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New study suggests weight loss drugs like Ozempic could help with knee pain. Here’s why there may be a link

<a href="https://theconversation.com/profiles/giovanni-e-ferreira-1030477">Giovanni E. Ferreira</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> and <a href="https://theconversation.com/profiles/christina-abdel-shaheed-425241">Christina Abdel Shaheed</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> The drug semaglutide, commonly known by the brand names Ozempic or Wegovy, was <a href="https://theconversation.com/the-rise-of-ozempic-how-surprise-discoveries-and-lizard-venom-led-to-a-new-class-of-weight-loss-drugs-219721">originally developed</a> to help people with type 2 diabetes manage their blood sugar levels. However, researchers have discovered it may help with other health issues, too. Clinical trials show semaglutide can be effective for <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2032183">weight loss</a>, and hundreds of thousands of people around the world are using it <a href="https://theconversation.com/considering-taking-a-weight-loss-drug-like-ozempic-here-are-some-potential-risks-and-benefits-219312">for this purpose</a>. Evidence has also shown the drug can help manage <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2306963">heart failure</a> and <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2403347">chronic kidney disease</a> in people with obesity and type 2 diabetes. Now, a study published in the <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2403664">New England Journal of Medicine</a> has suggested semaglutide can improve knee pain in people with obesity and osteoarthritis. So what did this study find, and how could semaglutide and osteoarthritis pain be linked? <h2>Osteoarthritis and obesity</h2> Osteoarthritis is a common joint disease, affecting <a href="https://www.aihw.gov.au/reports/chronic-musculoskeletal-conditions/osteoarthritis">2.1 million Australians</a>. Most people with osteoarthritis <a href="https://theconversation.com/do-you-have-knee-pain-from-osteoarthritis-you-might-not-need-surgery-heres-what-to-try-instead-236779">have pain</a> and find it difficult to perform common daily activities such as walking. The knee is <a href="https://pubmed.ncbi.nlm.nih.gov/37675071/">the joint most commonly affected</a> by osteoarthritis. Being overweight or obese is a <a href="https://pubmed.ncbi.nlm.nih.gov/25447976/">major risk factor</a> for osteoarthritis in the knee. The link between the two conditions <a href="https://pubmed.ncbi.nlm.nih.gov/26821091/">is complex</a>. It involves a combination of increased load on the knee, <a href="https://www.nature.com/articles/s41413-023-00301-9">metabolic factors</a> such as high cholesterol and high blood sugar, and inflammation. For example, elevated blood sugar levels increase the production of inflammatory molecules in the body, which can damage the cartilage in the knee, and lead to the <a href="https://pubmed.ncbi.nlm.nih.gov/30712918/">development of osteoarthritis</a>. Weight loss is strongly recommended to reduce the pain of knee osteoarthritis in people who are overweight or obese. <a href="https://pubmed.ncbi.nlm.nih.gov/31908149/">International</a> and <a href="https://www.safetyandquality.gov.au/sites/default/files/2024-08/osteoarthritis-knee-clinical-care-standard-2024.pdf">Australian guidelines</a> suggest losing as little as 5% of body weight can help. But losing weight with just diet and exercise can be difficult for many people. <a href="https://pubmed.ncbi.nlm.nih.gov/26180980/">One study</a> from the United Kingdom found the annual probability of people with obesity losing 5% or more of their body weight was less than one in ten. Semaglutide has recently entered the market as a potential alternative route to weight loss. It comes from a class of drugs known as GLP-1 receptor agonists and works by increasing a person’s sense of fullness. <h2>Semaglutide for osteoarthritis?</h2> The rationale for the <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2403664">recent study</a> was that while we know weight loss alleviates symptoms of knee osteoarthritis, the effect of GLP-1 receptor agonists was yet to be explored. So the researchers set out to understand what effect semaglutide might have on knee osteoarthritis pain, alongside body weight. They randomly allocated 407 people with obesity and moderate osteoarthritis into one of two groups. One group received semaglutide once a week, while the other group received a placebo. Both groups were treated for 68 weeks and received counselling on diet and physical activity. At the end of the treatment phase, researchers measured changes in knee pain, function, and body weight. As expected, those taking semaglutide lost more weight than those in the placebo group. People on semaglutide lost around 13% of their body weight on average, while those taking the placebo lost around 3% on average. More than 70% of people in the semaglutide group lost at least 10% of their body weight compared to just over 9% of people in the placebo group. The study found semaglutide reduced knee pain significantly more than the placebo. Participants who took semaglutide reported an additional 14-point reduction in pain on a 0–100 scale compared to the placebo group. This is much greater than the pain reduction in another <a href="https://pubmed.ncbi.nlm.nih.gov/36511925/">recent study</a> among people with obesity and knee osteoarthritis. This study investigated the effects of a diet and exercise program compared to an attention control (where participants are provided with information about nutrition and physical activity). The results here saw only a 3-point difference between the intervention group and the control group on the same scale. The amount of pain relief reported in the semaglutide trial is also larger than that reported with commonly used pain medicines such as <a href="https://pubmed.ncbi.nlm.nih.gov/35442752/">anti-inflammatories</a>, <a href="https://pubmed.ncbi.nlm.nih.gov/35137418/">opioids</a> and <a href="https://www.bmj.com/content/372/bmj.m4825">antidepressants</a>. Semaglutide also improved knee function compared to the placebo. For example, people who took semaglutide could walk about 42 meters further than those on the placebo in a six-minute walking test. <h2>How could semaglutide reduce knee pain?</h2> It’s not fully clear how semaglutide helps with knee pain from osteoarthritis. One explanation may be that when a person loses weight, there’s less stress on the joints, which reduces pain. But recent studies have also suggested semaglutide and other GLP-1 receptor agonists might have <a href="https://www.sciencedirect.com/science/article/pii/S1043661822002651">anti-inflammatory</a> properties, and could even protect against <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6731440/">cartilage wear and tear</a>. While the results of this new study are promising, it’s too soon to regard semaglutide as a “miracle drug” for knee osteoarthritis. And as this study was funded by the drug company that makes semaglutide, it will be important to have independent studies in the future, to confirm the findings, or not. The study also had strict criteria, excluding some groups, such as those taking opioids for knee pain. One in seven Australians seeing a GP for their knee osteoarthritis <a href="https://pubmed.ncbi.nlm.nih.gov/34527976/">are prescribed opioids</a>. Most participants in the trial were white (61%) and women (82%). This means the study may not fully represent the average person with knee osteoarthritis and obesity. It’s also important to consider semaglutide can have a range of <a href="https://theconversation.com/considering-taking-a-weight-loss-drug-like-ozempic-here-are-some-potential-risks-and-benefits-219312">side effects</a>, including gastrointestinal symptoms and fatigue. There are some concerns that semaglutide could reduce <a href="https://www.sciencealert.com/experts-are-concerned-drugs-like-ozempic-may-cause-muscle-loss">muscle mass</a> and <a href="https://www.healthline.com/health-news/ozempic-muscle-mass-loss">bone density</a>, though we’re still learning more about this. Further, it can be difficult to access. <h2>I have knee osteoarthritis, what should I do?</h2> Osteoarthritis is a disease caused by multiple factors, and it’s important to take <a href="https://www.safetyandquality.gov.au/standards/clinical-care-standards/osteoarthritis-knee-clinical-care-standard/information-consumers-osteoarthritis-knee-clinical-care-standard">a multifaceted approach</a> to managing it. Weight loss is an important component for those who are overweight or obese, but so are other aspects of <a href="https://theconversation.com/do-you-have-knee-pain-from-osteoarthritis-you-might-not-need-surgery-heres-what-to-try-instead-236779">self-management</a>. This might include physical activity, pacing strategies, and other positive lifestyle changes such as improving sleep, healthy eating, and so on.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/243159/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/giovanni-e-ferreira-1030477">Giovanni E. Ferreira</a>, NHMRC Emerging Leader Research Fellow, Institute of Musculoskeletal Health, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> and <a href="https://theconversation.com/profiles/christina-abdel-shaheed-425241">Christina Abdel Shaheed</a>, Associate Professor, School of Public Health, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> Image credits: Shutterstocl This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/new-study-suggests-weight-loss-drugs-like-ozempic-could-help-with-knee-pain-heres-why-there-may-be-a-link-243159">original article</a>.

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New study finds epilepsy drug could reduce sleep apnoea symptoms

New research has found that a drug used for epilepsy could be used to reduce the symptoms of sleep apnoea. Obstructive sleep apnoea, which affects about one in 20 people, according to the National Institute for Health and Care Excellence in England, includes symptoms like snoring and it causes a person's breathing to start and stop during the night, with many requiring an aid to help keep their airways open. An international study has identified that taking sulthiame, a drug sold under the brand name Ospolot in Europe, may help prevent patients' breathing from temporarily stopping. This provides an additional option for those unable to use mechanical breathing aids like the Cpap machines. “The standard treatment for obstructive sleep apnoea is sleeping with a machine that blows air through a face mask to keep the airways open. Unfortunately, many people find these machines hard to use over the long term, so there is a need to find alternative treatments,” Prof Jan Hedner from Sahlgrenska university hospital and the University of Gothenburg in Sweden said. Researchers conducted a randomised controlled trial of almost 300 obstructive sleep apnoea patients across Europe, who did not use Cpap machines. They were divided into four groups and given either a placebo or different strengths of sulthiame. The study measured patients’ breathing, oxygen levels, heart rhythm, eye movements, as well as brain and muscle activity while asleep. It found after 12 weeks, those taking sulthiame had up to 50% fewer occasions where their breathing stopped, and higher levels of oxygen in their blood. However, a bigger study needs to be done to confirm the beneficial effects on a larger group. The findings, were presented at the European Respiratory Society Congress in Vienna, Austria. Erika Radford, the head of health advice at Asthma + Lung UK said the findings were a positive step forward in moving away from having to rely on mechanical breathing equipment. “This potential alternative to the current main treatment would make it easier for people to manage their condition,” she said. Image: Shutterstock

Body

Common drug shows potential in reversing ageing

A common medication has been found to have anti-ageing qualities, with scientists finding that the drug can de-age monkeys. Metformin, a cheap and common diabetes drug that has been used since the 1950s, could be an anti-ageing elixir, with scientists from the Chinese Academy of Sciences and Beijing Institute of Genomics using the pill to "markedly" slow down ageing in the animals. According to the experts, the medication reduced deterioration of the brain and boosted cognitive abilities in the primates while also slowing down bone loss and aiding in the "rejuvenation" of several tissues and organs. The most significant improvements were seen in the liver and frontal lobe, the part of the brain responsible for language, reasoning, problem solving, memory, movement and personality. Researchers said all of the findings led to the conclusion that "metformin can reduce biological age indicators" up to six years, with the medication paving the way for ageing reversal in humans. The drug was previously tested on mice, but since testing the medication on Cynomolgus monkeys - that are both physiologically and functionally similar to humans - the tests have shown more promise for potential human trials. The researchers said of the 40-month study, "Our research pioneers the systemic reduction of multi-dimensional biological age in primates through metformin, paving the way for advancing pharmaceutical strategies against human ageing." The scientists added, "[The study] represents an important advance in the quest to delay human ageing, with geriatric medicine research gradually shifting its focus from treating individual chronic diseases to systemic intervention against ageing." Image credits: Shutterstock

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To tackle gendered violence, we also need to look at drugs, trauma and mental health

