three advantages the Reference Bank will have for healthy ageing. 1. Filtering disease and non-disease-causing variants The reference bank will be used to compare genomes from people with no disease history with those who have had disease to filter disease and non-disease variants. This will provide an ultimate genetic reference of what a healthy genome is and allow researchers to understand the genetic reason as to why some people do not get cancer and other diseases. “The primary motivation of the database is that it helps filter out those millions of variants that are what we call benign, they don’t have an impact on health and are just part of what makes each of us different,” Associate Professor Dinger said. This genomic data will allow experts to research whether healthy individuals are depleted of genetic variations that can cause neurological or cardiovascular disease or, if they have a genetic advantage that has a protective effect against diseases. This then “opens the opportunity for developing new therapeutics and may make it possible for other people to live longer if we understand the cause.” 2. Identifying people at risk “In the long term, it can help predict who is susceptible to disease, identify those people most at risk who can then be enrolled in screening programs,” Associate Professor Dinger explained. Associate Professor Dinger hopes that in the future, an individual at birth could be tested to see if they have diseasing causing variants. If they did, they could then have early intervention to prevent the disease. “I think what we might see as a general trend, is genomic sequencing moving from being used to diagnose patients – individuals that already have a disease – towards preventative medicine where you are able to anticipate disease or an individual’s predisposition to disease,” he said. “Normally, you only go to a doctor when you are sick whereas I think in the future, that genomics will start to play more of a role in disease prevention and health management.” 3. Interpreting the non-coding parts of the genome The genome is broken down into two parts of genetic material: the protein coding parts and the non-coding part of the genome. Associate Professor Dinger expects the Medical Genome Reference Bank will allow experts to interpret the non-coding parts of the genome, which is currently not well understood. “I think we will find a lot of the causes of disease, especially more complex disease, in the non-coding part of the genome, which tend to be responsible for controlling which genes are expressed and when. That’s a very new area for genomics,” he said. As more research is undertaken to identify disease-causing variants, Associate Professor Dinger believes that genomic data will have a transformative impact on the medical world in the immediate future. “Having genetic information available at the beginning of a person’s life has this enormous potential both to improve the quality of care and the efficiency of treatment for people with disease.” For more information or to support Garvan’s research into Genomes, please visit <a href="https://www.garvan.org.au/foundation/our-work/genomics/%20" target="_blank">garvan.org.au</a>. THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH THE <a href="https://www.garvan.org.au/" target="_blank">GARVAN INSTITUTE</a> OF MEDICAL RESEARCH. <div data-fsid="e.594b07a33b03300100460550" data-width="100%" data-height="auto"></div>

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Why Aussies need to take the diabetes epidemic more seriously

Diabetes has become one of today’s major health epidemics and is arguably the chief crisis facing Australia’s medical system in the immediate future. Diabetes Australia says 1.7 million Australians currently have some form of diabetes, with 280 Australians developing the condition every day. But we’re still some way from the public recognising the scope of the threat this condition presents, particularly when it comes to type 2 diabetes. Type 2 diabetes is a condition where the body fails to produce enough insulin in the pancreas, or becomes resistant to the normal effects of insulin. While some have a genetic predisposition towards the condition, lifestyle factors like high blood pressure, insufficient physical activity, obesity and a poor diet all play a part. Though it might not get as much press as other conditions, if left untreated the risks of type 2 diabetes can lead to serious long-term complications. Professor Mark Febbraio, Head of the Cellular and Molecular Metabolism Laboratory and Head of the Diabetes and Metabolism Division at the <a href="https://www.garvan.org.au/foundation/diseases-we-research/type-2-diabetes/%20" target="_blank">Garvan Institute for Medical Research</a>, says, “The concept of type 2 diabetes, because it’s a chronic disease, isn’t really that scary to people. But the consequences of diabetes are very dire. “If you have type 2 diabetes that isn’t managed effectively, then you’ll have much higher levels of glucose, or sugar, in your blood than you should. Too much glucose can cause terrible complications, especially over a long period of time. It can lead to problems like blindness, kidney failure and severe damage to blood supply which can result in amputations of limbs.” Diabetes Australia says that people with diabetes are four times more likely to suffer heart attacks and strokes, three times more likely to suffer kidney failure and 15 times more likely to have to undergo amputation. Diabetes is also the leading cause of preventable blindness in Australia, and more than 30 per cent of those diagnosed with the condition experience anxiety, depression and distress. Perhaps the most tragic thing about the prevalence of type 2 diabetes in Australia is the fact that plenty of measures can be taken to decrease the likelihood of it occurring. As Garvan’s Professor Febbraio states, “The thing is, people know what they need to do, they just don’t do it. And that’s why we have an obesity, type 2 diabetes epidemic. “If somebody is on the path to type 2 diabetes, the best thing they can do is exercise. While not being effective at reducing body weight in all individuals, it certainly has an effect in some individuals. And it has the added benefit of leading to insulin sensitivity. So, for people who have insulin resistance, exercise is certainly contributing to the healing process. “So, if you’re in pre-diabetes, even a half hour walk everyday would probably be of benefit.” While the threat of type 2 diabetes is very real, it’s by no means a death sentence and can be managed if you’re willing to make the appropriate lifestyle changes. Professor Febbraio says exercise and healthy eating choices are the best course of action. “If you exercise and you don’t lose weight, it doesn’t mean that it’s a failure,” he explains. “And the thing is, diabetes is linked to many diseases including liver cancer, breast cancer, colon cancer and Alzheimer’s. These diseases are what we call metabolic diseases now, because if people exercise these diseases can be prevented. “People also need to eat well, which means eating a lot of vegetables and less processed carbohydrates, so cutting down on bread and pasta, because they really play havoc with glucose control. And obviously being active is a big part of it.” Type 2 diabetes is one of the most significant challenges facing the Australian medical system today. <a href="https://www.garvan.org.au/foundation/diseases-we-research/type-2-diabetes/" target="_blank">The Garvan Institute</a> is leading the way in research into this debilitating condition, to point the way towards earlier, more-effective preventative measures, personalised treatments and ultimately a better understanding of the disease. For more information or to support Garvan’s research into Diabetes, please visit <a href="http://garvan.org.au/" target="_blank">garvan.org.au</a>. THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH THE <a href="https://www.garvan.org.au/" target="_blank">GARVAN INSTITUTE</a>.

