Search

Walking can prevent low back pain, a new study shows

<a href="https://theconversation.com/profiles/tash-pocovi-1293184">Tash Pocovi</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>; <a href="https://theconversation.com/profiles/christine-lin-346821">Christine Lin</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/mark-hancock-1463059">Mark Hancock</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>; <a href="https://theconversation.com/profiles/petra-graham-892602">Petra Graham</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>, and <a href="https://theconversation.com/profiles/simon-french-713564">Simon French</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a> Do you suffer from low back pain that recurs regularly? If you do, you’re not alone. Roughly <a href="https://pubmed.ncbi.nlm.nih.gov/31208917/">70% of people</a> who recover from an episode of low back pain will experience a new episode in the following year. The recurrent nature of low back pain is a major contributor to the <a href="https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(23)00098-X/fulltext">enormous burden</a> low back pain places on individuals and the health-care system. In our new study, published today in <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(24)00755-4/fulltext">The Lancet</a>, we found that a program combining walking and education can effectively reduce the recurrence of low back pain. <h2>The WalkBack trial</h2> We randomly assigned 701 adults who had recently recovered from an episode of low back pain to receive an individualised walking program and education (intervention), or to a no treatment group (control). Participants in the intervention group were guided by physiotherapists across six sessions, over a six-month period. In the first, third and fifth sessions, the physiotherapist helped each participant to develop a personalised and progressive walking program that was realistic and tailored to their specific needs and preferences. The remaining sessions were short check-ins (typically less than 15 minutes) to monitor progress and troubleshoot any potential barriers to engagement with the walking program. Due to the COVID pandemic, most participants received the entire intervention via telehealth, using video consultations and phone calls. The program was designed to be manageable, with a target of five walks per week of roughly 30 minutes daily by the end of the six-month program. Participants were also encouraged to continue walking independently after the program. Importantly, the walking program was combined with education provided by the physiotherapists during the six sessions. This education aimed to give people a better understanding of pain, reduce fear associated with exercise and movement, and give people the confidence to self-manage any minor recurrences if they occurred. People in the control group received no preventative treatment or education. This reflects what <a href="https://www.sciencedirect.com/science/article/abs/pii/S2468781222001308?via%3Dihub">typically occurs</a> after people recover from an episode of low back pain and are discharged from care. <h2>What the results showed</h2> We monitored the participants monthly from the time they were enrolled in the study, for up to three years, to collect information about any new recurrences of low back pain they may have experienced. We also asked participants to report on any costs related to their back pain, including time off work and the use of health-care services. The intervention reduced the risk of a recurrence of low back pain that limited daily activity by 28%, while the recurrence of low back pain leading participants to seek care from a health professional decreased by 43%. Participants who received the intervention had a longer average period before they had a recurrence, with a median of 208 days pain-free, compared to 112 days in the control group. Overall, we also found this intervention to be cost-effective. The biggest savings came from less work absenteeism and less health service use (such as physiotherapy and massage) among the intervention group. This trial, like all studies, had some limitations to consider. Although we tried to recruit a wide sample, we found that most participants were female, aged between 43 and 66, and were generally well educated. This may limit the extent to which we can generalise our findings. Also, in this trial, we used physiotherapists who were up-skilled in health coaching. So we don’t know whether the intervention would achieve the same impact if it were to be delivered by other clinicians. <h2>Walking has multiple benefits</h2> We’ve all heard the saying that “prevention is better than a cure” – and it’s true. But this approach has been largely neglected when it comes to low back pain. Almost all <a href="https://www.sciencedirect.com/science/article/pii/S0140673618304896?via%3Dihub">previous studies</a> have focused on treating episodes of pain, not preventing future back pain. A limited number of <a href="https://pubmed.ncbi.nlm.nih.gov/26752509/">small studies</a> have shown that exercise and education can help prevent low back pain. However, most of these studies focused on exercises that are not accessible to everyone due to factors such as high cost, complexity, and the need for supervision from health-care or fitness professionals. On the other hand, walking is a free, accessible way to exercise, including for people in rural and remote areas with limited access to health care. Walking also delivers many other <a href="https://www.vichealth.vic.gov.au/sites/default/files/VH_Benefits-of-Walking-Summary2020.pdf">health benefits</a>, including better heart health, improved mood and sleep quality, and reduced risk of several chronic diseases. While walking is not everyone’s favourite form of exercise, the intervention was well-received by most people in our study. Participants <a href="https://pubmed.ncbi.nlm.nih.gov/37271689/">reported</a> that the additional general health benefits contributed to their ongoing motivation to continue the walking program independently. <h2>Why is walking helpful for low back pain?</h2> We don’t know exactly why walking is effective for preventing back pain, but <a href="https://www.e-jer.org/journal/view.php?number=2013600295">possible reasons</a> could include the combination of gentle movements, loading and strengthening of the spinal structures and muscles. It also could be related to relaxation and stress relief, and the release of “feel-good” endorphins, which <a href="https://my.clevelandclinic.org/health/body/23040-endorphins">block pain signals</a> between your body and brain – essentially turning down the dial on pain. It’s possible that other accessible and low-cost forms of exercise, such as swimming, may also be effective in preventing back pain, but surprisingly, <a href="https://pubmed.ncbi.nlm.nih.gov/34783263/">no studies</a> have investigated this. Preventing low back pain is not easy. But these findings give us hope that we are getting closer to a solution, one step at a time.<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/231682/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/tash-pocovi-1293184">Tash Pocovi</a>, Postdoctoral research fellow, Department of Health Sciences, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>; <a href="https://theconversation.com/profiles/christine-lin-346821">Christine Lin</a>, Professor, Institute for Musculoskeletal Health, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/mark-hancock-1463059">Mark Hancock</a>, Professor of Physiotherapy, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>; <a href="https://theconversation.com/profiles/petra-graham-892602">Petra Graham</a>, Associate Professor, School of Mathematical and Physical Sciences, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>, and <a href="https://theconversation.com/profiles/simon-french-713564">Simon French</a>, Professor of Musculoskeletal Disorders, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie 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/walking-can-prevent-low-back-pain-a-new-study-shows-231682">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