<a href="https://theconversation.com/profiles/siobhan-odean-1356613">Siobhan O'Dean</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/lucinda-grummitt-1531503">Lucinda Grummitt</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/steph-kershaw-1466426">Steph Kershaw</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> After several highly publicised alleged murders of women in Australia, the Albanese government this week pledged <a href="https://ministers.pmc.gov.au/gallagher/2024/helping-women-leave-violent-partner-payment">more than A$925 million</a> over five years to address men’s violence towards women. This includes up to $5,000 to support those escaping violent relationships. However, to reduce and prevent gender-based and intimate partner violence we also need to address the root causes and contributors. These include alcohol and other drugs, trauma and mental health issues. <h2>Why is this crucial?</h2> The World Health Organization estimates <a href="https://iris.who.int/bitstream/handle/10665/341604/WHO-SRH-21.6-eng.pdf?sequence=1">30% of women</a> globally have experienced intimate partner violence, gender-based violence or both. In Australia, <a href="https://www.abs.gov.au/statistics/people/crime-and-justice/partner-violence/latest-release#key-statistics">27% of women</a> have experienced intimate partner violence by a co-habiting partner; <a href="https://pubmed.ncbi.nlm.nih.gov/37004184/">almost 40%</a> of Australian children are exposed to domestic violence. By gender-based violence we mean violence or intentionally harmful behaviour directed at someone due to their gender. But intimate partner violence specifically refers to violence and abuse occurring between current (or former) romantic partners. Domestic violence can extend beyond intimate partners, to include other family members. These statistics highlight the urgent need to address not just the aftermath of such violence, but also its roots, including the experiences and behaviours of perpetrators. <h2>What’s the link with mental health, trauma and drugs?</h2> The relationships between mental illness, drug use, traumatic experiences and violence are complex. When we look specifically at the link between mental illness and violence, most people with mental illness will not become violent. But there <a href="https://theconversation.com/bondi-attacker-had-mental-health-issues-but-most-people-with-mental-illness-arent-violent-227868">is evidence</a> people with serious mental illness can be more likely to become violent. The use of alcohol and other drugs also <a href="https://theconversation.com/alcohol-and-drug-use-exacerbate-family-violence-and-can-be-dealt-with-69986">increases the risk</a> of domestic violence, including intimate partner violence. About <a href="https://www.aihw.gov.au/family-domestic-and-sexual-violence/understanding-fdsv/factors-associated-with-fdsv">one in three</a> intimate partner violence incidents involve alcohol. These are more likely to result in physical injury and hospitalisation. The risk of perpetrating violence is even higher for people with mental ill health who are also <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525086/">using alcohol or other drugs</a>. It’s also important to consider traumatic experiences. Most people who experience trauma do not commit violent acts, but there are <a href="https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(23)00075-0/fulltext">high rates</a> of trauma among people who become violent. For example, experiences of childhood trauma (such as witnessing physical abuse) <a href="https://www.sciencedirect.com/science/article/pii/S1359178915000828?via%3Dihub">can increase the risk</a> of perpetrating domestic violence as an adult. Early traumatic experiences can affect the brain and body’s <a href="https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-017-0895-4">stress response</a>, leading to heightened fear and perception of threat, and difficulty regulating emotions. This can result in aggressive responses when faced with conflict or stress. This response to stress increases the risk of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9675346/">alcohol and drug problems</a>, developing <a href="https://pubmed.ncbi.nlm.nih.gov/30798897/">PTSD</a> (post-traumatic stress disorder), and <a href="https://psycnet.apa.org/record/2015-17349-001">increases the risk</a> of perpetrating intimate partner violence. <h2>How can we address these overlapping issues?</h2> We can reduce intimate partner violence by addressing these overlapping issues and tackling the root causes and contributors. The early intervention and treatment of <a href="https://doi.org/10.1186/s12905-019-0728-z">mental illness</a>, <a href="https://doi.org/10.1177/1541204020939645">trauma</a> (including PTSD), and <a href="https://doi.org/10.1016/j.avb.2015.06.001">alcohol and other drug use</a>, could help reduce violence. So extra investment for these are needed. We also need more investment to <a href="https://www.sciencedirect.com/science/article/pii/S2212657023000508">prevent mental health issues</a>, and preventing alcohol and drug use disorders from developing in the first place. <a href="https://www.sciencedirect.com/science/article/pii/S074937972200023X?via%3Dihub">Preventing trauma</a> from occuring and supporting those exposed is crucial to end what can often become a vicious cycle of intergenerational trauma and violence. <a href="https://journals.sagepub.com/doi/10.1177/070674371105600505">Safe and supportive</a> environments and relationships can protect children against mental health problems or further violence as they grow up and engage in their own intimate relationships. We also need to acknowledge the widespread <a href="https://store.samhsa.gov/product/practical-guide-implementing-trauma-informed-approach/pep23-06-05-005">impact of trauma</a> and its effects on mental health, drug use and violence. This needs to be integrated into policies and practices to reduce re-traumatising individuals. <h2>How about programs for perpetrators?</h2> Most existing standard intervention programs for perpetrators <a href="https://journals.sagepub.com/doi/10.1177/1524838018791268">do not consider</a> the links between trauma, mental health and perpetrating intimate partner violence. Such programs tend to have <a href="https://psycnet.apa.org/doi/10.1037/a0012718">little</a> or <a href="https://doi.org/10.1016/j.cpr.2021.101974">mixed effects</a> on the behaviour of perpetrators. But we could improve these programs with a <a href="http://rcfv.archive.royalcommission.vic.gov.au/MediaLibraries/RCFamilyViolence/Reports/RCFV_Full_Report_Interactive.pdf">coordinated approach</a> including treating mental illness, drug use and trauma at the same time. Such “<a href="https://www.sciencedirect.com/science/article/pii/S014976341930449X?via%3Dihub">multicomponent</a>” programs show promise in meaningfully reducing violent behaviour. However, we need more rigorous and large-scale evaluations of how well they work. <h2>What needs to happen next?</h2> Supporting victim-survivors and improving interventions for perpetrators are both needed. However, intervening once violence has occurred is arguably too late. We need to direct our efforts towards broader, holistic approaches to prevent and reduce intimate partner violence, including addressing the underlying contributors to violence we’ve outlined. We also need to look more widely at preventing intimate partner violence and gendered violence. We need developmentally appropriate <a href="https://theconversation.com/4-things-our-schools-should-do-now-to-help-prevent-gender-based-violence-228993">education and skills-based programs</a> for adolescents to prevent the emergence of unhealthy relationship patterns before they become established. We also need to address the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278040/">social determinants of health</a> that contribute to violence. This includes improving access to affordable housing, employment opportunities and accessible health-care support and treatment options. All these will be critical if we are to break the cycle of intimate partner violence and improve outcomes for victim-survivors. <hr /> The National Sexual Assault, Family and Domestic Violence Counselling Line – 1800 RESPECT (1800 737 732) – is available 24 hours a day, seven days a week for any Australian who has experienced, or is at risk of, family and domestic violence and/or sexual assault. If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14. In an emergency, call 000.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/229182/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/siobhan-odean-1356613">Siobhan O'Dean</a>, Postdoctoral Research Associate, The Matilda Centre for Research in Mental Health and Substance Use, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/lucinda-grummitt-1531503">Lucinda Grummitt</a>, Postdoctoral Research Fellow, The Matilda Centre for Research in Mental Health and Substance Use, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/steph-kershaw-1466426">Steph Kershaw</a>, Research Fellow, The Matilda Centre for Research in Mental Health and Substance Use, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/to-tackle-gendered-violence-we-also-need-to-look-at-drugs-trauma-and-mental-health-229182">original article</a>.

Caring

What happens when I stop taking a drug like Ozempic or Mounjaro?

<a href="https://theconversation.com/profiles/natasha-yates-1213624">Natasha Yates</a>, <a href="https://theconversation.com/institutions/bond-university-863">Bond University</a> Drugs like Ozempic are very <a href="https://dom-pubs.pericles-prod.literatumonline.com/doi/10.1111/dom.12932">effective</a> at helping most people who take them lose weight. Semaglutide (sold as Wegovy and Ozempic) and tirzepatide (sold as Zepbound and Mounjaro) are the most well known in the class of drugs that mimic hormones to reduce feelings of hunger. But does weight come back when you stop using it? The short answer is yes. Stopping <a href="https://jamanetwork.com/journals/jama/fullarticle/2812936">tirzepatide</a> and <a href="https://doi.org/10.1111/dom.14725">semaglutide</a> will result in weight regain in most people. So are these medications simply another (expensive) form of yo-yo dieting? Let’s look at what the evidence shows so far. <h2>It’s a long-term treatment, not a short course</h2> If you have a bacterial infection, antibiotics will help your body fight off the germs causing your illness. You take the full course of medication, and the infection is gone. For obesity, taking tirzepatide or semaglutide can help your body get rid of fat. However it doesn’t fix the reasons you gained weight in the first place because obesity is a chronic, complex condition. When you stop the medications, the weight returns. Perhaps a more useful comparison is with high blood pressure, also known as hypertension. Treatment for hypertension is lifelong. It’s the same with obesity. Medications work, but only while you are taking them. (Though obesity is more complicated than hypertension, as many different factors both cause and perpetuate it.) Therefore, several concurrent approaches are needed; taking medication can be an important part of effective management but on its own, it’s often insufficient. And in an unwanted knock-on effect, stopping medication can undermine other strategies to lose weight, like eating less. <h2>Why do people stop?</h2> Research trials show anywhere from <a href="https://asean-endocrinejournal.org/index.php/JAFES/article/view/1771">6%</a> to <a href="https://pubmed.ncbi.nlm.nih.gov/35015037/">13.5%</a> of participants stop taking these drugs, primarily because of <a href="https://www.health.harvard.edu/staying-healthy/glp-1-diabetes-and-weight-loss-drug-side-effects-ozempic-face-and-more">side effects</a>. But these studies don’t account for those forced to stop because of cost or <a href="https://www.tga.gov.au/safety/shortages/information-about-major-medicine-shortages/about-ozempic-semaglutide-shortage-2022-and-2023">widespread supply issues</a>. We don’t know how many people have needed to stop this medication over the past few years for these reasons. Understanding what stopping does to the body is therefore important. <h2>So what happens when you stop?</h2> When you stop using tirzepatide or semaglutide, it takes several days (or even a couple of weeks) to <a href="https://pubmed.ncbi.nlm.nih.gov/30565096/">move out of your system</a>. As it does, a number of things happen: <ul> <li>you start feeling hungry again, because both <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119845/">your brain and your gut</a> no longer have the medication working to make you feel full</li> </ul> <ul> <li> blood sugars increase, because the medication is no longer acting on the pancreas to help control this. If you have diabetes as well as obesity you may need to take other medications to keep these in an acceptable range. Whether you have diabetes or not, you may need to eat foods with a <a href="https://www.betterhealth.vic.gov.au/health/healthyliving/carbohydrates-and-the-glycaemic-index">low glycemic index</a> to stabilise your blood sugars </li> <li> over the longer term, most people experience a return to their <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10092593/">previous blood pressure and cholesterol levels</a>, as the weight comes back </li> <li> weight regain will mostly be in the form of fat, because it will be gained faster than skeletal muscle. </li> </ul> While you were on the medication, you will have lost <a href="https://academic.oup.com/jes/article/5/Supplement_1/A16/6240360">proportionally less skeletal muscle than fat</a>, muscle loss is inevitable when you lose weight, no matter whether you use medications or not. The problem is, when you stop the medication, your body preferentially puts on fat. <h2>Is stopping and starting the medications a problem?</h2> People whose weight fluctuates with tirzepatide or semaglutide may experience some of the downsides of <a href="https://pubmed.ncbi.nlm.nih.gov/21829159/">yo-yo dieting</a>. When you keep going on and off diets, it’s like a rollercoaster ride for your body. Each time you regain weight, your body has to <a href="https://www.jomes.org/journal/view.html?doi=10.7570/jomes.2017.26.4.237">deal with</a> spikes in blood pressure, heart rate, and how your body handles sugars and fats. This can <a href="https://cardiab.biomedcentral.com/articles/10.1186/s12933-022-01735-x">stress</a> your heart and overall cardiovascular system, as it has to respond to greater fluctuations than usual. Interestingly, the risk to the body from weight fluctuations is greater for people who are <a href="https://jech.bmj.com/content/74/8/662">not obese</a>. This should be a caution to those who are not obese but still using tirzepatide or semaglutide to try to lose unwanted weight. <h2>How can you avoid gaining weight when you stop?</h2> Fear of regaining weight when stopping these medications is valid, and needs to be addressed directly. As obesity has many causes and perpetuating factors, many evidence-based approaches are needed to reduce weight regain. This might include: <ul> <li> getting quality <a href="https://www.hindawi.com/journals/ije/2010/270832/">sleep</a> </li> <li> exercising in a way that builds and maintains muscle. While on the medication, you will <a href="https://pubmed.ncbi.nlm.nih.gov/32628589/">likely have lost muscle</a> as well as fat, although this is not inevitable, especially if you <a href="https://www.europeanreview.org/article/34169">exercise regularly</a> while taking it </li> </ul> <ul> <li> addressing emotional and cultural aspects of life that contribute to over-eating and/or eating unhealthy foods, and how you view your body. Stigma and shame around body shape and size is not cured by taking this medication. Even if you have a healthy relationship with food, we live in a culture that is <a href="https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2009.159491">fat-phobic and discriminates</a> against people in larger bodies </li> <li> eating in a healthy way, hopefully continuing with habits that were formed while on the medication. Eating meals that have high nutrition and fibre, for example, and lower overall portion sizes. </li> </ul> Many people will stop taking tirzepatide or semaglutide at some point, given it is expensive and in short supply. When you do, it is important to understand what will happen and what you can do to help avoid the consequences. Regular reviews with your GP are also important. <hr /> Read the other articles in The Conversation’s <a href="https://theconversation.com/au/topics/ozempic-series-154673">Ozempic series</a> here.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/224972/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/natasha-yates-1213624">Natasha Yates</a>, General Practitioner, PhD Candidate, <a href="https://theconversation.com/institutions/bond-university-863">Bond University</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/what-happens-when-i-stop-taking-a-drug-like-ozempic-or-mounjaro-224972">original article</a>.

Body

No, taking drugs like Ozempic isn’t ‘cheating’ at weight loss or the ‘easy way out’