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Is it possible to detect Parkinson’s sooner?

Parkinson’s disease has long been a source of confusion, misinformation and misunderstanding, with many believing it to simply be “the shakes”. But there is so much more to this cruel and complex disease. According to <a href="http://www.parkinsons.org.au/" target="_blank">Parkinson’s Australia</a>, there are currently around 70,000 people affected by the disease in this country alone. The average age of diagnosis is 65 years, but for some, the dreaded news can come much earlier. “My mother had Parkinson’s,” Over60 community member Pauline Marrone explains. “She was first diagnosed at 43 years old and passed away at 73. The last 10 years of her life, once she became bedridden, were terrible to watch, particularly the involuntary jumping of her legs after she had taken her medication. My dad was her carer. He passed away in his sleep, in bed next to her, and she was unable to do anything but lay there next to him until help arrived. It was very traumatic.” Not only is its cause currently almost impossible to pinpoint, it’s also notoriously difficult to diagnose, as there are currently no laboratory tests available – diagnosis is all down to examinations conducted by neurologists. To understand a bit more about the disease, and learn about an exciting breakthrough that may lead to the development of an effective treatment, we spoke to Associate Professor Antony Cooper. As head of the neuroscience division at the <a href="https://www.garvan.org.au" target="_blank">Garvan Institute of Medical Research</a>, his work focuses on a number of neurodegenerative diseases – primarily, Parkinson’s disease. “We’re looking at two things,” he explains. “One, to try and understand what are the early events that cause or contribute to Parkinson’s, because if we can identify them, it gives us a way of trying to find a therapy that would stop this disease. And two, to search for biomarkers (indicators of disease). “In Parkinson’s, you start to get neurons that either degenerate (which means they die) or simply aren’t working, which is really the same outcome – in that different parts ofyour brain stops working properly. “With one part of your brain not working it produces specific symptoms but then the problem “spreads” to another brain region, causing that region to fail which results in a new set of symptoms. As time goes on, you get more and more brain regions affected, and therefore you gain new symptoms and the symptoms you already have get worse. This is disease progression.” There may be hope, however, in slowing the progression of the disease. Current therapies only treat certain symptoms rather than tackling the disease as a whole. Associate Professor Cooper believes his team’s research could lead to the development of a treatment, which would get to the root of the problem and prevent the disease getting worse. “There’s a protein called alpha-synuclein which is quite central to the disease. It’s recently been proposed that the progression of the disease – that is, the timing pattern in which parts of the brain fail – is that this protein might be moving from one brain cell to another, where it triggers the next cell (which was healthy) to fail or degenerate. “We’re also looking at a second Parkinson’s disease gene called PARK9 (or ATP13A2), which is involved with how the cell copes with toxic levels of alpha-synuclein. It protects the cell against rising levels of alpha-synuclein and also impacts how that alpha-synuclein is perhaps transmitted from one cell to another. A number of us at the Garvan are investigating if we could interfere with that transmission of alpha-synuclein between cells, we might be able to stop the disease getting worse, which would be fantastic.” Therapy will be most beneficial if we can give it to people very early in the disease course. “Part of our problem is that by the time some people are diagnosed, they’ve already got a resting tremor in their hand, and by that stage, you’re probably in the mid-course of the disease,” he explains. “So, we need to be able to diagnose people much earlier. And that’s pretty hard, because the really early symptoms don’t necessarily suggest Parkinson’s, so we need earlier indicators – biomarkers. Some people may have had the disease for five years before they began to show symptoms. So, the earlier we can detect it, if we have a therapy, we could give those to people before they even have symptoms, and we may stop the progression really early on. Pre-symptomatic diagnosis, that’s our goal.” Associate Professor Cooper hopes that, one day, if the search for biomarkers is successful, diagnosing early Parkinson’s will be as simple as a trip to the doctor. However, without proper funding, diagnosis will remain a struggle. “If you wonder whether you’re diabetic or have high blood glucose, you go and have a blood test where they take a measurement and say, ‘you’ve got 5, that’s healthy,’ or ‘you’ve got 7, that’s a concern’. That’s a biomarker for diabetes. So, we’re looking for biomarkers that we can measure so that, maybe at the age of 50, you can stop by your GP and as part of your blood test they screen you for Parkinson’s and say, “‘hey, your markers indicate very early stages of Parkinson’, we’ve got this therapy,’ or ‘we’re going to monitor you for another year and see if it gets worse,’ and ideally, we’d be able to significantly slow the disease and add an extra five or more years of being symptom free.” If you’re interested in finding out more information about Parkinson’s, why not consider attending a free seminar at the Garvan Institute on Tuesday April 11 from 10am to 12pm? <a href="https://www.garvan.org.au/get-involved/public-seminars" target="_blank">Click here</a> to register now. If you would like to help Associate Professor Antony Cooper and his team at the Garvan Institute as they continue their research to find an early diagnosis test for Parkinson’s, <a href="https://www.giving.garvan.org.au/donate-now" target="_blank">click here</a> to find out how you can donate now. For more information or to support Garvan’s research into Parkinson’s, please visit <a href="http://garvan.org.au/parkinsons" target="_blank">garvan.org.au/parkinsons</a>. THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH <a href="https://www.garvan.org.au" target="_blank">GARVAN INSTITUTE</a>.