Alzheimer’s may have once spread from person to person, but the risk of that happening today is incredibly low

<a href="https://theconversation.com/profiles/steve-macfarlane-4722">Steve Macfarlane</a>, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a> An article published this week in the prestigious journal <a href="https://www.nature.com/articles/s41591-023-02729-2">Nature Medicine</a> documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person. The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors. Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s. The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop <a href="https://www.vdh.virginia.gov/epidemiology/epidemiology-fact-sheets/creutzfeldt-jakob-disease-cjd/">Creuztfeldt-Jakob disease</a> (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million. <h2>What’s CJD got to do with Alzehimer’s?</h2> CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell. Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised <a href="https://en.wikipedia.org/wiki/United_Kingdom_BSE_outbreak">public health concerns</a> over the eating of beef products in the United Kingdom in the 1980s. <h2>Human growth hormone used to come from donated organs</h2> Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue. But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around <a href="https://www.cdc.gov/mmwr/preview/mmwrhtml/00000563.htm">16,000 donated glands</a>. An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people. hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk. <h2>What are the latest findings about Alzheimer’s disease?</h2> The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission. The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease. They considered other explanations for the findings but concluded donated hGH was the likely cause. Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease. Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is <a href="https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-017-0488-7">increasing evidence</a> these proteins spread in the brain in a <a href="https://pubmed.ncbi.nlm.nih.gov/8086126/">similar way to prion diseases</a>. So the mode of transmission the authors propose is certainly plausible. However, given the amyloid protein deposits in the brain <a href="https://www.nia.nih.gov/news/estimates-amyloid-onset-may-predict-alzheimers-progression">at least 20 years</a> before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident. <h2>When was this process used in Australia?</h2> In Australia, donated pituitary material <a href="https://www.health.gov.au/sites/default/files/documents/2022/07/the-cjd-review-final-report.pdf">was used</a> from 1967 to 1985 to treat people with short stature and infertility. <a href="https://www.health.gov.au/sites/default/files/documents/2022/07/the-cjd-review-final-report.pdf">More than 2,000 people</a> received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch. The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are <a href="https://www.mja.com.au/journal/2010/193/6/iatrogenic-creutzfeldt-jakob-disease-australia-time-amend-infection-control">considered to be</a> incredibly small. Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4356853/">around 5%</a> of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution. <h2>The risk is very low – and you can’t ‘catch’ it like a virus</h2> The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide. Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk. The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.<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/222374/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/steve-macfarlane-4722">Steve Macfarlane</a>, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, <a href="https://theconversation.com/institutions/monash-university-1065">Monash 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/alzheimers-may-have-once-spread-from-person-to-person-but-the-risk-of-that-happening-today-is-incredibly-low-222374">original article</a>.

Mind

Can I actually target areas to lose fat, like my belly?