<a href="https://theconversation.com/profiles/clare-collins-7316">Clare Collins</a>, <a href="https://theconversation.com/institutions/university-of-newcastle-1060">University of Newcastle</a> Obesity medication that is effective has been a long time coming. Enter semaglutide (sold as Ozempic and Wegovy), which is helping people improve weight-related health, including <a href="https://pubmed.ncbi.nlm.nih.gov/37952131/">lowering the risk</a> of a having a heart attack or stroke, while also silencing “<a href="https://theconversation.com/some-ozempic-users-say-it-silences-food-noise-but-there-are-drug-free-ways-to-stop-thinking-about-food-so-much-208467">food noise</a>”. As demand for semaglutide increases, so are <a href="https://www.smh.com.au/lifestyle/health-and-wellness/in-a-fat-phobic-world-ozempic-is-hardly-the-easy-way-out-20240401-p5fgjd.html">claims</a> that taking it is “cheating” at weight loss or the “easy way out”. We don’t tell people who need statin medication to treat high cholesterol or drugs to manage high blood pressure they’re cheating or taking the easy way out. Nor should we shame people taking semaglutide. It’s a drug used to treat diabetes and obesity which needs to be taken long term and comes with risks and side effects, as well as benefits. When prescribed for obesity, it’s given alongside advice about diet and exercise. <h2>How does it work?</h2> Semaglutide is a <a href="https://en.wikipedia.org/wiki/GLP-1_receptor_agonist">glucagon-like peptide-1</a> receptor agonist (GLP-1RA). This means it makes your body’s own glucagon-like peptide-1 hormone, called <a href="https://en.wikipedia.org/wiki/Glucagon-like_peptide-1">GLP-1</a> for short, work better. GLP-1 gets secreted by cells in your gut when it <a href="https://pubmed.ncbi.nlm.nih.gov/38218319/">detects increased nutrient levels</a> after eating. This stimulates insulin production, which lowers blood sugars. GLP-1 also slows gastric emptying, which makes you feel full, and reduces hunger and feelings of reward after eating. <iframe id="tc-infographic-1031" class="tc-infographic" style="border: none;" src="https://cdn.theconversation.com/infographics/1031/c11b606581d4bc58a71f066492d7f740b52c04e1/site/index.html" width="100%" height="400px" frameborder="0"></iframe> GLP-1 receptor agonist (GLP-1RA) medications like Ozempic help the body’s own GLP-1 work better by mimicking and extending its action. Some studies have found less GLP-1 gets released after meals in <a href="https://pubmed.ncbi.nlm.nih.gov/38218319/">adults with obesity or type 2 diabetes mellitus</a> compared to adults with normal glucose tolerance. So having less GLP-1 circulating in your blood means you don’t feel as full after eating and get hungry again sooner compared to people who produce more. GLP-1 has a very short half-life of about <a href="https://pubmed.ncbi.nlm.nih.gov/28443255/">two minutes</a>. So GLP-1RA medications were designed to have a very long half-life of about <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/">seven days</a>. That’s why semaglutide is given as a weekly injection. <h2>What can users expect? What does the research say?</h2> Higher doses of semaglutide are prescribed to treat obesity compared to type 2 diabetes management (up to 2.4mg versus 2.0mg weekly). A large group of <a href="https://pubmed.ncbi.nlm.nih.gov/36691309/">randomised controlled trials</a>, called STEP trials, all tested weekly 2.4mg semaglutide injections versus different interventions or placebo drugs. Trials lasting 1.3–2 years consistently found weekly 2.4 mg semaglutide injections <a href="https://pubmed.ncbi.nlm.nih.gov/36691309/">led to 6–12% greater weight loss</a> compared to placebo or alternative interventions. The average weight change depended on how long medication treatment lasted and length of follow-up. Weight reduction due to semaglutide also leads to a <a href="https://pubmed.ncbi.nlm.nih.gov/36769420/">reduction in systolic and diastolic blood pressure</a> of about 4.8 mmHg and 2.5 mmHg respectively, a reduction in <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/triglycerides">triglyceride levels</a> (a type of blood fat) and <a href="https://pubmed.ncbi.nlm.nih.gov/38041774/">improved physical function</a>. Another recent trial in adults with pre-existing heart disease and obesity, but without type 2 diabetes, found adults receiving weekly 2.4mg semaglutide injections had a <a href="https://pubmed.ncbi.nlm.nih.gov/37952131/">20% lower risk</a> of specific cardiovascular events, including having a non-fatal heart attack, a stroke or dying from cardiovascular disease, after three years follow-up. <h2>Who is eligible for semaglutide?</h2> Australia’s regulator, the Therapeutic Goods Administration (TGA), has <a href="https://www.tga.gov.au/safety/shortages/information-about-major-medicine-shortages/about-ozempic-semaglutide-shortage-2022-and-2023">approved</a> semaglutide, sold as Ozempic, for treating type 2 diabetes. However, due to shortages, the TGA had advised doctors not to start new Ozempic prescriptions for “off-label use” such as obesity treatment and the Pharmaceutical Benefits Scheme doesn’t currently subsidise off-label use. The TGA has <a href="https://www.tga.gov.au/resources/prescription-medicines-registrations/wegovy-novo-nordisk-pharmaceuticals-pty-ltd">approved Wegovy to treat obesity</a> but it’s not currently available in Australia. When it’s available, doctors will be able to prescribe <a href="https://pubmed.ncbi.nlm.nih.gov/36934408/">semaglutide to treat obesity</a> in conjunction with lifestyle interventions (including diet, physical activity and psychological support) in adults with obesity (a BMI of 30 or above) or those with a BMI of 27 or above who also have weight-related medical complications. <h2>What else do you need to do during Ozempic treatment?</h2> Checking details of the <a href="https://pubmed.ncbi.nlm.nih.gov/36691309/">STEP trial intervention components</a>, it’s clear participants invested a lot of time and effort. In addition to taking medication, people had brief lifestyle counselling sessions with dietitians or other health professionals every four weeks as a minimum in most trials. Support sessions were designed to help people stick with consuming 2,000 kilojoules (500 calories) less daily compared to their energy needs, and performing 150 minutes of <a href="https://www.healthdirect.gov.au/tips-for-getting-active">moderate-to-vigorous physical activity</a>, like brisk walking, dancing and gardening each week. STEP trials varied in other components, with follow-up time periods varying from 68 to 104 weeks. The aim of these trials was to show the effect of adding the medication on top of other lifestyle counselling. A <a href="https://pubmed.ncbi.nlm.nih.gov/38041774/">review of obesity medication trials</a> found people reported they needed less <a href="https://pubmed.ncbi.nlm.nih.gov/28652832/">cognitive behaviour training</a> to help them stick with the reduced energy intake. This is one aspect where drug treatment may make adherence a little easier. Not feeling as hungry and having environmental food cues “switched off” may mean less support is required for goal-setting, self-monitoring food intake and <a href="https://theconversation.com/9-ways-wont-power-is-better-than-willpower-for-resisting-temptation-and-helping-you-eat-better-71267">avoiding things that trigger eating</a>. <h2>But what are the side effects?</h2> Semaglutide’s side-effects <a href="https://pubmed.ncbi.nlm.nih.gov/38041774/">include</a> nausea, diarrhoea, vomiting, constipation, indigestion and abdominal pain. In one study these <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/">led to</a> discontinuation of medication in 6% of people, but interestingly also in 3% of people taking placebos. More severe side-effects included gallbladder disease, acute pancreatitis, hypoglycaemia, acute kidney disease and injection site reactions. To reduce risk or severity of side-effects, <a href="https://pubmed.ncbi.nlm.nih.gov/36934408/">medication doses are increased very slowly</a> over months. Once the full dose and response are achieved, research indicates you need to take it long term. Given this long-term commitment, and associated <a href="https://www.health.gov.au/topics/private-health-insurance/what-private-health-insurance-covers/out-of-pocket-costs#:%7E:text=An%20out%20of%20pocket%20cost,called%20gap%20or%20patient%20payments">high out-of-pocket cost of medication</a>, when it comes to taking semaglutide to treat obesity, there is no way it can be considered “cheating”. <hr /> Read the other articles in The Conversation’s <a href="https://theconversation.com/au/topics/ozempic-series-154673">Ozempic series</a> here.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/219116/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/clare-collins-7316">Clare Collins</a>, Laureate Professor in Nutrition and Dietetics, <a href="https://theconversation.com/institutions/university-of-newcastle-1060">University of Newcastle</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/no-taking-drugs-like-ozempic-isnt-cheating-at-weight-loss-or-the-easy-way-out-219116">original article</a>.

Body

Drugs like Ozempic won’t ‘cure’ obesity but they might make us more fat-phobic

<a href="https://theconversation.com/profiles/emma-beckett-22673">Emma Beckett</a>, <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a> Many have <a href="https://www.economist.com/leaders/2023/03/02/new-drugs-could-spell-an-end-to-the-worlds-obesity-epidemic">declared</a> drugs like Ozempic could “end obesity” by reducing the appetite and waistlines of millions of people around the world. When we look past the hype, this isn’t just untrue – it can also be harmful. The focus on weight, as opposed to health, is a feature of <a href="https://www.sciencedirect.com/science/article/abs/pii/S0277539521001217">diet culture</a>. This frames the pursuit of thinness as more important than other aspects of physical and cultural wellbeing. The Ozempic buzz isn’t just rooted in health and medicine but plays into ideas of <a href="https://butterfly.org.au/weight-bias-fatphobia-diet-culture/#:%7E:text=Weight%20bias%2C%20sometimes%20also%20called,or%20being%20around%20fat%20people.">fat stigma and fat phobia</a>. This can perpetuate fears of fatness and fat people, and the behaviours that <a href="https://link.springer.com/article/10.1186/S12916-018-1116-5">harm people who live in larger bodies</a>. <h2>Not the first ‘miracle’ weight-loss drug</h2> This isn’t the first time we have heard that weight-loss drugs will change the world. Ozempic and <a href="https://www.ncbi.nlm.nih.gov/books/NBK551568/">its family</a> of GLP-1-mimicking drugs are the <a href="https://theconversation.com/ozempic-is-in-the-spotlight-but-its-just-the-latest-in-a-long-and-strange-history-of-weight-loss-drugs-209324">latest in a long line of weight loss drugs</a>. Each looked promising at the time. But none have lived up to the hype in the long term. Some have even been withdrawn from sale due to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5126837/">severe side effects</a>. Science does improve <a href="https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30028-8/fulltext">incrementally</a>, but diet culture also keeps us on a cycle of hope for the next <a href="https://sahrc.org/2022/04/diet-culture-a-brief-history/">miracle cure</a>. So drugs like Ozempic might not deliver the results individuals expect, continuing the cycle of hope and shame. <h2>Ozempic doesn’t work the same for everyone</h2> When we talk about the results of studies using Ozempic, we often <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719041/">focus on the average</a> (also known as the mean) results or the maximum (or peak) results. So, studies might <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">show</a> those using the drug lost an average of 10.9% of their body weight, but some lost more than 20% and others less than 5% What we don’t talk about as much is that responses are variable. Some people are “<a href="https://www.sciencedirect.com/science/article/pii/S2212877820301769">non-responders</a>”. This means not everyone loses as much weight as the average, and some don’t lose weight at all. For some people, the side-effects will outweigh the benefits. When people are on drugs like Ozempic, their blood sugar is better controlled by enhancing the release of insulin and reducing the levels of another hormone called glucagon. But there is greater variability in the amount of <a href="https://www.sciencedirect.com/science/article/pii/S2212877820301769#bib88">weight lost</a> than the variability in blood sugar control. It isn’t clear why, but is likely due to differences in genetics and lifestyles, and weight being more complex to regulate. <h2>Treatment needs to be ongoing. What will this mean?</h2> When weight-loss drugs do work, they are only effective while they’re being taken. This means that to keep the weight off people need to keep taking them long term. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9542252/">One study found</a> an average weight loss of more than 17% after a year on Ozempic became an average net weight loss of 5.6% more than two years after stopping treatment. Short-term side effects of drugs like Ozempic include dizziness, nausea, vomiting and other gastrointestinal upsets. But because these are new drugs, we simply don’t have data to tell us if side effects will increase as people take them for longer periods. Nor do we know if <a href="https://www.medicalnewstoday.com/articles/why-weight-loss-drugs-stop-working-how-to-break-past-ozempic-plateau#:%7E:text=A%20lifetime%20commitment%20to%20Ozempic&text=By%20these%20standards%2C%20such%20drugs,long%2Dterm%20risk%20is%20unknown.">effectiveness will be reduced</a> in the long term. This is called <a href="https://www.cancer.gov/publications/dictionaries/cancer-terms/def/drug-tolerance#:%7E:text=A%20condition%20that%20occurs%20when,or%20different%20medicine%20is%20needed.">drug tolerance</a> and is documented for other long-term treatments such as antidepressants and chemotherapies. <h2>Biology is only part of the story</h2> For some people, using GLP-1-mimicking drugs like Ozempic will be validating and empowering. They will feel like their biology has been “normalised” in the same way that blood pressure or cholesterol medication can return people to the “normal” range of measures. But biologically, obesity <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202176/#:%7E:text=Obesity%20behaves%20as%20complex%20polygenic,about%2080%25%20(3).">isn’t solely about GLP-1 activity</a> with <a href="https://www.worldobesity.org/what-we-do/our-policy-priorities/the-roots-of-obesity">many other</a> hormones, physical activity, and even our gut microbes involved. Overall, <a href="https://www.ncbi.nlm.nih.gov/books/NBK278977/">obesity is complex and multifaceted</a>. Obesity isn’t just driven by personal biology and choice; it has social, cultural, political, environmental and economic determinants. <h2>A weight-centred approach misses the rest of the story</h2> The weight-centred approach <a href="https://butterfly.org.au/body-image/health-not-weight/#:%7E:text=Health%20and%20wellbeing%20are%20multi,on%20their%20size%20or%20appearance.">suggests that leading with thinness means health will follow</a>. But changing appetite is only part of the story when it comes to health. Obesity often <a href="https://www.sciencedirect.com/science/article/pii/S2667368123000335#:%7E:text=Obesity%20related%20malnutrition%20can%20also,%5D%2C%20%5B7%5D%5D.">co-exists with malnutrition</a>. We try to separate the effects in research using statistics, but focusing on the benefits of weight-loss drugs without addressing the underlying malnutrition means we aren’t likely to see the <a href="https://www.wsj.com/articles/ozempic-diet-exercise-healthy-43eee86c">improved health outcomes in everyone who loses weight</a>. <h2>Obesity isn’t an issue detached from people</h2> Even when it is well-intentioned, the rhetoric around the joy of “ending the obesity epidemic” can <a href="https://theconversation.com/ozempic-the-miracle-drug-and-the-harmful-idea-of-a-future-without-fat-211661">harm people</a>. Obesity doesn’t occur in isolation. It is people who are obese. And the celebration and hype of these weight-loss drugs can reinforce harmful fat stigma. The framing of these drugs as a “cure” exacerbates the binary view of thin versus fat, and healthy versus unhealthy. These are not binary outcomes that are good or bad. Weight and health exist on a spectrum. Ironically, while fat people are told they need to lose weight for their health, they are also <a href="https://www.dailytelegraph.com.au/news/nsw/ozempic-shame-why-users-are-embarrassed-to-admit-using-weight-loss-wonder-drug/news-story/ee52a819c69459afe6576d25988f9bd6">shamed for “cheating” or taking shortcuts</a> by using medication. <h2>Drugs are tools, not silver bullets</h2> The creation of these drugs is a start, but they remain expensive, and the hype has been followed by <a href="https://www.tga.gov.au/safety/shortages/information-about-major-medicine-shortages/about-ozempic-semaglutide-shortage-2022-and-2023#:%7E:text=Consumer%20Medicine%20Information%20.-,Why%20the%20Ozempic%20shortage%20happened,label%20prescribing%20for%20weight%20loss.">shortages</a>. Ultimately, complex challenges aren’t addressed with simple solutions. This is particularly true when people are involved, and even more so when there isn’t even an agreement on what the challenge is. Many organisations and individuals see obesity is a disease and believe this framing helps people to seek treatment. Others think it’s unnecessary to attach medical labels to body types and <a href="https://www.forbes.com/sites/geoffreykabat/2013/07/09/why-labeling-obesity-as-a-disease-is-a-big-mistake/?sh=5ca95cc2103b">argue</a> it confuses risk factors (things that are linked to increased risk of illness) with illness itself. Regardless, two things will always remain true. Drugs can only ever be tools, and those tools need to be applied in a context. To use these tools ethically, we need to remain mindful of who this application harms along the way. <hr /> Read the other articles in The Conversation’s <a href="https://theconversation.com/au/topics/ozempic-series-154673">Ozempic series</a> here.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/219309/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/emma-beckett-22673">Emma Beckett</a>, Adjunct Senior Lecturer, Nutrition, Dietetics & Food Innovation - School of Health Sciences, <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/drugs-like-ozempic-wont-cure-obesity-but-they-might-make-us-more-fat-phobic-219309">original article</a>.