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Find out your bone fracture risk with new online tool

<img width="117" height="74" src="https://oversixtydev.blob.core.windows.net/media/22722/kyb_logo_v2_117x74.jpg" alt="KYB_Logo _V2 (2)"/> THIS IS AN ADVERTORIAL FEATURE An Australian-first bone health self-assessment tool designed to help consumers understand their bone fracture risk, is now available to all adults, including the 7.5 million Australians living with brittle bones. The “Know Your Bones” online tool – an inaugural Garvan Institute of Medical Research and Osteoporosis Australia joint initiative – helps adults assess their likelihood of fractures, including those diagnosed with osteopenia and osteoporosis – two common bone conditions that, together with fractures, will cost the nation more than $3 billion this year. The evidence-based, consumer-friendly tool summarises bone fracture risk by assessing age, gender, weight, history of fracture, bone mineral density, and history of falls and lifestyle factors within the past 12 months. Risk of fracture over five and 10 years respectively, is assessed for people aged 50 and above, and a general, actionable summary is provided for all users (18+), for further discussion with their GP. The launch of the innovative tool coincides with the release of Osteoporosis Australia fracture figures revealing more than 155,000 fractures will occur Australia-wide this year, with a bone broken every 3.4 minutes due to poor bone health. Furthermore, men will account for up to 30 per cent of all fractures related to osteopenia and osteoporosis, and their associated costs. In 2016, the total annual cost of fractures is estimated to be $2.15 billion. Two-thirds of Australians aged 50 and above, have poor bone health and many don’t know it, even when they have obvious risk factors, or have experienced a previous fracture. Unfortunately, only around 20 per cent of those women who sustain a fracture and go to hospital, are either treated or properly investigated for osteoporosis. Even fewer men are followed up appropriately. Poor bone health can lead to fractures. Don’t wait to break a bone, take the Know Your Bones health assessment today. The Know Your Bones fracture risk self-assessment takes only five minutes. Simply visit www.knowyourbones.org.au, print out a report and take it to your doctor to discuss your risk and a suitable action plan. It’s estimated that 1.2 million Australians are living with osteoporosis and 6.3 million have low bone density. Osteoporosis affects women and men, and occurs when bones lose their density and quality, weakening the skeleton. Osteoporosis can affect almost any of your body’s 206 bones, though fractures most often occur in the hip, spine, wrist, ribs, and pelvis. However, the Know Your Bones tool can help people understand when they may need to speak to their GP about managing risks, proper medical investigation and management can approximately halve the risk of further fracture. Risk factors for osteoporosis include a family history of the disease, fractures from minimal trauma, low bone density and falls. Medical risk factors include low body weight, early menopause, low testosterone, inflammatory conditions, malabsorption disorders (such as coeliac disease), corticosteroid use (e.g. for asthma), some cancer treatments (particularly for breast and prostate cancer), loss of height (3 cm or more), overactive thyroid and parathyroid conditions. Lifestyle issues include calcium and vitamin D deficiency, smoking, insufficient exercise and excessive alcohol consumption. To check out the online test, visit <a href="http://www.knowyourbones.org.au/" target="_blank">www.knowyourbones.org.au</a> now.

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Find out your bone fracture risk with new online tool

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