<a href="https://theconversation.com/profiles/nick-fuller-219993">Nick Fuller</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> Spend some time scrolling social media and you’re all-but-guaranteed to see an ad promising to help you with targeted fat loss. These ads promote a concept known as “spot reduction”, claiming you can burn fat in a specific body area, usually the belly, with specially designed exercises or workouts. It’s also common to see ads touting special diets, pills and supplements that will blast fat in targeted areas. These ads – which often feature impressive before and after photos taken weeks apart – can seem believable. Unfortunately, spot reduction is another weight-loss myth. It’s simply not possible to target the location of fat loss. Here’s why. <h2>1. Our bodies are hardwired to access and burn all our fat stores for energy</h2> To understand why spot reduction is a myth, it’s important to understand how body fat is stored and used. The fat stored in our bodies takes the form of triglycerides, which are a type of lipid or fat molecule we can use for energy. Around 95% of the dietary fats <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/triglycerides">we consume are triglycerides</a>, and when we eat, our bodies also convert any unused energy consumed into triglycerides. Triglycerides are stored in special fat cells called adipocytes, and they’re released into our bloodstream and transported to adipose tissue – tissue we more commonly refer to as body fat. This body fat is found all over our bodies, but it’s primarily stored as subcutaneous fat under our skin and as visceral fat around our internal organs. These fat stores serve as a vital energy reserve, with our bodies mobilising to access stored triglycerides to provide energy during periods of prolonged exercise. We also draw on these reserves when we’re dieting and fasting. However, contrary to what many spot-reduction ads would have us think, our muscles can’t directly access and burn specific fat stores when we exercise. Instead, they use a process called lipolysis to convert triglycerides into free fatty acids and a compound called glycerol, which then travels to our muscles via our bloodstream. As a result, the fat stores we’re using for energy when we exercise come from everywhere in our bodies – not just the areas we’re targeting for fat loss. Research reinforces how our bodies burn fat when we exercise, confirming spot reduction is a weight-loss myth. This includes a randomised <a href="https://pubmed.ncbi.nlm.nih.gov/25766455/">12-week clinical trial</a> which found no greater improvement in reducing belly fat between people who undertook an abdominal resistance program in addition to changes in diet compared to those in the diet-only group. Further, <a href="https://www.termedia.pl/A-proposed-model-to-test-the-hypothesis-of-exerciseinduced-localized-fat-reduction-spot-reduction-including-a-systematic-review-with-meta-analysis,129,45538,0,1.html">a 2021 meta-analysis</a> of 13 studies involving more than 1,100 participants found that localised muscle training had no effect on localised fat deposits. That is, exercising a specific part of the body did not reduce fat in that part of the body. <a href="https://www.mdpi.com/1660-4601/18/7/3845">Studies</a> purporting to show spot-reduction benefits have small numbers of participants with results that aren’t clinically meaningful. <h2>2. Our bodies decide where we store fat and where we lose it from first</h2> Factors outside of our control influence the areas and order in which our bodies store and lose fat, namely: <ul> <li> our genes. Just as DNA prescribes whether we’re short or tall, genetics plays a significant role in how our fat stores are managed. Research shows our genes can account for <a href="https://pubmed.ncbi.nlm.nih.gov/24632736/">60% of where fat is distributed</a>. So, if your mum tends to store and lose weight from her face first, there’s a good chance you will, too </li> <li> our gender. Our bodies, by nature, have distinct fat storage characteristics <a href="https://pubmed.ncbi.nlm.nih.gov/11706283/">driven by our gender</a>, including females having more fat mass than males. This is primarily because the female body is designed to hold fat reserves to support pregnancy and nursing, with women tending to lose weight from their face, calves and arms first because they impact childbearing the least, while holding onto fat stored around the hips, thighs and buttocks </li> <li> our age. The ageing process triggers changes in muscle mass, metabolism, and hormone levels, which can impact where and how quickly fat is lost. Post-menopausal <a href="https://theconversation.com/is-menopause-making-me-put-on-weight-no-but-its-complicated-198308">women</a> and middle-aged <a href="https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/sex-differences-in-fat-storage-fat-metabolism-and-the-health-risks-from-obesity-possible-evolutionary-origins/00950AD6710FB3D0414B13EAA67D4327">men</a> tend to store visceral fat around the midsection and find it a stubborn place to shift fat from. </li> </ul> <h2>3. Over-the-counter pills and supplements cannot effectively target fat loss</h2> Most advertising for these pills and dietary supplements – including products claiming to be “the best way to lose belly fat” – will also proudly claim their product’s results are backed by “clinical trials” and “scientific evidence”. But the reality is a host of independent studies don’t support these claims. This includes two recent studies by the University of Sydney that examined data from more than 120 placebo-controlled trials of <a href="https://pubmed.ncbi.nlm.nih.gov/31984610/">herbal</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/33976376/">dietary</a> supplements. None of the supplements examined provided a clinically meaningful reduction in body weight among overweight or obese people. <h2>The bottom line</h2> Spot reduction is a myth – we can’t control where our bodies lose fat. But we can achieve the results we’re seeking in specific areas by targeting overall fat loss. While you may not lose the weight in a specific spot when exercising, all physical activity helps to burn body fat and preserve muscle mass. This will lead to a change in your body shape over time and it will also help you with long-term weight management. This is because your metabolic rate – how much energy you burn at rest – is determined by how much muscle and fat you carry. As muscle is more metabolically active than fat (meaning it burns more energy than fat), a person with a higher muscle mass will have a faster metabolic rate than someone of the same body weight with a higher fat mass. Successfully losing fat long term comes down to losing weight in small, manageable chunks you can sustain – periods of weight loss, followed by periods of weight maintenance, and so on, until you achieve your goal weight. It also requires gradual changes to your lifestyle (diet, exercise and sleep) to ensure you form habits that last a lifetime. At the Boden Group, Charles Perkins Centre, we are studying the science of obesity and running clinical trials for weight loss. You can <a href="https://redcap.sydney.edu.au/surveys/?s=RKTXPPPHKY">register here</a> to express your interest.<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/205203/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/nick-fuller-219993">Nick Fuller</a>, Charles Perkins Centre Research Program Leader, <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/can-i-actually-target-areas-to-lose-fat-like-my-belly-205203">original article</a>.

Body

6 signs you’re low in iron

Feeling constantly tired, looking pale and having heart palpitations? Well you could be one of the two billion people thought to suffer from some degree of iron deficiency. Low iron is the most common and widespread nutritional disorder in the world, and is the only nutrient deficiency that is significantly prevalent in the western world, according to the World Health Organization. Here's how to know, and what to do if you tick all the low iron boxes 1. You suffer from fatigue (aka feel tired ALL of the time) The body uses iron to make haemoglobin, the substance in red blood cells that transports oxygen around the body. When you don't have enough healthy red blood cells, you start to feel pretty exhausted. 2. You seem to get out of breath easily – even if you’re fit When the body is not efficiently transporting oxygen to the lungs, you can feel breathlessness after minimal exertion. Low iron levels can also cause your endurance to suffer too. 3. You look pale and washed out In addition to looking pale, if the inside of your lips, your gums, and the inside of your bottom eyelids are less red than usual, low iron may be the reason behind this. 4. You get sick often Ever felt like you’re fighting an endless cold? Research has shown iron deficiency can affect the immune system, making you more likely to pick up infections and viruses. 5. You experience heart palpitations Your heart may feel like it's pounding, fluttering or beating irregularly, often for just a few seconds or minutes. 6. You get unusual cravings for non-food substances such as dirt, ice, paint, or clay Yes, this does sound very strange, but it's a real symptom that can occur when your body is low in iron – it's called pica. Image credits: Getty Images

Body

What is cognitive functional therapy? How can it reduce low back pain and get you moving?