Body

Considering taking a weight-loss drug like Ozempic? Here are some potential risks and benefits

<a href="https://theconversation.com/profiles/lauren-ball-14718">Lauren Ball</a>, <a href="https://theconversation.com/institutions/the-university-of-queensland-805">The University of Queensland</a> and <a href="https://theconversation.com/profiles/emily-burch-438717">Emily Burch</a>, <a href="https://theconversation.com/institutions/southern-cross-university-1160">Southern Cross University</a> After weight-loss drugs like Ozempic exploded onto the market, celebrities and social media influencers were quick to spruik their benefits, leading to their rapid rise in use. In the last three months of 2022, clinicians in the United States alone wrote <a href="https://www.washingtonpost.com/business/2023/09/27/ozempic-prescriptions-data-analysis/">more than nine million prescriptions</a> for these drugs. As they’ve grown in popularity, we’ve also heard more about the potential side effects – from common gastrointestinal discomforts, to more serious mental health concerns. But what does the science say about how well Ozempic and Wegovy (which are both brand names of the drug semaglutide) work for weight loss? And what are the potential side effects? Here’s what to consider if you or a loved one are thinking of taking the drug. <h2>Potential benefits</h2> 1) It’s likely to help you lose weight The largest, well-conducted <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/">research study</a> of semaglutide was from United Kingdom in 2021. Some 1,961 people who were classified as “overweight” or “obese” were randomly assigned to have either semaglutide or a placebo and followed for 68 weeks (about 1.3 years). All participants also had free access to advice about healthy eating and physical activity. The study found those taking semaglutide lost weight – significantly more than people who had the placebo (-14.9% of their body weight compared with -2.4% of body weight). In another <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">study</a> in the United States, one health-care clinic gave 408 people weekly injections of semaglutide. Over the first three months, those included in the final analysis (175 people) lost an average of 6.7kg. Over the first six months, they lost an average of 12.3kg. Large weight losses have been found in a more <a href="https://www.nature.com/articles/s41591-022-02026-4">recent trial</a> of semaglutide, suggesting weight loss is a very likely outcome of ongoing use of the medication. 2) It may reduce your chronic disease risk factors When people in the overweight or obese weight categories lose <a href="https://www.sciencedirect.com/science/article/pii/S1550413116300535">at least 5%</a> of their body weight, physiological changes often occur beyond a change in weight or shape. This <a href="https://www.nih.gov/news-events/nih-research-matters/research-context-obesity-metabolic-health">might include</a> lowered cholesterol levels, lowered blood pressure and lowered blood glucose levels, which all reduce the risk of chronic diseases. In one of the semaglutide <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">trials</a>, most people (87.3%) lost at least 5% of their body weight. Although most of the large studies of semaglutide excluded people with metabolic health conditions such as type 2 diabetes, metabolic health gains were <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/">observed</a>, including lowered blood pressure, blood glucose levels and fasting blood lipid (fat) levels. In the UK <a href="https://pubmed.ncbi.nlm.nih.gov/33567185/">study</a> from 2021, people taking semaglutide had greater improvements in physical capabilities and risk factors for heart disease and diabetes, including reductions in waist circumference, markers of inflammation, blood pressure and blood glucose levels. 3) It might improve your quality of life, emotional wellbeing or sense of achievement The original trial of semaglutide did not focus on this bundle of benefits, but further follow-ups show additional benefits associated with the medication. Compared to the placebo, people taking semaglutide saw significant <a href="https://www.tandfonline.com/doi/full/10.1080/00325481.2022.2150006">improvements</a> in their physical functioning and perceptions of their general health, social functioning and mental health. Anecdotally (not based on scientific research), people using semaglutide, such as <a href="https://people.com/oprah-winfrey-reveals-weight-loss-medication-exclusive-8414552">Oprah Winfrey</a>, report a reclaiming or turning point of their life, social situation and body image. <h2>What about the risks?</h2> 1) You may experience gastrointestinal symptoms In the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">US clinical trial</a>, nearly half (48.6%) of people taking semaglutide reported experiencing adverse effects. Nausea and vomiting were the most frequently experienced (36.6%) followed by diarrhea (8.6%), fatigue (6.3%) and constipation (5.7%). In the UK study, nausea and diarrhoea were also commonly reported. In <a href="https://www.nejm.org/doi/10.1056/NEJMoa2032183?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">another trial</a>, many participants (74.2%) using semaglutide reported gastrointestinal symptoms. However, nearly half (47.9%) using the placebo also reported gastrointestinal symptoms, indicating that symptoms may be similar to those experienced during normal daily living. Most gastrointestinal symptoms were mild to moderate in severity, and resolved for most people without the need to stop participating in the study. 2) You might feel fatigued Fatigue was the second most common side effect for participants in the US <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">clinical trial</a>, affecting 6.3% of participants. 3) You might be among the minority who don’t tolerate the drug Australia’s Therapeutic Goods Administration (TGA) has <a href="https://www.tga.gov.au/news/safety-alerts/compounding-safety-information-semaglutide-products">approved</a> Ozempic as safe to use, for the treatment of type 2 diabetes but it has not yet been approved for weight loss. The TGA has also <a href="https://www.tga.gov.au/resources/prescription-medicines-registrations/wegovy-novo-nordisk-pharmaceuticals-pty-ltd">approved Wegovy</a> (a higher dose of semagtlutide) for weight loss, however it’s not yet available in Australia. In the US <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9486455/">clinical trial</a>, no unexpected safety issues were reported. However, five patients (2.9%) had to stop taking the medication because they could not tolerate the adverse effects. Fifteen (8.6%) had to either reduce the dose or remain on the same dose to avoid the adverse effects. In <a href="https://www.nejm.org/doi/10.1056/NEJMoa2032183?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">other studies</a>, some patients stopped the trial due to gastrointestinal symptoms being so severe they could not tolerate continuing. More severe safety concerns reported in <a href="https://www.nejm.org/doi/10.1056/NEJMoa2032183?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">studies</a> include gallbladder-related disorders (mostly cholelithiasis, also known as gallstones) in 34 patients (2.6%) and mild acute pancreatitis in three patients (0.2%). All people recovered during the trial period. A 2024 European <a href="https://link.springer.com/article/10.1007/s11096-023-01694-7">study</a> analysed psychiatric adverse events associated with semaglutide, liraglutide and tirzepatide (which work in a similar way to semaglutide). Between January 2021 and May 2023, the drug database recorded 481 psychiatric events (about 1.2% of the total reported) associated with these drugs. About half of these events were reported as depression, followed by anxiety (39%) and suicidal ideation (19.6%). Nine deaths and 11 life-threatening outcomes were reported during the study period. Due to the severity and fatal outcomes of some of these reports, <a href="https://www.fda.gov/drugs/drug-safety-and-availability/update-fdas-ongoing-evaluation-reports-suicidal-thoughts-or-actions-patients-taking-certain-type">the US Food and Drug Administration</a> investigated further but did not find evidence that use of these medicines caused suicidal thoughts or actions. 4) It might be difficult to access Despite being considered safe, the TGA has <a href="https://www.tga.gov.au/safety/shortages/medicine-shortage-alerts/update-prescribers-advised-not-start-new-patients-ozempic#:%7E:text=Ozempic%27s%20TGA%2Dapproved%20indication%20is,consult%20the%20appropriate%20prescribing%20guidelines.">warned</a> significant Ozempic access barriers are likely to continue throughout 2024. To manage the shortage, pharmacists are instructed to give preference to people with type 2 diabetes who are seeking the medication. 5) You might not always get clear information from vested interests Given the popularity of Ozempic and Wegovy, health organisations such as the World Obesity Federation have expressed <a href="https://www.theguardian.com/society/2023/mar/12/orchestrated-pr-campaign-how-skinny-jab-drug-firm-sought-to-shape-obesity-debate">concern</a> about the medication’s marketing, PR and strong <a href="https://www.theguardian.com/australia-news/2023/jan/06/tga-investigates-influencers-after-diabetes-drug-ozempic-promoted-as-weight-loss-treatment">social media presence</a>. Some journalists have <a href="https://www.theguardian.com/society/2023/mar/12/orchestrated-pr-campaign-how-skinny-jab-drug-firm-sought-to-shape-obesity-debate">raised conflict of interest concerns</a> about the relationship between some obesity researchers and Novo Nordrisk, Ozempic and Wegovy’s manufacturer. The worry is that researchers might be influenced by their relationship with Novo Nordrisk to produce study results that are more favourable to the medications. <h2>Bottom line</h2> Ozempic is a medication that should be used in conjunction with your health care provider. But remember, weight is only one aspect of your health and wellbeing. It’s important to take a holistic view of your health and prioritise eating well, moving more and getting enough sleep. <hr /> Read the other articles in The Conversation’s <a href="https://theconversation.com/au/topics/ozempic-132745">Ozempic series</a> here.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/219312/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/lauren-ball-14718">Lauren Ball</a>, Professor of Community Health and Wellbeing, <a href="https://theconversation.com/institutions/the-university-of-queensland-805">The University of Queensland</a> and <a href="https://theconversation.com/profiles/emily-burch-438717">Emily Burch</a>, Lecturer, <a href="https://theconversation.com/institutions/southern-cross-university-1160">Southern Cross University</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/considering-taking-a-weight-loss-drug-like-ozempic-here-are-some-potential-risks-and-benefits-219312">original article</a>.

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How dieting, weight suppression and even misuse of drugs like Ozempic can contribute to eating disorders

<a href="https://theconversation.com/profiles/samantha-withnell-1504436">Samantha Withnell</a>, <a href="https://theconversation.com/institutions/western-university-882">Western University</a> and <a href="https://theconversation.com/profiles/lindsay-bodell-1504260">Lindsay Bodell</a>, <a href="https://theconversation.com/institutions/western-university-882">Western University</a> Up to 72 per cent of women and 61 per cent of men are dissatisfied with their weight or <a href="https://doi.org/10.1016/j.eatbeh.2014.04.010">body image</a>, according to a U.S. study. Globally, millions of people <a href="https://doi.org/10.1111%2Fobr.12466">attempt to lose weight</a> every year with the hope that weight loss will have positive effects on their body image, health and quality of life. However, these motivated individuals often struggle to maintain new diets or exercise regimens. The rise of medications such as semaglutides, like <a href="https://dhpp.hpfb-dgpsa.ca/dhpp/resource/101298">Ozempic</a> or <a href="https://dhpp.hpfb-dgpsa.ca/dhpp/resource/101765">Wegovy</a>, <a href="https://www.cbc.ca/news/health/ozempic-weight-loss-1.6772021">might be viewed as an appealing “quick fix”</a> alternative to meet weight loss goals. Research led by our team and others suggests that such attempts to lose weight often do more harm than good, and even increase the risk of <a href="https://osf.io/9stq2">developing an eating disorder</a>. <h2>Weight loss and eating disorders</h2> Eating disorders are <a href="https://doi.org/10.1002/eat.20589">serious mental health conditions</a> primarily characterized by extreme patterns of under- or over-eating, concerns about one’s shape or body weight or other behaviours intended to influence body shape or weight such as exercising excessively or self-inducing vomiting. Although once thought to only affect young, white adolescent girls, eating disorders do not discriminate; eating disorders can develop in people of <a href="https://doi.org/10.1002/erv.2553">any age, sex, gender or racial/ethnic background</a>, with an estimated <a href="https://nedic.ca/general-information/">one million Canadians</a> suffering from an eating disorder at any given time. Feb. 1 to 7 is <a href="https://nedic.ca/edaw/">National Eating Disorders Awareness Week</a>. As a clinical psychologist and clinical psychology graduate student, our research has focused on how eating disorders develop and what keeps them going. Pertinent to society’s focus on weight-related goals, our research has examined associations between weight loss and eating disorder symptoms. <h2>Eating disorders and ‘weight suppression’</h2> In eating disorders research, the state of maintaining weight loss is referred to as “weight suppression.” Weight suppression is typically defined as the difference between a person’s current weight and their highest lifetime weight (excluding pregnancy). Despite the belief that weight loss will improve body satisfaction, we found that in a sample of over 600 men and women, weight loss had no impact on women’s negative body image and was associated with increased body dissatisfaction in <a href="https://doi.org/10.1016/j.bodyim.2023.01.011">men</a>. Importantly, being more weight suppressed has been associated with the <a href="https://doi.org/10.1093/ajcn/nqaa146">onset of eating disorders</a>, including anorexia nervosa and bulimia nervosa. <a href="https://doi.org/10.1007/s11920-018-0955-2">One proposed explanation</a> for the relationship between weight suppression and eating disorders is that maintaining weight loss becomes increasingly difficult as body systems that <a href="https://doi.org/10.3945/ajcn.110.010025">reduce metabolic rate and energy expenditure, and increase appetite</a>, are activated to promote weight gain. There is growing awareness that <a href="https://doi.org/10.1136/bmj.g2646">weight regain is highly likely following conventional diet programs</a>. This might lead people to engage in more and more extreme behaviours to control their weight, or they might shift between extreme restriction of food intake and episodes of overeating or binge eating, the characteristic symptoms of bulimia nervosa. <h2>Ozempic and other semaglutide drugs</h2> Semaglutide drugs like Ozempic and Wegovy are part of a class of drug called <a href="https://pdf.hres.ca/dpd_pm/00067924.PDF">glucagon-like peptide-1 agonists (GLP-1As)</a>. These drugs work by mimicking the hormone GLP-1 to interact with neural pathways that signal satiety (fullness) and slow stomach emptying, leading to reduced food intake. Although GLP-1As are indicated to treat Type 2 diabetes, <a href="https://www.cbc.ca/news/canada/london/ozempic-off-label-1.6884141">they are increasingly prescribed off-label</a> or being <a href="https://www.bbc.com/news/health-67414203">illegally purchased</a> without a prescription because of their observed effectiveness at inducing weight loss. Although medications like Ozempic do often lead to weight loss, the rate of weight loss may <a href="https://doi.org/10.1001/jama.2021.3224">slow down or stop over time</a>. Research by Lindsay Bodell, one of the authors of this story, and her colleagues on weight suppression may help explain why effects of semaglutides diminish over time, as <a href="https://doi.org/10.1016/j.physbeh.2019.112565">weight suppression is associated with reduced GLP-1 response</a>. This means those suppressing their weight could become less responsive to the satiety signals activated by GLP-1As. Additionally, weight loss effects are only seen for as long as the medication is taken, meaning those who take these drugs to achieve some weight loss goal are <a href="https://doi.org/10.1111/dom.14725">likely to regain most, if not all, weight lost</a> when they stop taking the medication. <h2>Risks of dieting and weight-loss drugs</h2> The growing market for off-label weight loss drugs is concerning, because of the exacerbation of <a href="https://theconversation.com/ozempic-the-miracle-drug-and-the-harmful-idea-of-a-future-without-fat-211661">weight stigma</a> and the serious <a href="https://doi.org/10.1016/j.jand.2022.01.004">health risks</a> associated with unsupervised weight loss, including developing eating disorders. Researchers and health professionals are already raising the alarm about the use of GLP-1As in children and adolescents, due to concerns about their possible <a href="https://doi.org/10.1017/cts.2023.612">impact on growth and development</a>. Moreover, popular weight-loss methods, whether they involve pills or “crash diets,” often mimic symptoms of eating disorders. For example, intermittent fasting diets that involve long periods of fasting followed by short periods of food consumption may mimic and <a href="https://doi.org/10.1016/j.eatbeh.2022.101681">increase the risk of developing binge eating problems</a>. The use of diet pills or laxatives to lose weight has been found to increase the risk of <a href="https://doi.org/10.2105/AJPH.2019.305390">being diagnosed with an eating disorder in the next one to three years</a>. Drugs like Ozempic may also be <a href="https://doi.org/10.1002/eat.24109">misused by individuals already struggling with an eating disorder</a> to suppress their appetite, compensate for binge eating episodes or manage fear of weight gain. Individuals who are already showing signs of an eating disorder, such as limiting their food intake and intense concerns about their weight, may be most at risk of spiralling from a weight loss diet or medication into an eating disorder, <a href="https://doi.org/10.1002/eat.24116">even if they only lose a moderate amount of weight</a>. People who are dissatisfied with their weight or have made multiple attempts to lose weight often feel pressured to try increasingly drastic methods. However, any diet, exercise program or weight-loss medication promising a quick fix for weight loss should be treated with extreme caution. At best, you may gain the weight back; at worst, you put yourself at risk for much more serious eating disorders and other health problems.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/221514/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/samantha-withnell-1504436">Samantha Withnell</a>, PhD Candidate, Clinical Psychology, <a href="https://theconversation.com/institutions/western-university-882">Western University</a> and <a href="https://theconversation.com/profiles/lindsay-bodell-1504260">Lindsay Bodell</a>, Assistant Professor of Psychology, <a href="https://theconversation.com/institutions/western-university-882">Western University</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/how-dieting-weight-suppression-and-even-misuse-of-drugs-like-ozempic-can-contribute-to-eating-disorders-221514">original article</a>.

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Do you really need antibiotics? Curbing our use helps fight drug-resistant bacteria

<a href="https://theconversation.com/profiles/minyon-avent-1486987">Minyon Avent</a>, <a href="https://theconversation.com/institutions/the-university-of-queensland-805">The University of Queensland</a>; <a href="https://theconversation.com/profiles/fiona-doukas-1157050">Fiona Doukas</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/kristin-xenos-1491653">Kristin Xenos</a>, <a href="https://theconversation.com/institutions/university-of-newcastle-1060">University of Newcastle</a> Antibiotic resistance occurs when a microorganism changes and no longer responds to an antibiotic that was previously effective. It’s <a href="https://thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00502-2/fulltext">associated with</a> poorer outcomes, a greater chance of death and higher health-care costs. In Australia, antibiotic resistance means some patients are admitted to hospital because oral antibiotics are <a href="https://www.who.int/news-room/fact-sheets/detail/antibiotic-resistance">no longer effective</a> and they need to receive intravenous therapy via a drip. Antibiotic resistance is rising to high levels in certain parts of the world. Some hospitals <a href="https://www.reactgroup.org/news-and-views/news-and-opinions/year-2022/the-impact-of-antibiotic-resistance-on-cancer-treatment-especially-in-low-and-middle-income-countries-and-the-way-forward/">have to consider</a> whether it’s even viable to treat cancers or perform surgery due to the risk of antibiotic-resistant infections. Australia is <a href="https://www.safetyandquality.gov.au/our-work/antimicrobial-resistance/antimicrobial-use-and-resistance-australia-aura/aura-2023-fifth-australian-report-antimicrobial-use-and-resistance-human-health">one of the highest users</a> of antibiotics in the developed world. We need to use this precious resource wisely, or we risk a future where a simple infection could kill you because there isn’t an effective antibiotic. <h2>When should antibiotics not be used?</h2> Antibiotics only work for some infections. They work against bacteria but <a href="https://www.safetyandquality.gov.au/publications-and-resources/resource-library/do-i-really-need-antibiotics">don’t treat</a> infections caused by viruses. Most community acquired infections, even those caused by bacteria, are likely to get better without antibiotics. Taking an antibiotic when you don’t need it won’t make you feel better or recover sooner. But it can increase your chance of side effects like nausea and diarrhoea. Some people think green mucus (or snot) is a sign of bacterial infection, requiring antibiotics. But it’s actually <a href="https://www.safetyandquality.gov.au/sites/default/files/2023-11/aura_2023_do_i_really_need_antibiotics.pdf">a sign</a> your immune system is working to fight your infection. <h2>If you wait, you’ll often get better</h2> <a href="https://www.tg.org.au/">Clinical practice guidelines</a> for antibiotic use aim to ensure patients receive antibiotics when appropriate. Yet 40% of GPs say they prescribe antibiotics <a href="https://doi.org/10.1071/HI13019">to meet patient expectations</a>. And <a href="https://pubmed.ncbi.nlm.nih.gov/35973750/">one in five</a> patients expect antibiotics for respiratory infections. It can be difficult for doctors to decide if a patient has a viral respiratory infection or are at an early stage of serious bacterial infection, particularly in children. One option is to “watch and wait” and ask patients to return if there is clinical deterioration. An alternative is to prescribe an antibiotic but advise the patient to not have it dispensed unless specific symptoms occur. This can <a href="https://doi.org/10.1002/14651858.CD004417.pub5">reduce antibiotic use by 50%</a> with no decrease in patient satisfaction, and no increase in complication rates. <h2>Sometimes antibiotics are life-savers</h2> For some people – particularly those with a weakened immune system – a simple infection can become more serious. Patients with life-threatening suspected infections should receive an appropriate antibiotic <a href="https://www.safetyandquality.gov.au/our-work/clinical-care-standards/antimicrobial-stewardship-clinical-care-standard">immediately</a>. This includes serious infections such as <a href="https://www.hopkinsmedicine.org/health/conditions-and-diseases/bacterial-meningitis#:%7E:text=What%20is%20bacterial%20meningitis%3F,can%20cause%20life%2Dthreatening%20problems.">bacterial meningitis</a> (infection of the membranes surrounding the brain) and <a href="https://clinicalexcellence.qld.gov.au/priority-areas/safety-and-quality/sepsis/adult-sepsis#:%7E:text=Adult%20patients%20with%20sepsis%20also,adult%20emergency%20department%20sepsis%20pathway.">sepsis</a> (which can lead to organ failure and even death). <h2>When else might antibiotics be used?</h2> Antibiotics are sometimes used to prevent infections in patients who are undergoing surgery and are at significant risk of infection, such as those undergoing bowel resection. These patients will <a href="https://www.tg.org.au">generally receive</a> a single dose before the procedure. Antibiotics may also <a href="https://www.tg.org.au">be given</a> to patients undergoing chemotherapy for solid organ cancers (of the breast or prostate, for example), if they are at high risk of infection. While most sore throats are caused by a virus and usually resolve on their own, some high risk patients with a bacterial strep A infection which can cause “scarlet fever” are given antibiotics to prevent a more serious infection like <a href="https://www.rhdaustralia.org.au/">acute rheumatic fever</a>. <h2>How long is a course of antibiotics?</h2> The recommended duration of a course of antibiotics depends on the type of infection, the likely cause, where it is in your body and how effective the antibiotics are at killing the bacteria. In the past, courses were largely arbitrary and based on assumptions that antibiotics should be taken for long enough to eliminate the infecting bacteria. More recent research does not support this and shorter courses are <a href="https://www.acpjournals.org/doi/full/10.7326/M19-1509">nearly always as effective as longer ones</a>, particularly for community acquired respiratory infections. For <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736742/">community acquired pneumonia</a>, for example, research shows a three- to five-day course of antibiotics is at least as effective as a seven- to 14-day course. The “take until all finished” approach is no longer recommended, as the longer the antibiotic exposure, the greater the chance the bacteria will develop resistance. However, for infections where it is more difficult to eradicate the bacteria, such as tuberculosis and bone infections, a combination of antibiotics for many months is usually required. <h2>What if your infection is drug-resistant?</h2> You may have an antibiotic-resistant infection if you don’t get better after treatment with standard antibiotics. Your clinician will collect samples for lab testing if they suspect you have antibiotic-resistant infection, based on your travel history (especially if you’ve been hospitalised in a country with high rates of antibiotic resistance) and if you’ve had a recent course of antibiotics that hasn’t cleared your infection. Antibiotic-resistant infections are managed by prescribing broad-spectrum antibiotics. These are like a sledgehammer, wiping out many different species of bacteria. (Narrow-spectrum antibiotics conversely can be thought of as a scalpel, more targeted and only affecting one or two kinds of bacteria.) Broad-spectrum antibiotics are usually more expensive and come with more severe side effects. <h2>What can patients do?</h2> Decisions about antibiotic prescriptions should be made using <a href="https://www.safetyandquality.gov.au/our-work/partnering-consumers/shared-decision-making/decision-support-tools-specific-conditions">shared decision aids</a>, where patients and prescribers discuss the risks and benefits of antibiotics for conditions like a sore throat, middle ear infection or acute bronchitis. Consider asking your doctor questions such as: <ul> <li>do we need to test the cause of my infection?</li> <li>how long should my recovery take?</li> <li>what are the risks and benefits of me taking antibiotics?</li> <li>will the antibiotic affect my regular medicines?</li> <li>how should I take the antibiotic (how often, for how long)?</li> </ul> Other ways to fight antibiotic resistance include: <ul> <li>returning leftover antibiotics to a pharmacy for safe disposal</li> <li>never consuming leftover antibiotics or giving them to anyone else</li> <li>not keeping prescription repeats for antibiotics “in case” you become sick again</li> <li>asking your doctor or pharmacist what you can do to feel better and ease your symptoms rather than asking for antibiotics.</li> </ul> <a href="https://theconversation.com/profiles/minyon-avent-1486987">Minyon Avent</a>, Antimicrobial Stewardship Pharmacist, <a href="https://theconversation.com/institutions/the-university-of-queensland-805">The University of Queensland</a>; <a href="https://theconversation.com/profiles/fiona-doukas-1157050">Fiona Doukas</a>, PhD candidate, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/kristin-xenos-1491653">Kristin Xenos</a>, Research Assistant, College of Health, Medicine and Wellbeing, School of Biomedical Science and Pharmacy, <a href="https://theconversation.com/institutions/university-of-newcastle-1060">University of Newcastle</a> Image credits: Shutterstock This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/do-you-really-need-antibiotics-curbing-our-use-helps-fight-drug-resistant-bacteria-217920">original article</a>.

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Drug resistance may make common infections like thrush untreatable

<a href="https://theconversation.com/profiles/christine-carson-109004">Christine Carson</a>, <a href="https://theconversation.com/institutions/the-university-of-western-australia-1067">The University of Western Australia</a> We’ve all heard about antibiotic resistance. This happens when bacteria develop strategies to avoid being destroyed by an antibiotic. The consequences of antibiotic resistance mean an antibiotic previously used to cure bacterial infections no longer works effectively because the bacteria have become resistant to the drug. This means it’s getting harder to cure the infections some bacteria cause. But unfortunately, it’s only one part of the problem. The same phenomenon is also happening with other causes of infections in humans: fungi, viruses and parasites. “Antimicrobial resistance” means the drugs used to treat diseases caused by microbes (bugs that cause infection) no longer work. This occurs with antibacterial agents used against bacteria, antifungal agents used against fungi, anti-parasitic agents used against parasites and antiviral agents used against viruses. This means a wide range of previously controllable infections are becoming difficult to treat – and may become untreatable. <h2>Fighting fungi</h2> Fungi are responsible for a range of infections in humans. Tinea, ringworm and vulvovaginal candidiasis (thrush) are some of the more familiar and common superficial fungal infections. There are also life-threatening fungal infections such as aspergillosis, cryptococcosis and invasive fungal bloodstream infections including those caused by Candida albicans and Candida auris. Fungal resistance to antifungal agents is a problem for several reasons. First, the range of antifungal agents available to treat fungal infections is limited, especially compared to the range of antibiotics available to treat bacterial infections. There are only four broad families of antifungal agents, with a small number of drugs in each category. Antifungal resistance further restricts already limited options. Life-threatening fungal infections happen less frequently than life-threatening bacterial infections. But they’re rising in frequency, especially among people whose immune systems are compromised, including by <a href="https://7news.com.au/news/qld/first-heart-transplant-patient-to-die-from-fungal-infection-at-brisbanes-prince-charles-hospital-identified-as-mango-hill-gp-muhammad-hussain-c-12551559">organ transplants</a> and chemotherapy or immunotherapy for cancer. The threat of getting a drug-resistant fungal infection makes all of these health interventions riskier. The greatest <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2017.00735/full">burden of serious fungal disease</a> occurs in places with limited health-care resources available for diagnosing and treating the infections. Even if infections are diagnosed and antifungal treatment is available, antifungal resistance reduces the treatment options that will work. But even in Australia, common fungal infections are impacted by resistance to antifungal agents. Vulvovaginal candidiasis, known as thrush and caused by Candida species and some closely related fungi, is usually reliably treated by a topical antifungal cream, sometimes supplemented with an oral tablet. However, instances of <a href="https://www.theage.com.au/national/victoria/they-can-t-sit-properly-doctors-treat-growing-number-of-women-with-chronic-thrush-20230913-p5e499.html">drug-resistant thrush</a> are increasing, and new treatments are needed. <h2>Targeting viruses</h2> Even <a href="https://theconversation.com/why-are-there-so-many-drugs-to-kill-bacteria-but-so-few-to-tackle-viruses-137480">fewer antivirals</a> are available than antibacterial and antifungal agents. Most antimicrobial treatments work by exploiting differences between the microbe causing the infection and the host (us) experiencing the infection. Since viruses use our cells to replicate and cause their infection, it’s difficult to find antiviral treatments that selectively target the virus without damaging us. With so few antiviral drugs available, any resistance that develops to one of them significantly reduces the treatment options available. Take COVID, for example. Two antiviral medicines are in widespread use to treat this viral infection: Paxlovid (containing nirmatrelvir and ritonavir) and Lagevrio (molnupiravir). So far, SARS-CoV-2, the virus that causes COVID, has not developed significant resistance to either of these <a href="https://www.cidrap.umn.edu/covid-19/low-levels-resistance-paxlovid-seen-sars-cov-2-isolates">treatments</a>. But if SARS-CoV-2 develops resistance to either one of them, it halves the treatment options. Subsequently relying on one would likely lead to its increased use, which may heighten the risk that resistance to the second agent will develop, leaving us with no antiviral agents to treat COVID. The threat of antimicrobial resistance makes our ability to treat serious COVID infections rather precarious. <h2>Stopping parasites</h2> Another group of microbes that cause infections in humans are single-celled microbes such as Plasmodium, Giardia, Leishmania, and Trypanosoma. These microbes are sometimes referred to as parasites, and they are becoming increasingly resistant to the very limited range of anti-parasitic agents used to treat the infections they cause. Several Plasmodium species cause malaria and anti-parasitic drugs have been the cornerstone of malaria treatment for decades. But their usefulness has been significantly reduced by the <a href="https://www.mmv.org/our-work/mmvs-pipeline-antimalarial-drugs/antimalarial-drug-resistance">development of resistance</a>. Giardia parasites cause an infection called giardiasis. This can resolve on its own, but it can also cause severe gastrointestinal symptoms such as diarrhea, nausea, and bloating. These microbes have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6207226/">developed resistance</a> to the main treatments and patients infected with drug-resistant parasites can have protracted, unpleasant infections. <h2>Resistance is a natural consequence</h2> Treating infections influences microbes’ evolutionary processes. Exposure to drugs that stop or kill them pushes microbes to either evolve or die. The exposure to antimicrobial agents provokes the evolutionary process, selecting for microbes that are resistant and can survive the exposure. The pressure to evolve, provoked by the antimicrobial treatment, is called “selection pressure”. While most microbes will die, a few will evolve in time to overcome the antimicrobial drugs used against them. The evolutionary process that leads to the emergence of resistance is inevitable. But some things can be done to minimise this and the problems it brings. Limiting the use of antimicrobial agents is one approach. This means reserving antimicrobial agents for when their use is known to be necessary, rather than using them “just in case”. Antimicrobial agents are precious resources, holding at bay many infectious diseases that would otherwise sicken and kill millions. It is imperative we do all we can to preserve the effectiveness of those that remain, and give ourselves more options by working to discover and develop new ones.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/213460/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/christine-carson-109004">Christine Carson</a>, Senior Research Fellow, School of Medicine, <a href="https://theconversation.com/institutions/the-university-of-western-australia-1067">The University of Western Australia</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/drug-resistance-may-make-common-infections-like-thrush-untreatable-213460">original article</a>.