<a href="https://theconversation.com/profiles/peter-osullivan-48973">Peter O'Sullivan</a>, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin University</a>; <a href="https://theconversation.com/profiles/jp-caneiro-1463060">JP Caneiro</a>, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin University</a>; <a href="https://theconversation.com/profiles/mark-hancock-1463059">Mark Hancock</a>, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>, and <a href="https://theconversation.com/profiles/peter-kent-1433302">Peter Kent</a>, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin University</a> If you haven’t had lower back pain, it’s likely you know someone who has. It affects <a href="https://pubmed.ncbi.nlm.nih.gov/22231424/">around 40% of adults</a> in any year, ranging from adolescents to those in later life. While most people recover, <a href="https://pubmed.ncbi.nlm.nih.gov/29112007/">around 20%</a> go on to develop chronic low back pain (lasting more than three months). There is a <a href="https://bjsm.bmj.com/content/54/12/698">common view</a> that chronic low back pain is caused by permanent tissue damage including “wear and tear”, disc degeneration, disc bulges and arthritis of the spine. This “damage” is often described as resulting from injury and loading of the spine (such as bending and lifting), ageing, poor posture and weak “core” muscles. We’re often told to “protect” our back by sitting tall, bracing the core, keeping a straight back when bending and lifting, and avoiding movement and activities that are painful. Health practitioners often <a href="https://theconversation.com/having-good-posture-doesnt-prevent-back-pain-and-bad-posture-doesnt-cause-it-183732">promote and reinforce these messages</a>. But this is <a href="https://bjsm.bmj.com/content/54/12/698">not based on evidence</a>. An emerging treatment known as <a href="https://pubmed.ncbi.nlm.nih.gov/29669082/">cognitive functional therapy</a> aims to help patients undo some of these unhelpful and restrictive practices, and learn to trust and move their body again. <h2>People are often given the wrong advice</h2> People with chronic back pain are often referred for imaging scans to detect things like disc degeneration, disc bulges and arthritis. But these findings are very common in people without low back pain and research shows they <a href="https://pubmed.ncbi.nlm.nih.gov/24276945/">don’t accurately predict</a> a person’s current or future experience of pain. Once serious causes of back pain have been ruled out (such as cancer, infection, fracture and nerve compression), there is <a href="https://pubmed.ncbi.nlm.nih.gov/27745712/">little evidence</a> scan findings help guide or improve the care for people with chronic low back pain. In fact, scanning people and telling them they have arthritis and disc degeneration can <a href="https://pubmed.ncbi.nlm.nih.gov/33748882/">frighten them</a>, resulting in them avoiding activity, worsening their pain and distress. It can also lead to potentially harmful treatments such as <a href="https://pubmed.ncbi.nlm.nih.gov/27213267/">opioid</a> pain medications, and invasive treatments such as spine <a href="https://pubmed.ncbi.nlm.nih.gov/19127161/">injections</a>, spine <a href="https://pubmed.ncbi.nlm.nih.gov/12709856/">surgery</a> and battery-powered electrical stimulation of spinal nerves. <h2>So how should low back pain be treated?</h2> A complex range of factors <a href="https://pubmed.ncbi.nlm.nih.gov/29112007/">typically contribute</a> to a person developing chronic low back pain. This includes over-protecting the back by avoiding movement and activity, the belief that pain is related to damage, and negative emotions such as pain-related fear and anxiety. Addressing these factors in an individualised way is <a href="https://pubmed.ncbi.nlm.nih.gov/29573871/">now considered</a> best practice. <a href="https://pubmed.ncbi.nlm.nih.gov/15936976/">Best practice care</a> also needs to be person-centred. People suffering from chronic low back pain want to be heard and validated. They <a href="https://pubmed.ncbi.nlm.nih.gov/35384928/">want</a> to understand why they have pain in simple language. They want care that considers their preferences and gives a safe and affordable pathway to pain relief, restoring function and getting back to their usual physical, social and work-related activities. An example of this type of care is cognitive functional therapy. <h2>What is cognitive functional therapy?</h2> <a href="https://pubmed.ncbi.nlm.nih.gov/29669082/">Cognitive functional therapy</a> is about putting the person in the drivers’ seat of their back care, while the clinician takes the time to guide them to develop the skills needed to do this. It’s led by physiotherapists and can be used once serious causes of back pain have been ruled out. The therapy helps the person understand the unique contributing factors related to their condition, and that pain is usually not an accurate sign of damage. It guides patients to relearn how to move and build confidence in their back, without over-protecting it. It also addresses other factors such as sleep, relaxation, work restrictions and engaging in physical activity based on the <a href="https://www.restorebackpain.com/patient-journey">person’s preferences</a>. Cognitive functional therapy usually involves longer physiotherapy sessions than usual (60 minutes initially and 30-45 minute follow-ups) with up to seven to eight sessions over three months and booster sessions when required. <h2>What’s the evidence for this type of therapy?</h2> Our recent clinical trial of cognitive functional therapy, published in <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(23)00441-5/fulltext">The Lancet</a>, included 492 people with chronic low back pain. The participants had pain for an average of four years and had tried many other treatments. We first trained 18 physiotherapists to competently deliver cognitive functional therapy across Perth and Sydney over six months. We compared the therapy to the patient’s “usual care”. We found large and sustained improvements in function and reductions in pain intensity levels for people who underwent the therapy, compared with those receiving usual care. The effects remained at 12 months, which is unusual in low back pain trials. The effects of most recommended interventions such as exercise or psychological therapies are <a href="https://pubmed.ncbi.nlm.nih.gov/34580864/">modest in size</a> and tend to be of <a href="https://pubmed.ncbi.nlm.nih.gov/32794606/">short duration</a>. People who underwent cognitive functional therapy were also more confident, less fearful and had a more positive mindset about their back pain at 12 months. They also liked it, with 80% of participants satisfied or highly satisfied with the treatment, compared with 19% in the usual care group. The treatment was as safe as usual care and was also cost-effective. It saved more than A$5,000 per person over a year, largely due to increased participation at work. <h2>What does this mean for you?</h2> This trial shows there are safe, relatively cheap and effective treatments options for people living with chronic pain, even if you’ve tried other treatments without success. <a href="https://www.restorebackpain.com/cft-clinicians">Access to clinicians</a> trained in cognitive functional therapy is currently limited but will expand as training is scaled up. The costs depend on how many sessions you have. Our studies show some people improve a lot within two to three sessions, but most people had seven to eight sessions, which would cost around A$1,000 (aside from any Medicare or private health insurance rebates). <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/207009/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/peter-osullivan-48973">Peter O'Sullivan</a>, Professor of Musculoskeletal Physiotherapy, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin University</a>; <a href="https://theconversation.com/profiles/jp-caneiro-1463060">JP Caneiro</a>, Research Fellow in physiotherapy, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin University</a>; <a href="https://theconversation.com/profiles/mark-hancock-1463059">Mark Hancock</a>, Professor of Physiotherapy, <a href="https://theconversation.com/institutions/macquarie-university-1174">Macquarie University</a>, and <a href="https://theconversation.com/profiles/peter-kent-1433302">Peter Kent</a>, Adjunct Associate Professor of Physiotherapy, <a href="https://theconversation.com/institutions/curtin-university-873">Curtin 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/what-is-cognitive-functional-therapy-how-can-it-reduce-low-back-pain-and-get-you-moving-207009">original article</a>.