Body

5 reasons why climate change may see more of us turn to alcohol and other drugs

<a href="https://theconversation.com/profiles/helen-louise-berry-8608">Helen Louise Berry</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a> and <a href="https://theconversation.com/profiles/francis-vergunst-230743">Francis Vergunst</a>, <a href="https://theconversation.com/institutions/university-of-oslo-934">University of Oslo</a> Climate change will affect every aspect of our <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(23)01859-7/fulltext">health and wellbeing</a>. But its potential harms go beyond the body’s ability to handle extreme heat, important as this is. Extreme weather events, such as floods, droughts, storms and wildfires, are becoming more frequent and severe. These affect our <a href="https://pubmed.ncbi.nlm.nih.gov/36165756/">mental health</a> in a multitude of <a href="https://www.nature.com/articles/s41558-018-0102-4">ways</a>. Coping with climate change can be overwhelming. Sometimes, the best someone can do is to seek refuge in alcohol, tobacco, over-the-counter and prescription drugs, or other psychoactive substances. This is understandable, but dangerous, and can have serious consequences. We outline <a href="https://journals.sagepub.com/doi/full/10.1177/17456916221132739">five ways</a> climate change could increase the risk of harmful substance use. <h2>1. Mental health is harmed</h2> Perhaps the most obvious way climate change can be linked to harmful substance use is by damaging mental health. This <a href="https://onlinelibrary.wiley.com/doi/10.1111/dar.12448">increases the risk</a> of new or worsened substance use. People with a mental disorder are <a href="https://www.hindawi.com/journals/psychiatry/2018/5697103/">at high risk</a> of also having a <a href="https://bmcpsychiatry.biomedcentral.com/articles/10.1186/1471-244X-11-25#:%7E:text=Prevalence%20of%20comorbidity%20in%20epidemiological%20studies&text=Among%20subjects%20with%20an%20alcohol,a%20comorbid%20SUD%20%5B39%5D.">substance-use disorder</a>. This often precedes their mental health problems. Climate change-related increases in the number and nature of extreme events, in turn, are escalating risks to mental health. For example, extreme heat is linked to increased <a href="https://pubmed.ncbi.nlm.nih.gov/27727320/">distress</a> across the whole population. In extreme heat, more people go to the <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2789481">emergency department</a> for psychiatric problems, including for <a href="https://www.sciencedirect.com/science/article/abs/pii/S0048969720338249">alcohol</a> and <a href="https://www.nature.com/articles/s43856-023-00346-1">substance use</a> generally. This is even true for <a href="https://www.sciencedirect.com/science/article/pii/S0048969720325572">a single very hot day</a>. Post-traumatic stress disorder, depression, anxiety and <a href="https://onlinelibrary.wiley.com/doi/abs/10.5694/mja13.10307">other mental health</a> problems are <a href="https://www.frontiersin.org/articles/10.3389/fpubh.2019.00367/full">common</a> at the time of extreme weather events and can persist for months, even years afterwards, especially if people are exposed to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9116266/">multiple events</a>. This can <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6101235/">increase</a> the likelihood of using substances as a way to cope. <h2>2. Worry increases</h2> With <a href="https://climatecommunication.yale.edu/publications/climate-change-in-the-american-mind-beliefs-attitudes-december-2022/">increasing public awareness</a> of how climate change is endangering wellbeing, people are <a href="https://www.ons.gov.uk/peoplepopulationandcommunity/wellbeing/articles/worriesaboutclimatechangegreatbritain/septembertooctober2022#:%7E:text=The%20level%20of%20worry%20about,lives%20right%20now%20(29%25).">increasingly worried</a> about what will happen if it remains unchecked. Worrying isn’t the same as meeting the criteria for a mental disorder. But <a href="https://www.undp.org/publications/peoples-climate-vote">surveys</a> show climate change generates complex emotional responses, <a href="https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(21)00278-3/fulltext">especially in children</a>. As well as feelings of worry, there is anxiety, fear, guilt, anger, grief and helplessness. Some <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904966/">emotional states</a>, such as <a href="https://www.pnas.org/doi/full/10.1073/pnas.1909888116">sadness</a>, are linked with long-term tobacco use and also make substance use <a href="https://pubmed.ncbi.nlm.nih.gov/16011392/">relapse</a> more likely. <h2>3. Physical injuries hurt us in many ways</h2> Physical injuries caused by extreme weather events – such as smoke inhalation, burns and flood-related cuts and infections – increase the risk of harmful substance use. That’s partly because they <a href="https://pubmed.ncbi.nlm.nih.gov/20033251/">increase</a> the risk of psychological distress. If injuries cause long-term illness or disability, consequent feelings of hopelessness and depression can dispose some people to self-medicate with alcohol or other drugs. Substance use itself can also generate long-term physiological harm, disabilities or other chronic health problems. These are <a href="https://www.tandfonline.com/doi/abs/10.3109/00952999609001655">linked with</a> higher rates of harmful substance use. <h2>4. Our day-to-day lives change</h2> A single catastrophic event, such as a storm or flood, can devastate lives overnight and change the way we live. So, too, can the more subtle changes in climate and day-to-day weather. Both can disrupt behaviour and routines in ways that risk new or worsened substance use, for example, using stimulants to cope with fatigue. Take, for example, hotter temperatures, which disrupt <a href="https://www.cell.com/one-earth/fulltext/S2590-3322(22)00209-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2590332222002093%3Fshowall%3Dtrue">sleep</a>, undermine <a href="https://jhr.uwpress.org/content/57/2/400">academic performance</a>, <a href="https://www.nature.com/articles/s41562-017-0097">reduce physical activity</a>, and promote <a href="https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(22)00173-5/fulltext">hostile language</a> and <a href="https://www.cambridge.org/core/elements/abs/climate-change-and-human-behavior/F64471FA47B8A6F5524E7DDDDE571D57">violent behaviour</a>. <h2>5. It destabilises communities</h2> Finally, climate change is destabilising the socioeconomic, natural, built and geopolitical <a href="https://www.nature.com/articles/s41558-018-0102-4">systems</a> on which human wellbeing – <a href="https://theconversation.com/climate-change-and-health-ipcc-reports-emerging-risks-emerging-consensus-24213">indeed survival</a> – depends. Damaged infrastructure, agricultural losses, school closures, homelessness and displacement are significant <a href="https://www.nature.com/articles/s41558-018-0102-4">sources of psychosocial distress</a> that prompt acute (short-term) and chronic (long-term) stress responses. <a href="https://doi.org/10.1196/annals.1441.030">Stress</a>, in turn, can <a href="https://doi.org/10.1007/s002130100917">increase</a> the risk of <a href="https://link.springer.com/article/10.1007/s002130100917">harmful substance use</a> and make people more likely to relapse. <h2>Why are we so concerned?</h2> Substance-use disorders are economically and socially <a href="https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(18)30337-7/fulltext">very costly</a>. Risky substance use that doesn’t meet the criteria for a formal diagnosis <a href="https://digitalcommons.fiu.edu/srhreports/health/health/32/">can also harm</a>. Aside from its direct physical harm, harmful substance use disrupts <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3843305/">education</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3234116/">employment</a>. It increases the risk of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676144/">accidents</a> and <a href="https://www.tandfonline.com/doi/abs/10.1080/09595230600944479">crime</a>, and it undermines social relationships, intimate <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4795906/#:%7E:text=Results%20indicated%20that%20alcohol%20use,drinkers%20with%20low%20relationship%20satisfaction.">partnerships</a> and <a href="https://www.cambridge.org/core/journals/development-and-psychopathology/article/abs/longitudinal-relations-between-parental-drinking-problems-family-functioning-and-child-adjustment/CE508589A9E799FD6DC9E23DF364FB8F">family functioning</a>. <h2>Politicians take note</h2> As we head towards the <a href="https://www.cop28.com">COP28 global climate talks</a> in Dubai, climate change is set to hit the headlines once more. Politicians know climate change is undermining human health and wellbeing. It’s well past time to insist they act. As we have seen for populations as a whole, there are multiple possible ways for climate change to cause a rise in harmful substance use. This means multidimensional <a href="https://www.nature.com/articles/s41558-018-0102-4">prevention strategies</a> are needed. As well as addressing climate change more broadly, we need strategies including: <ul> <li> supporting vulnerable individuals, especially <a href="https://journals.sagepub.com/doi/full/10.1177/21677026211040787">young people</a>, and marginalised commmunities, who are <a href="https://www.nature.com/articles/s41558-018-0102-4">hit hardest</a> by extreme weather-related events </li> <li> focusing health-related policies more on broadscale health promotion, for example, healthier eating, active transport and community-led mental health support </li> <li> investing in climate-resilient infrastructure, such as heat-proofing buildings and greening cities, to prevent more of the destabilising effects and stress we know contributes to mental health problems and harmful substance use. </li> </ul> There is now <a href="https://news.un.org/en/story/2022/10/1129912">no credible pathway</a> to avoiding dangerous climate change. However, if <a href="https://carnegieendowment.org/2023/01/12/climate-protests-tracking-growing-unrest-pub-88778#:%7E:text=These%20are%20just%20a%20few,even%20more%20numerous%20and%20influential.">increasing rates</a> of climate protests are anything to go by, the world may finally be ready for radical change – and perhaps for reduced harmful substance use.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/217894/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/helen-louise-berry-8608">Helen Louise Berry</a>, Honorary Professor, Centre for Health Systems and Safety Research, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a> and <a href="https://theconversation.com/profiles/francis-vergunst-230743">Francis Vergunst</a>, Associate Professor, Psychosocial Difficulties, <a href="https://theconversation.com/institutions/university-of-oslo-934">University of Oslo</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/5-reasons-why-climate-change-may-see-more-of-us-turn-to-alcohol-and-other-drugs-217894">original article</a>.

Mind

Ozempic is in the spotlight but it’s just the latest in a long and strange history of weight-loss drugs