Body

Censorship or sensible: is it bad to listen to Fat Bottomed Girls with your kids?

<a href="https://theconversation.com/profiles/liz-giuffre-105499">Liz Giuffre</a>, <a href="https://theconversation.com/institutions/university-of-technology-sydney-936">University of Technology Sydney</a> International music press has reported this week that Queen’s song Fat Bottomed Girls <a href="https://www.billboard.com/music/music-news/queen-fat-bottomed-girls-greatest-hits-1235396348/">has not been included</a> in a greatest hits compilation aimed at children. While there was no formal justification given, presumably lyrics “fat bottomed” and “big fat fatty” were the problem, and even the very singable hook, “Oh, won’t you take me home tonight”. Predictably, The Daily Mail and similar outlets used it as an excuse to bemoan cancel culture, political correctness and the like, with the headline “<a href="https://www.dailymail.co.uk/tvshowbiz/article-12424449/We-woke-Classic-Queen-song-Fat-Bottomed-Girls-mysteriously-dropped-groups-new-Greatest-Hits-collection.html">We Will Woke You</a>” quickly out of the gate. Joke headlines aside, should children be exposed to music with questionable themes or lyrics? The answer is not a hard yes or no. My colleague Shelley Brunt and I studied a range of factors and practices relating to <a href="https://www.routledge.com/Popular-Music-and-Parenting/Brunt-Giuffre/p/book/9780367367138">Popular Music and Parenting</a>, and we found that more important than individual songs or concerts is the support children are given when they’re listening or participating. A parent or caregiver should always be part of a conversation and some sort of relationship when engaging with music. This can involve practical things like making sure developing ears aren’t exposed to too harsh a volume or that they know how to find a trusted adult at a concert. But this also extends to the basics of media and cultural literacy, like what images and stories are being presented in popular music, and how we want to consider those in our own lives. In the same way you’d hope someone would talk to a child to remind them that superheroes can’t actually fly (and subsequently if you’re dressed as a superhero for book week don’t go leaping off tall buildings!), popular music of all types needs to be contextualised. <figure><iframe src="https://www.youtube.com/embed/VMnjF1O4eH0?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> <h2>Should we censor, or change, the way popular music is presented for kids?</h2> There is certainly a long tradition of amending popular songs to make them child or family friendly. On television, this has happened as long as the medium has been around, with some lyrics and dance moves toned down to appease concerned parents and tastemakers about the potential evils of pop. Famously, <a href="https://www.youtube.com/watch?v=oim51kUg748">Elvis Presley serenaded a literal Hound Dog</a> rather than the metaphorical villain of his 1950s hit. In Australia, the local TV version of <a href="https://nostalgiacentral.com/music/music-on-film-and-tv/bandstand-australia/">Bandstand</a> from the 1970s featured local artists singing clean versions of international pop songs while <a href="https://www.youtube.com/watch?v=guembJBOOyI">wearing modest hems and neck lines</a>. This continued with actual children also re-performing pop music, from the Mickey Mouse Club versions of songs from the US to our own wonderful star factory that was <a href="https://theconversation.com/all-my-loving-young-talent-time-still-glows-50-years-since-first-airing-on-australian-tv-159533">Young Talent Time</a>. The tradition continues today with family-friendly, popular music-based programming like The Voice and The Masked Singer. <figure><iframe src="https://www.youtube.com/embed/oim51kUg748?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> In America, there is a huge industry for children’s versions of pop music via the Kidz Bop franchise. Its formula of child performers covering current hits has been wildly successful for over 20 years. Some perhaps obvious substitutions are made – the <a href="https://www.youtube.com/watch?v=zkctByJbtNY">cover of Lizzo’s About Damn Time</a> is now “About That Time”, with the opening lyric changed to “Kidz Bop O’Clock” rather than “Bad Bitch O’Clock”. In some other Kidz Bop songs, though, <a href="https://pudding.cool/2020/04/kidz-bop/">references to violence and drugs have been left in</a>. Other longer-standing children’s franchises have also made amendments to pop lyrics, but arguably with a bit more creativity and fun. The Muppets’ cover of Bohemian Rhapsody, replacing the original murder with a rant from Animal, is divine. <figure><iframe src="https://www.youtube.com/embed/tgbNymZ7vqY?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> <h2>Should music ever just be for kids?</h2> Context is key when deciding what is for children or for adults. And hopefully we’re always listening (in some way) together. Caregivers should be able to make an informed decision about whether a particular song is appropriate for their child, however they consider that in terms of context. By the same token, the resurgence of <a href="https://www.theguardian.com/music/2022/apr/05/how-the-wiggles-took-over-the-world-and-got-the-cool-kids-on-side-too">millennial love</a> for The Wiggles has shown us no one should be considered “too old” for Hot Potato or Fruit Salad. <figure><iframe src="https://www.youtube.com/embed/quHus3DwN4Q?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> When considering potential harm for younger listeners, factors like <a href="https://kidsafeqld.com.au/risks-noise-exposure-baby/">volume and tone</a> can be more dangerous than whether or not there’s a questionable lyric. Let’s remember, too, lots of “nursery rhymes” aimed at children are also quite violent if you listen to their words closely. French writer Jacques José Attali <a href="https://www.google.com.au/books/edition/Noise/OHe7AAAAIAAJ?hl=en">famously argued</a> the relationship between music, noise and harm is politics and power – even your most beloved song can become just noise if played too loudly or somewhere where you shouldn’t be hearing it. As an academic, parent and fat-bottomed girl myself, my advice is to keep having conversations with the children in your life about what you and they are listening to. Just like reminding your little superhero to only pretend to fly rather than to actually jump – when we sing along to Queen, we remember that using a word like “fat” and even “girl” isn’t how everyone likes to be treated these days.<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/212093/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/liz-giuffre-105499">Liz Giuffre</a>, Senior Lecturer in Communication, <a href="https://theconversation.com/institutions/university-of-technology-sydney-936">University of Technology 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/censorship-or-sensible-is-it-bad-to-listen-to-fat-bottomed-girls-with-your-kids-212093">original article</a>.