<a href="https://theconversation.com/profiles/laura-dawes-1445353">Laura Dawes</a>, <a href="https://theconversation.com/institutions/australian-national-university-877">Australian National University</a> Losing weight conveniently, cheaply, safely. That’s been the holy grail of weight-loss ever since 19th century English undertaker and weight-loss celebrity William Banting’s 1863 <a href="https://www.gutenberg.org/files/57545/57545-h/57545-h.htm">Letter on Corpulence</a> spruiked his “miraculous” method of slimming down. Since then, humans have tried many things – diet, exercise, psychotherapy, surgery – to lose weight. But time and again we return to the promise of a weight-loss drug, whether it’s a pill, injection, or tonic. A “diet drug”. The <a href="https://www.hup.harvard.edu/catalog.php?isbn=9780674281448#:%7E:text=Childhood%2520Obesity%2520in%2520America%2520traces,problem%2520facing%2520American%2520children%2520today.">history of diet drugs</a> is not a glowing one, however. There have been so many popular drug treatments for excess weight over the years. All, however, have eventually lost their shine and some have even been banned. <h2>Ozempic is a recent arrival</h2> <a href="https://www.novonordisk.com/our-products/our-medicines.html">Ozempic and its sister drug Wegovy</a>, both manufactured by Novo Nordisk, are the latest offerings in a long history of drug treatments for people who are overweight. They contain the same active ingredient – semaglutide, which mimics a hormone, <a href="https://www.sciencedirect.com/science/article/abs/pii/S1544319118303273">GLP-1</a> (glucagon-like peptide-1) that acts on the hypothalamus (the brain’s “hunger centre”) to regulate appetite. As an obesity treatment, semaglutide appears to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573908/">work</a> in part by reducing appetite. These are injections. And there can be <a href="https://www.novonordisk.com.au/content/dam/nncorp/au/en/pdfs/Ozempic-1mg-cmi-v3.0.pdf%22%22">side effects</a>, most commonly nausea and diarrhoea. Although marketed as treatments for chronic obesity and diabetes, they have <a href="https://www.forbes.com/health/body/ozempic-for-weight-loss/#footnote_1">exploded in popularity</a> as diet drugs, largely thanks to social media. This has helped drive a <a href="https://www.tga.gov.au/safety/shortages/information-about-major-medicine-shortages/about-ozempic-semaglutide-shortage-2022-and-2023#:%7E:text=Why%2520the%2520Ozempic%2520shortage%2520happened,label%2520prescribing%2520for%2520weight%2520loss.">shortage of Ozempic</a> for diabetes treatment. <h2>From ‘gland treatment’ to amphetamines</h2> But Ozempic is not the first weight-loss drug. For example, organotherapy (gland treatment) was <a href="https://www.hup.harvard.edu/catalog.php?isbn=9780674281448#:%7E:text=Childhood%20Obesity%20in%20America%20traces,problem%20facing%20American%20children%20today.">hugely popular</a> in the 1920s to 1940s. It rode on a wave of enthusiasm for endocrinology and specifically the discovery that “ductless glands” – such as the thyroid, pituitary and renal glands – secreted chemical messengers (or “hormones”, as they came to be known). These hormones coordinate the activities and growth of different parts of the body. Doctors prescribed overweight people extracts of animal glands – either eaten raw or dried in pill form or injected – to treat their <a href="https://www.hup.harvard.edu/catalog.php?isbn=9780674281448#:%7E:text=Childhood%20Obesity%20in%20America%20traces,problem%20facing%20American%20children%20today.">supposedly “sluggish glands”</a>. For slaughterhouse companies, this was a lucrative new market for offal. But organotherapy soon fell from favour. There was no evidence excess weight was usually caused by underperforming glands or that gland extracts (thyroid in particular) were doing anything other than <a href="https://my.clevelandclinic.org/health/diseases/21741-thyrotoxicosis">poisoning you</a>. <a href="https://nyupress.org/9780814776391/on-speed/">Amphetamines</a> were first used as a nasal decongestant in the 1930s, but quickly found a market for weight-loss. Why they worked was complex. The drug operated on the hypothalamus but also had an effect on mental state. Amphetamine is, of course, an “upper”. The theory was it helped people feel up to dieting and gave pleasure not found on a plate. Amphetamines too, <a href="https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2007.110593">fell from treatment use</a> in the 1970s with Nixon’s “war on drugs” and recognition they were addictive. <h2>Another decade, another drug</h2> Each decade seems to produce its own briefly popular weight-loss drug. For example, the popular <a href="https://www.nytimes.com/1997/09/23/science/how-fen-phen-a-diet-miracle-rose-and-fell.html">diet drug</a> of the 1980s and 90s was fen-phen, which contained appetite suppressants fenfluramine and phentermine. During the height of its craze, vast numbers of users testified to dramatic weight loss. But after users experienced heart valve and lung disease, fen-phen was <a href="https://pubmed.ncbi.nlm.nih.gov/9688104/">withdrawn</a> from the market in 1997. Its producer allocated a <a href="https://www.bloomberg.com/news/articles/2012-08-23/pfizer-asks-end-to-fen-phen-suits-linked-to-lung-ailment">reported US$21 billion</a> to settle the associated lawsuits. The hormone <a href="https://www.webmd.com/obesity/features/the-facts-on-leptin-faq">leptin</a> aroused excitement in the mid-1990s. Leptin seemed, for a brief moment, to hold the key to how the hypothalamus regulated fat storage. Pharmaceutical company Amgen <a href="https://www.science.org/doi/10.1126/science.7732366">wagered millions</a> buying the <a href="https://pubmed.ncbi.nlm.nih.gov/30532682/">rights</a> to the research in the hope this discovery could be turned into a treatment, only to discover it didn’t translate from mice into people. Far from not having enough leptin, people with obesity tend to be <a href="https://www.healthline.com/nutrition/leptin-101">leptin-resistant</a>. So taking more leptin doesn’t help with weight-loss. Amgen <a href="https://news.harvard.edu/gazette/story/2009/01/obesity-reviving-the-promise-of-leptin/">sold</a> the rights it had paid so much for. <a href="https://www.healthline.com/nutrition/ephedra-sinica">Ephedra</a> was popular as a weight-loss treatment and as a stimulant in the 1990s and 2000s, finding buyers among athletes, body builders and in the military. But the US Food and Drug Administration <a href="https://ods.od.nih.gov/HealthInformation/Ephedra.aspx">banned</a> the sale of dietary supplements containing ephedra in 2004 after it was linked to <a href="https://www.nejm.org/doi/full/10.1056/nejmc1502505">health problems</a> ranging from heart attacks and seizures to strokes and even death, and in Australia ephedra is <a href="https://www.legislation.gov.au/Details/F2023L00864">prescription-only</a>. Now we have Ozempic. Just because the history of diet drugs has <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362858/">been so dire</a>, we shouldn’t jump to conclusions about new ones – Ozempic is not a drug of the 1920s or 1960s or 1990s. And as <a href="https://www.hup.harvard.edu/catalog.php?isbn=9780674281448#:%7E:text=Childhood%2520Obesity%2520in%2520America%2520traces,problem%2520facing%2520American%2520children%2520today.">history recognises</a>, multiple complexities can combine to push a drug into popularity or damn it to history’s rubbish bin. These include patients’, physicians’ and industry interests; social attitudes about drug treatment; evidence about safety and efficacy; beliefs and knowledge about the cause of excess weight. One noticeable contrast with past diet drug experiences is that now, many people are <a href="https://www.nytimes.com/2022/11/22/well/ozempic-diabetes-weight-loss.html">happy to talk</a> about using Ozempic. It seems to be increasingly socially acceptable to use a drug to achieve weight-loss for primarily aesthetic reasons. (Due to Ozempic shortages in Australia, though, doctors have been <a href="https://www.tga.gov.au/safety/shortages/medicine-shortage-alerts/ozempic-semaglutide-supply-update">asked</a> to direct current supplies to people with type 2 diabetes who satisfy certain criteria. In other words, it’s not really meant to be used just to treat obesity). <h2>Our enduring search for weight-loss drugs</h2> Ozempic is predicted to earn Novo Nordisk <a href="https://www.pharmaceutical-technology.com/comment/novo-nordisk-ozempic/">US$12.5 billion this year alone</a>, but it’s not just industry interests stoking this enduring desire for weight-loss drugs. Patients on an endless cycle of dieting and exercise want something more convenient, with a more certain outcome. And doctors, too, want to offer patients effective treatment, and a drug prescription is a workable option given the constraints of appointment times. The body positivity movement has not yet ousted anti-fat bias or stigma. And despite <a href="https://www.who.int/teams/health-promotion/enhanced-wellbeing/first-global-conference">decades of recognition</a> of the major role our physical and social environment plays in human health, there’s little political, public or industry appetite for change. Individuals are left to personally defend against an obesogenic environment, where economic, cultural, social, health and urban design policies can conspire to make it easy to gain weight but hard to lose it. It is no wonder demand for weight-loss drugs continues to soar.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/209324/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/laura-dawes-1445353">Laura Dawes</a>, Research Fellow in Medico-Legal History, <a href="https://theconversation.com/institutions/australian-national-university-877">Australian National University</a> Image credits: Shutterstock This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/ozempic-is-in-the-spotlight-but-its-just-the-latest-in-a-long-and-strange-history-of-weight-loss-drugs-209324">original article</a>.

Body

Promising Alzheimer’s drug offers hope for a bright future in treatment

A remarkable and significant breakthrough in the fight against Alzheimer’s disease is ushering in a new era of hope and possibilities for patients grappling with early onset dementia. Scientists and researchers are celebrating this groundbreaking development, viewing it as a tremendous opportunity to transform the landscape of Alzheimer's treatment. The drug in question, donanemab, developed by Eli Lilly, has shown remarkable success in clinical trials and is anticipated to receive approval from the Food and Drug Administration later this year, according to a report in the <a href="https://nypost.com/2023/07/17/alzheimers-drug-donanemab-lowers-risk-of-dementia/" target="_blank" rel="noopener">New York Post</a>. Individuals who participated in the donanemab trials experienced a remarkable 40% reduction in the risk of transitioning from mild cognitive impairment to mild or moderate dementia. This is an extraordinary advancement that brings renewed optimism to those affected by this devastating condition. Donanemab would be the third Alzheimer’s drug to emerge in recent months, following the introduction of Leqembi and Aduhelm. This is just the beginning of an exciting new chapter in the realm of molecular therapies for Alzheimer's, as expressed by Dr. Gil Rabinovici, director of the University of California San Francisco’s Memory and Ageing Centre, in an editorial for JAMA. Dr. Daniel Skovronsky, the chief scientific and medical officer at Lilly, has emphasised the significance of this breakthrough. He states, "This will be a very important and meaningful drug," as quoted in Fierce Biotech. Skovronsky further adds, "[T]here’s a huge opportunity here for patients." Such resolute optimism is inspiring, reflecting the tremendous potential this drug holds for transforming lives. Similar to Leqembi and Aduhelm, donanemab is a monoclonal antibody designed to target plaque in the brain, specifically the amyloid protein. These amyloid plaques are responsible for the propagation of another protein called tau, which contributes to the development of Alzheimer's disease. Notably, the donanemab trial also revealed that the drug slowed cognitive decline by an impressive 35% compared to a placebo in individuals with low to intermediate levels of tau protein in the brain. In fact, donanemab demonstrated superior efficacy in clearing amyloid plaques when compared to Aduhelm and Leqembi. Moreover, unlike Leqembi, which necessitates long-term usage, patients taking donanemab may follow a fixed-duration dosing schedule, potentially allowing some individuals to discontinue the treatment after a certain period. "I expect that many patients will be able to stop dosing even as soon as 12 months," Skovronsky affirmed. This stands as a significant departure from being prescribed a lifelong medication, providing an exciting and meaningful prospect for patients. While it is important to note that these new Alzheimer’s drugs do carry limitations and risks, medical experts remain cautiously optimistic. Donanemab, along with the other emerging drugs, has been associated with brain swelling and bleeding. Tragically, three individuals in the donanemab clinical trial lost their lives due to these side effects. The risk of brain swelling and bleeding is heightened among those carrying the APOE4 gene, which is associated with an increased susceptibility to Alzheimer’s. Furthermore, individuals with more advanced stages of the disease showed minimal to no benefit compared to those who received a placebo. As a result, it is possible that donanemab will be recommended primarily for individuals with low to intermediate levels of tau proteins, indicating milder forms of the disease. Nevertheless, Skovronsky and other medical experts maintain their optimism regarding the FDA's approval, expressing the urgent need for it to come to fruition. Skovronsky highlights, "Every day that goes by, there are some patients who pass through this early stage of Alzheimer’s disease and become more advanced, and they won’t benefit from treatment. That’s a very pressing sense of urgency." While challenges and risks remain, the emergence of donanemab and its potential approval by the FDA represents a beacon of hope for the millions of individuals and families affected by Alzheimer's disease. It symbolises the start of a new chapter in the fight against this debilitating condition, offering renewed prospects for a brighter future filled with effective treatments and improved quality of life. Image: Shutterstock

Mind

Firing squad demanded for teen in Bali

Prosecutors are calling for a 19-year-old woman to be executed by firing squad after she was arrested for allegedly smuggling drugs into Bali. The Brazilian teenager, Manuela Vitoria de Araujo Farias, has been in custody since her initial arrest in January 2023, after allegedly being sprung with 3kg of cocaine in her luggage. According to global press agency Newsflash, prosecutors demanded the maximum penalty. If she is convicted of trafficking drugs into Indonesia, she could face execution by firing squad or a lifetime prison sentence. Authorities allege she was involved with a drug gang, but according to her lawyer, Davi Lira da Silva, the teen sold lingerie and perfume for a living and was tricked by people she trusted. Mr da Silva claimed the 19-year-old was tricked into cooperating after the gang who hired her told her about temples in Bali where they pray for the ill. Her mother had recently suffered a stroke and her lawyers claimed she was going to seek Buddhist prayers for a cure. They also alleged that the gang had promised to pay for surf lessons for Ms Farias following her arrival to the country. Her arrest made international headlines after the case was confirmed to local media by Bali Police Chief Inspector Gen Putu Jayan Danu Putra in Denpasar on January 27, 2023. The Bali Sun reported that Ms Farias had arrived at Bali Airport around 3 am on January 1 on a Qatar Airways flight, travelling from Brazil to Bali via Qatar. “The drug smuggling attempt was thwarted by the Bali airport customs. We really appreciate what customs have done,” Chief Inspector Putra said at a press conference on January 27, according to the outlet. Ms Farias’ case has been adjourned with the sentences to be announced on a later date in April. Image credit: Twitter

Travel Trouble

Prince Harry reveals “fundamental” drug use

Prince Harry has opened up about his recreational drug use in a livestream chat with trauma expert Dr Gabor Maté. During the session, the Duke of Sussex revealed to Dr Maté that he has turned to drugs to help him deal with - and overcome - the traumas of his past, and how it all began as a recreational activity for the 38-year-old. “It was the cleaning of the windscreen,” he explained, “the removal of life’s filters - these layers of filters - it removed it all for me and brought me a sense of relaxation, relief, comfort, a lightness that I managed to hold back for a period of time. “I started doing it recreationally and then started to realise how good it was for me. “I would say it is one of the fundamental parts of my life that changed me and helped me deal with the traumas and the pains of the past. They’re unlocking so much of what we’ve suppressed.” This is not the first time Harry has admitted to his drug usage, having opened up about his cocaine abuse in his controversial memoir, Spare. In the book, he made reference to tabloid stories from his teenage years at boarding school, and dubbed his father - King Charles - a “harried single dad coping with a drug-addled child”. Despite Buckingham Palace denying claims about Harry’s drug use at the time, he confessed in Spare that “of course” he was “doing cocaine around this time”, and that he was “at someone’s country house, during a shooting weekend” when he was offered the drug for the first time. “I’d been offered a line,” he later admitted, “and I’d done a few more since.” And while he decided that drug use wasn’t “much fun”, and that cocaine didn’t “make [him] particularly happy”, it helped him achieve his goal of feeling different. In his memoir, Harry also made note of the time he tried magic mushrooms during a party at actress Courteney Cox’s house, after discovering a box full of “black diamond mushroom chocolates.” “My mate and I grabbed several, gobbled them, washed them down with tequila,” he said, before going on to recall his drug-induced hallucinations - namely, a bin transforming into a head. “I stepped on the pedal and the head opened its mouth,” Harry described, “a huge open grin.” However, Harry’s story didn’t exactly line up with Courtney’s account, with the 58-year-old denying his story in the wake of the memoirs release, telling Variety, “I’m not saying there were mushrooms! I definitely wasn’t passing them out.” Whether or not the story is entirely factually accurate, the Duke of Sussex credits his experience with substances as the thing that helped him see the world, and his life, for what they were, writing in Spare that “under the influence of these substances I was able to let go of rigid preconcepts, to see that there was another world beyond my heavily filtered senses. “A world that was equally real and doubly beautiful.” Images: Getty