Music

Rob Lowe's West Wing confession

Rob Lowe has spoken candidly about leaving one of his most acclaimed TV shows. The 59-year-old actor has opened up about leaving The West Wing, which first aired in 1999 with Lowe playing the character of Sam Seaborn, the Bartlet administration's deputy communications director, on the very first episode of the show. The show ran for seven seasons and went off the air in 2006, although Lowe left the show during season four. Despite the show's popularity, Lowe said that leaving the show when he did was the best decision to make for him and his future career. Speaking candidly on the Stitcher Studios' podcast Podcrushed, Lowe was asked about why he left the show, and he summed up his departure with an analogy. He said, "I walked away from the most popular girl at school, but I also knew that it was a super unhealthy relationship, and it was the best thing I ever did." The unofficial story when Lowe left the show, as reported by <a href="https://www.cnn.com/2002/SHOWBIZ/TV/07/24/west.wing.lowe/index.html" target="_blank" rel="nofollow noopener" data-i13n="cpos:3;pos:1" data-ylk="slk:Daily Variety;cpos:3;pos:1;elm:context_link;itc:0" data-rapid_p="33" data-v9y="1">Daily Variety</a>, was that he was doing so because he couldn't get the salary that he wanted. As Lowe explained to Podcrushed hosts Penn Badgley, Nava Kavelin and Sophie Ansari, his decision had boiled down to one thing. "I felt very undervalued," said Lowe, the author of 2012's Stories I Only Tell My Friends. "Whenever I talk to actors who complain about, you know, their relationships on their shows, it happens. It happens in any workplace. You could be in an environment where people sandbag you, want to see you fail, don't appreciate you, whatever it is and whenever I share my stories, people are like, 'I will never share my own stories again.'" "They would make your hair stand up and there's some of them I wrote. I shared some of them in my book, but I purposely didn't share half of the other ones because it would make the people involved look so bad that I didn't want to do it to them." "So, I did not have a good experience. Tried to make it work and tried to make it work and tried to make it work and then what happened was my kids were getting to a certain age where I could see them having first girlfriends or friends and being in a relationship that was abusive and taking it," said Lowe, the father of sons John Owen, a 27-year-old actor, and venture capitalist Matthew, 29. "She's the popular girl, everybody likes her, she's beautiful, it must be great. All the things that people would say about making The West Wing to me. It's so popular, it's so amazing, it must be amazing, but I know what it's like and if I couldn't walk away from it, then how could I empower my kids to walk away from it?" When Lowe did leave the show, he issued a statement on why his character would be written out. "As much as it hurts to admit it, it has been increasingly clear, for quite a while, that there was no longer a place for Sam Seaborn on The West Wing," he said, <a href="https://www.cnn.com/2002/SHOWBIZ/TV/07/24/west.wing.lowe/index.html" target="_blank" rel="nofollow noopener" data-i13n="cpos:5;pos:1" data-ylk="slk:per CNN;cpos:5;pos:1;elm:context_link;itc:0" data-rapid_p="36" data-v9y="1">per CNN</a>. "However, Warner Bros. has allowed me an opportunity to leave the show as I arrived ... grateful for it, happy to have been on it and proud of it. We were a part of television history and I will never forget it." Image credits: Getty Images