Body

Experimental Alzheimer’s drug shows promise

The first drug that can slow the rate of decline in Alzheimer’s patients has been found. The experimental drug, called lecanemab, is an antibody that targets the toxic clumps of amyloid protein associated with the mind-robbing disease. While these results are cause for celebration, there are still significant questions about its safety and rollout. The full results of the phase 3 lecanemab drug trial (the final stage of testing in humans) have <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2212948">been published in the New England Journal of Medicine</a>. The trial showed that patients receiving the drug had a 27% slower disease progression than those receiving a placebo after 18 months of treatment. Overall, this is good news. For the first time, we have a potential treatment that has a demonstrated effect on both the symptoms and underlying pathology of Alzheimer’s disease. These results are a breakthrough in the search for treatments for this devastating disease and give a strong indication that the course of the disease can be altered. But the results paint a mixed picture for those with Alzheimer’s. On one hand, this is the first drug that has been shown to have any effect on slowing the progression of the disease. On the other hand, the apparent effects are slight and the risks are not inconsiderable. About 1,800 people with early-stage Alzheimer’s took part in the global trial. The participants were randomly assigned to receive either lecanemab or placebo intravenously every two weeks. The study was “double blind”, meaning neither the participants nor the researchers knew who was receiving the experimental drug and who was receiving the placebo until the end of the trial. Throughout the study, the participants’ disease progression was tracked using the clinical dementia rating scale, which scores the patient on cognition and ability to live independently. The participants’ brains were also scanned for the two proteins commonly associated with Alzheimer’s disease: amyloid and tau. Alzheimer’s scores in both groups worsened during the 18 months of the study, but the rate of decline was slower in those receiving the lecanemab. Also, the magnitude of the slowing, while statistically significant (not likely to be due to chance) was small – a 0.45 reduction on an 18-point scale. Some experts are concerned that this effect may not be clinically meaningful. In a <a href="https://www.sciencemediacentre.org/expert-reaction-to-phase-3-trial-results-of-lecanemab-for-early-alzheimers-disease/">statement to the Science Media Centre</a>, Rob Howard, professor of old age psychiatry at UCL, said that “none of the reported results, including the primary outcome, reached accepted levels of improvement to constitute a clinically meaningful treatment effect”. The success of lecanemab was also measured by the amount of amyloid and tau protein in those on the experimental drug compared with those receiving the placebo infusion. The results showed a reduction in these proteins in those receiving lecanemab. Indeed, the levels of brain amyloid were reduced to below the threshold needed for a positive Alzheimer’s diagnosis. However, markers of brain cell death were unaffected, indicating that amyloid in Alzheimer’s disease is just one mechanism in a complicated disease landscape. <h2>Side-effects</h2> About one in four participants (26.6%) in the lecanemab group experienced brain swelling or a bleed on the brain (which can be both minor or major). STAT, a medical news website, <a href="https://www.statnews.com/2022/10/28/patient-death-lecanemab-alzheimers-trial/">reported that a man died of a brain haemorrhage</a> after receiving lecanemab, citing a possible interaction with his blood thinning medication. A short while later, the <a href="https://www.science.org/content/article/second-death-linked-potential-antibody-treatment-alzheimer-s-disease">journal Science reported</a> a second death of a trial patient, also after receiving treatment for a stroke. However, the drug’s developer, Eisa, told Science: “All the available safety information indicates that lecanemab therapy is not associated with an increased risk of death overall or from any specific cause.” Nevertheless, given the possibility that patients may be on the drug for the rest of their lives, more research is needed on safety and interactions with existing medications. It’s also important to find out how long-lived the improvements in cognition are, and whether the drug continues to slow the rate of decline, or if the results plateau – or even decline. It should be noted that only patients who had a sufficient level of amyloid detected in the brain or spinal fluid – which requires a PET brain scan or an invasive lumbar puncture – were eligible to take part in this phase 3 trial. In the UK, Alzheimer’s is currently diagnosed via an interview with a doctor. Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, says the <a href="https://www.sciencemediacentre.org/expert-reaction-to-phase-3-trial-results-of-lecanemab-for-early-alzheimers-disease/">NHS is not ready for a new era of dementia treatment</a>. <blockquote> We estimate that unless there are drastic changes in how people access specialist diagnostic tests for Alzheimer’s disease, only 2% of people eligible for drugs like lecanemab will be able to access them. </blockquote> Restructuring NHS dementia services to provide routine and timely PET scans or lumbar punctures would be a costly and lengthy process. Based on previous results, Eisai applied to the US drug regulator (the Food and Drug Administration) for accelerated approval of their drug. A decision is expected by January 6 2023. If accelerated approval is granted by the regulator, these latest results will probably support an application for full approval. <figure class="align-right "><figcaption></figcaption></figure> Listen to The Conversation’s podcast series <a href="https://theconversation.com/uk/topics/uncharted-brain-decoding-dementia-128903">Uncharted Brain: Decoding Dementia</a> to find out more about the latest research unlocking clues to the ongoing mystery of how dementia works in the brain. Find all episodes via <a href="https://podfollow.com/the-anthill/view">The Anthill podcast</a>.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/195383/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/ritchie-williamson-1346959">Ritchie Williamson</a>, Director of research, Associate Professor in Therapeutics, <a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a> and <a href="https://theconversation.com/profiles/stuart-dickens-1397610">Stuart Dickens</a>, Post Doctoral Research Assistant, <a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a> Image: Shutterstock This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/experimental-alzheimers-drug-shows-promise-but-there-are-many-hurdles-still-to-overcome-195383">original article</a>.

Caring

Drugs – 4 essential reads on how they’re made, how they work and how context can make poison a medicine

Pandemics and disease outbreaks put a spotlight on the hurdles researchers face to get a drug on the shelves. From finding prospective drug candidates to balancing time and financial pressures with ensuring safety and efficacy, there are many aspects of drug development that determine whether a treatment ever makes it out of the lab. Broadening the definition of “medicine” and where it can be found, however, could help expand the therapeutic options available for both researchers and patients. Here are four facets of how drugs are developed and how they work in the body, drawn from stories in The Conversation’s archive. <h2>1. Matching drug to target</h2> The most effective drugs are, in a sense, the product of good matchmaking – they bind to a specific disease-causing receptor in the body, elicit a desired effect and ideally ignore healthy parts of the body. Drugs <a href="https://theconversation.com/how-do-drugs-know-where-to-go-in-the-body-a-pharmaceutical-scientist-explains-why-some-medications-are-swallowed-while-others-are-injected-182488" target="_blank" rel="noopener">travel through the bloodstream</a> to reach their targets. Because of this, most drugs circulate throughout the body and can bind to unintended sites, potentially causing undesired side effects. Researchers can increase the precision and effectiveness of a drug by designing different ways to take it. An inhaler, for example, delivers a drug directly to the lungs without its having to travel through the rest of the body to get there. Whether patients take drugs as prescribed is also essential to ensuring the right dose gets to where it needs to be often enough to have a desired effect. “Even with all the science that goes into understanding a disease well enough to develop an effective drug, it is often up to the patient to make it all work as designed,” writes pharmaceutical scientist <a href="https://www.researchgate.net/profile/Thomas-Anchordoquy" target="_blank" rel="noopener">Tom Anchordoquy</a> of the University of Colorado Anschutz. <h2>2. Searching for drug candidates</h2> Researchers have discovered a number of drugs by chance, including <a href="https://www.pbs.org/newshour/health/the-real-story-behind-the-worlds-first-antibiotic" target="_blank" rel="noopener">penicillin</a> for bacterial infections, <a href="https://www.bbc.com/future/article/20200928-how-the-first-vaccine-was-born" target="_blank" rel="noopener">vaccines for smallpox</a> and <a href="https://doi.org/10.1038/nrcardio.2017.172" target="_blank" rel="noopener">warfarin</a> for blood clots. While serendipity still plays a role in modern drug discovery, most drug developers take a systematic approach. Scientists typically start by identifying a particular molecular target, usually receptors that trigger a specific response in the body. Then, they look for chemical compounds that react with that target. Technology called <a href="https://theconversation.com/discovering-new-drugs-is-a-long-and-expensive-process-chemical-compounds-that-dupe-screening-tools-make-it-even-harder-175972" target="_blank" rel="noopener">high-throughput screening</a> allows researchers to quickly test thousands of potential drug candidates at once. Compounds that match screening criteria advance to further development and refinement. Once optimized for their intended use, compounds go on to safety and efficacy testing in animals and people. One way to ease the search for optimal drug candidates is to work with compounds that are already optimized to work in living beings. <a href="https://theconversation.com/nature-is-the-worlds-original-pharmacy-returning-to-medicines-roots-could-help-fill-drug-discovery-gaps-176963" target="_blank" rel="noopener">Natural products</a>, derived from organisms like microbes, fungi, plants and animals, share similar structures and functions across species. Though not without their own development challenges, they could aid the search for related compounds that work in people. “There are thousands of microorganisms in the ocean left to explore as potential sources of drug candidates, not to mention all the ones on land,” writes medical chemist <a href="https://scholar.google.com/citations?user=8_T1ueYAAAAJ&hl=en" target="_blank" rel="noopener">Ashu Tripathi</a> of the University of Michigan. “In the search for new drugs to combat antibiotic resistance, natural products may still be the way to go.” <h2>3. A drug by any other name may be just as effective</h2> Existing drugs can find a second (or third, fourth and fifth) life through repurposing. Most drugs <a href="https://theconversation.com/many-medications-affect-more-than-one-target-in-the-body-some-drug-designers-are-embracing-the-side-effects-that-had-been-seen-as-a-drawback-184922" target="_blank" rel="noopener">have many functions</a> beyond what researchers originally designed them to do. While this multifunctionality is often the cause of unwanted side effects, sometimes these results are exactly what’s needed to treat a completely unrelated condition. Sildenafil, for example, failed to treat severe chest pain from coronary artery disease, but proved to be potent at inducing erections as Viagra. Similarly, thalidomide, a compound that caused birth defects in thousands of infants around the world as a morning sickness drug, found redemption as a cancer treatment. Because drugs inherently have more than one function in the body, <a href="https://theconversation.com/repurposing-generic-drugs-can-reduce-time-and-cost-to-develop-new-treatments-but-low-profitability-remains-a-barrier-174874" target="_blank" rel="noopener">repurposing existing drugs</a> can help fill a gap where pharmaceutical companies and other developers cannot or will not. <a href="https://scholar.google.com/citations?user=iDKZaA4AAAAJ&hl=en" target="_blank" rel="noopener">Gregory Way</a>, a researcher at the University of Colorado Anschutz, uses artificial intelligence to predict the various effects a drug can have and believes that this lack of specificity is something to explore rather than eliminate. Instead of trying to home in on one specific target, he suggests that scientists “embrace the complexity of biology and try to leverage the multifaceted effects drugs can offer.” <h2>4. Poison as medicine</h2> If so many drugs can have toxic effects in the body, be it through side effects or taking the wrong dose or for the wrong condition, what determines whether a drug is a “medicine” or a “poison”? Biomedical scientists evaluate drugs based on their active ingredient, or a specific compound that has a specific effect in the body. But reducing medicines to just a single molecule ignores another important factor that determines whether a drug is therapeutic – the context in which it is used. Opioids treat intractable pain but can lead to debilitating and lethal addiction when improperly administered. Chemotherapy kills tumors but causes collateral damage to healthy tissues in the process. Another pharmaceutical paradigm, <a href="https://theconversation.com/poison-or-cure-traditional-chinese-medicine-shows-that-context-can-make-all-the-difference-163337" target="_blank" rel="noopener">traditional Chinese medicine</a>, has historically acknowledged the malleability of drugs through the use of poisons as therapeutics. <a href="https://scholar.google.com/citations?user=4q0hYSwAAAAJ&hl=en" target="_blank" rel="noopener">Yan Liu</a>, a medical historian at University of Buffalo who studies this practice, notes that ancient texts did not distinguish between poisons and nonpoisons – rather, Chinese doctors examined drugs based on a continuum of potency, or ability to harm and heal. They used different processing and administration techniques to adjust the potency of poisons. They also took a personalized approach to treatment, aware that each drug works differently based on a number of different individual factors. “The paradox of healing with poisons in traditional Chinese medicine reveals a key message: There is no essential, absolute or unchanging core that characterizes a medicine,” Liu writes. “Instead, the effect of any given drug is always relational – it is contingent on how the drug is used, how it interacts with a particular body and its intended effects.” This article originally appeared on <a href="https://theconversation.com/drugs-4-essential-reads-on-how-theyre-made-how-they-work-and-how-context-can-make-poison-a-medicine-192590" target="_blank" rel="noopener">The Conversation</a> and is a roundup of of articles from The Conversation’s archives. Image: Shutterstock

Books

Doctors say cheese could be as addictive as drugs

Look, we’ve all be there: you’re enjoying a tasty cheese platter, perhaps with a glass of red, and before you know it, you’ve devoured the entire wheel of camembert. You’re not even sure how it happened; all you know is the cheese was too delicious to stop. But before you berate yourself for your lack of willpower, stop – because it may not be your willpower but that the cheese is simply too addictive. According to Thrillist, Dr Neal Barnard, founder and president of the Physicians Committee for Responsible Medicine, has called cheese “dairy crack” because your brain reacts to a particular protein in it the way it would any other addictive substance. “These protein fragments can attach to the opiate receptors in your brain,” Dr Barnard says. “As the name implies, casomorphins are casein-derived morphine-like compounds.” Cheese also has high fat and salt content – two other things that our brains enjoy. However, lucky for all the cheese lovers out there, even though our brains may react to cheese similarly to morphine, it doesn’t have any brain-destroying compounds as the drug. Image: Getty

Body

"Dramatic result": New drug shows hope for slowing down Alzheimer's disease

A trial drug has shown "significant" results in slowing down Alzheimer's disease, with Australian healthcare experts hopeful in where this breakthrough can take their research. The drug, known as Lecanemab, has been proven to reduce cognitive decline by 27 per cent compared to placebo, according to an overseas study. More than 1,700 patients with mild cognitive impairment were enrolled in the study and the results were collected over 18 months. "Functionally and cognitively, it seems they did better and so that is a dramatic result," Dr Lawrence Honig, one of the study investigators from Columbia University Medical Centre, said. The drug works by removing the build-up of amyloid plaques in the brain which is one of the hallmarks of the disease, which featured in the scans of each study participant. Australian experts are excited about the findings, and how this can further their research. "This is the first time we've seen a drug like this have these kinds of effects," Professor Sharon Naismith, Clinical Neuropsychologist & NHMRC Dementia Leadership Fellow at the University of Sydney, said. "The results of this trial have massive implications for our resourcing." Naismith warns there's a need to spend more money on better diagnosing patients with mild cognitive impairment. "In the past there has been a lot of reluctance from healthcare physicians to diagnose or ask about cognitive impairment, even in primary care," she said. She said being able to access a drug that can slow cognitive decline will change the paradigm and conversation around Alzheimer's disease. "I do think we're going to get a real avalanche of people coming to GPs and coming to memory clinics for that reason," she said. Professor Kathryn Goozee, Director of KaRa Minds at Macquarie Park said the study showed using an antibody to target amyloid in the brain can help with cognition. "To date there has been no disease-modifying medication so we want to be offering studies that can potentially change that trajectory," Goozee said. The full details of the results will be presented at an international conference of experts in the US in late November. Image credits: 9News

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Drugs – 4 essential reads on how they’re made, how they work and how context can make poison a medicine

Doctors say cheese could be as addictive as drugs

"Dramatic result": New drug shows hope for slowing down Alzheimer's disease