Weight loss: why you don’t just lose fat when you’re on a diet

<a href="https://theconversation.com/profiles/adam-collins-1179004">Adam Collins</a>, <a href="https://theconversation.com/institutions/university-of-surrey-1201">University of Surrey</a> When you go on a diet, you don’t just lose fat – you lose muscle too. This can have many repercussions – not only on your fitness and strength, but on your metabolism. To lose weight (body fat), you need to be in a calorie deficit. This means consuming fewer calories than your body uses, or exercising to burn more calories than you consume. During the first few days in a calorie deficit, the body uses up its small reservoir of <a href="https://pubmed.ncbi.nlm.nih.gov/1615908/">glycogen stores</a> for energy. Glycogen is a string of glucose (sugar) that comes from the carbohydrates you eat. Since carbs are the body’s main energy source, this is why any glucose the body doesn’t immediately use is stored to use for energy later. But as carbohydrate molecules bind with water, this means that when the body stores glycogen, it also stores water in the muscles. As these glycogen stores are used up, the body also releases a significant amount of water. This is often called “water weight”, and explains why some may feel they lose considerable weight early in their diet. Given you only have days’ worth of glycogen stores, this is why the body uses fat to store extra calories for when you need it. Once the glycogen stores are used up, the body shifts to metabolising fat to get the energy it needs to function. But not all tissues can use fat for energy – such as the brain. This is why the body needs to metabolise your muscles when you’re in a calorie deficit. Protein (from the food you eat) is stored in your muscles. The body can convert this stored protein into glucose for energy. But this means you subsequently lose the muscle tissue itself when that happens. This has significant consequences – including <a href="https://pubmed.ncbi.nlm.nih.gov/35103583/">slowing the metabolism</a>, which may ultimately drive weight regain after losing weight. <h2>Muscle loss</h2> Many factors can affect how much muscle you lose while in a calorie deficit. While it was once thought that the more fat you had, the <a href="https://pubmed.ncbi.nlm.nih.gov/10673906/">less muscle you lost</a> in a calorie deficit, this has since been disproved – with both <a href="https://pubmed.ncbi.nlm.nih.gov/3066619/">lean</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/17367567/">obese people</a> losing significant rates of muscle when dieting. <a href="https://pubmed.ncbi.nlm.nih.gov/29957829/">Ethnicity</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/32734691/">genetics</a> may, however, play a role – with studies showing black people tend to lose more muscle mass in a calorie deficit than white people do. Some research also suggests that genetic variants may make some people more susceptible to <a href="https://pubmed.ncbi.nlm.nih.gov/32734691/">certain dietary changes</a>, which may determine how much muscle mass they end up losing. Muscle loss will also happen regardless of whether you lose weight <a href="https://pubmed.ncbi.nlm.nih.gov/30925026/">gradually or quickly</a>. A better determinant of how much muscle you’ll lose depends on <a href="https://pubmed.ncbi.nlm.nih.gov/30925026/">how much weight you end up losing</a>. If a person loses 10% of their body weight, typically around 20% of this is fat-free mass (the proportion of body mass that isn’t fat – such as muscle). This can equate to several kilograms of muscle. Many people also think that what you eat while losing weight may determine how much muscle you lose, with it commonly believed that if you eat plenty of protein you’re less likely to lose muscle mass. This is <a href="https://pubmed.ncbi.nlm.nih.gov/19246357/">debatable</a>, with research showing people lose as much muscle on high-protein weight loss diets as people who followed other types of diets. Low-carb diets have also been claimed to promote more fat loss. But studies comparing <a href="https://pubmed.ncbi.nlm.nih.gov/22258266/">different types of diets</a> have found that low-fat high-carb diets seem to offer <a href="https://pubmed.ncbi.nlm.nih.gov/28193517/">the same, if not better, fat loss</a> than low-carb, high-fat diets – with no differences in muscle loss. <h2>Protein and exercise</h2> Given all that has been said, the only way to prevent muscle loss somewhat while losing weight is to combine exercise (particularly <a href="https://pubmed.ncbi.nlm.nih.gov/18356845/">resistance exercise</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/28507015/">endurance exercise</a>) with a diet higher in protein. This is because exercise stimulates muscle growth – but this process can only happen if you have an adequate supply of protein. It’s suggested adults normally aim to consume <a href="https://pubmed.ncbi.nlm.nih.gov/34371981/">0.8g of protein per kilogram of body weight</a> per day to maintain muscle mass. But given the extra demand exercise places on the muscles, a person will probably need to consume 1.2-1.5g of protein per kilogram of body weight to preserve muscle during weight loss. People who exercise a lot may need to increase that to more than <a href="https://pubmed.ncbi.nlm.nih.gov/28642676/">2g per kilogram of body weight</a> when losing weight. <a href="https://pubmed.ncbi.nlm.nih.gov/22221216/">Older people</a> may also need to consume more protein than average. Just be wary of consuming too much protein (more than 2.5g per kilogram of body weight) as eating more than your body uses could have an <a href="https://pubmed.ncbi.nlm.nih.gov/28507015/">adverse effect</a> on your metabolism by potentially making the body less able to draw upon glucose for energy. It may also put greater pressure on the kidneys and liver – which could lead to serious <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460905/#:%7E:text=High%20dietary%20protein%20intake%20can,a%20role%20in%20kidney%20health.">health issues</a>, such as liver and kidney damage. Even if you prevent muscle loss when losing weight, other metabolic changes still happen that promote weight regain – such as changes in your metabolic rate (the minimum amount of calories your body needs to survive) and <a href="https://pubmed.ncbi.nlm.nih.gov/21677272/">increases in appetite and hunger</a>. This is why, when trying to lose weight, the most important thing to consider is how sustainable your diet and lifestyle changes are. The easier these are to maintain, the better chances you have of keeping the weight off.<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/209258/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/adam-collins-1179004">Adam Collins</a>, Principal Teaching Fellow, Nutrition, <a href="https://theconversation.com/institutions/university-of-surrey-1201">University of Surrey</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/weight-loss-why-you-dont-just-lose-fat-when-youre-on-a-diet-209258">original article</a>.

Body

Harrison Ford is back as an 80-year-old Indiana Jones – and a 40-something Indy. The highs (and lows) of returning to iconic roles

<a href="https://theconversation.com/profiles/ben-mccann-398197">Ben McCann</a>, <a href="https://theconversation.com/institutions/university-of-adelaide-1119">University of Adelaide</a> Saddle up, don the fedora and crack that whip: Harrison Ford is back as the intrepid archaeologist in Indiana Jones and the Dial of Destiny. The film premiered at Cannes, where Ford was <a href="https://www.hollywoodreporter.com/movies/movie-news/harrison-ford-honorary-palme-dor-cannes-1235495463/">awarded</a> an Honorary Palme d’Or in recognition of his life’s work. Reviews for the fifth film in the franchise <a href="https://www.hollywoodreporter.com/movies/movie-news/indiana-jones-5-review-roundup-1235495961/">have been mixed</a>, and it is the first Indy film not to be directed by Steven Spielberg (this time, it’s James Mangold, best known for his motor-racing drama Ford v Ferrari). But this is “event” cinema that combines nostalgia, old-school special effects and John Williams’ <a href="https://theconversation.com/from-jaws-to-star-wars-to-harry-potter-john-williams-90-today-is-our-greatest-living-composer-176245">iconic score</a>. So, Ford is back, aged 80. What draws actors back after all this time? <figure><iframe src="https://www.youtube.com/embed/eQfMbSe7F2g?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> <h2>Role returns</h2> Ford first played Indy in 1981 and last played him in 2008. That is a full 15 years since the most recent film in the series, and 42 years since his first outing in Raiders of the Lost Ark. Ford has form in returning to celebrated characters. One of the great pleasures of watching The Force Awakens back in 2015 was seeing Ford play Han Solo again for the <a href="https://www.dailymotion.com/video/x3j2j09">first time in over 30 years</a>. <figure><iframe src="https://www.youtube.com/embed/0xQSIdSRlAk?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> Actors return to roles for numerous reasons: <ul> <li>financial (Ford was reportedly paid <a href="https://okmagazine.com/exclusives/harrison-ford-paid-indiana-jones-5-plagued-with-problems/">US$25 million</a> for Dial of Destiny)</li> <li>protection of their brand, image and star persona (Michael Keaton <a href="https://www.fortressofsolitude.co.za/the-flash-movies-biggest-hero-how-michael-keaton-saved-the-film/">returning to play Batman</a> after three decades and three other actors who have embodied the role)</li> <li>professional (Tom Cruise admitted over the 36 years between Top Gun films he wanted to make sure the sequel <a href="https://screenrant.com/top-gun-maverick-tom-cruise-return-how-explained/">could live up to the original</a>)</li> <li>personal (once-huge stars are working less and less, and only feel the need to return to a built-in fan base every few years – Bill Murray in the 2021 Ghostbusters sequel springs to mind).</li> </ul> It’s not always a successful endeavour. Arnold Schwarzenegger and Sylvester Stallone – two of the biggest action stars of the 1980s off the back of iconic roles as The Terminator, Rocky Balboa and John Rambo – have repeatedly returned to those roles, and critics have been <a href="https://screenrant.com/terminator-dark-fate-undermined-john-connor-storyline-franchise-bad/">particularly harsh</a>. It did not work for Sigourney Weaver in <a href="https://www.rogerebert.com/reviews/alien-resurrection-1997">Alien: Resurrection</a> in 1997, 18 years after her first time as Ripley; nor for Keanu Reeves in <a href="https://www.theguardian.com/film/2021/dec/21/the-matrix-resurrections-review-keanu-reeves">The Matrix Resurrections</a> in 2021, 23 years after the original. And still, I’m intrigued to see what Michael Mann could do with his long-rumoured sequel to Heat, his definitive 1995 crime film. Ever since Mann published his novel Heat 2 last year – a kind of origin story for Heat’s key protagonists – fans have been hoping a de-aged Al Pacino (now aged 83) <a href="https://deadline.com/2023/04/michael-mann-heat-2-warner-bros-adam-driver-young-neil-mccauley-1235316777/">might return</a> as LA cop Vincent Hanna. <h2>Undoing time</h2> “Digital de-ageing” first entered the Hollywood mainstream in 2019 with The Irishman and Captain Marvel. <a href="https://www.indiewire.com/features/craft/de-aging-actors-history-benjamin-button-dial-of-destiny-harrison-ford-1234863938/">Via this process</a>, older actors (Robert De Niro, Al Pacino and Samuel L. Jackson have all been subject to the technology) move back and forwards in time without younger actors having to play them. <figure><iframe src="https://www.youtube.com/embed/OF-lElIlZM0?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> Films still tend to cast two actors to play older and younger versions of the same character, a choice that dates back at least to 1974’s The Godfather Part II, in which a young Robert de Niro plays Vito Corleone, portrayed by the much older Marlon Brando in the first film. In 1989, Indiana Jones and the Last Crusade features a delightful opening scene where River Phoenix plays the young version of Indiana Jones, before Ford takes over for the rest of the film. <figure><iframe src="https://www.youtube.com/embed/AwH6-Yh7_SM?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> Actors used to just play characters of their own age when reprising earlier roles. Paul Newman finally won a Best Actor Oscar for his role as “Fast Eddie” Felson in The Color of Money (1986), a quarter of a century after first playing him in The Hustler. The sequel plays on Newman’s age, and his role as a mentor to an upcoming Tom Cruise, and bathes viewers in nostalgia and memories of <a href="https://faroutmagazine.co.uk/paul-newman-schooled-tom-cruise-the-color-of-money/">a younger Newman</a>. <figure><iframe src="https://www.youtube.com/embed/k7gmrKAFshE?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> But actors no longer have to exclusively play their age. The first part of Dial of Destiny is an extended flashback, set in 1944, in which Ford has been digitally de-aged to appear in his 40s. This process used an AI system that scanned used and unused reels of footage of Ford from <a href="https://www.cbr.com/harrison-ford-de-aging-indiana-jones-dial-of-destiny/">the first three Indy films</a> to match his present-day performance. Here, it is as if we are getting two Fords for the price of one: the “younger”, fitter Indy and the older, more world-weary version. It makes for a powerfully emotional connection on screen. Yet there are some <a href="https://variety.com/2023/film/awards/indiana-jones-5-harrison-ford-de-aging-not-working-1235618698/">pitfalls to de-ageing</a>. Some viewers complain that the whole process is distracting and that the hyper-real visual look of de-aged scenes resembles a video game. Even so, de-ageing in Hollywood cinema is here to stay. Tom Hanks’s <a href="https://variety.com/2023/film/news/tom-hanks-robin-wright-digitally-deaged-robert-zemeckis-movie-1235507766/">next film</a> is using AI-based generative technology to digitally de-age him. Given its reduced cost, speed and reduced human input, AI-driven innovation might have <a href="https://filmstories.co.uk/news/new-ai-driven-de-ageing-tools-to-be-used-in-tom-hanks-project/">industry-changing ramifications</a>. <h2>The star of Ford</h2> Harrison Ford remains a bona fide “movie star” in an industry profoundly buffeted by COVID, the rise of streaming platforms, the demise of the monoculture, and the changing nature of who constitutes a star. In the midst of all this industry uncertainty, it seems there is no longer a statute of limitations on actors returning to much-loved characters. The next big ethical issue for the film industry as it further embraces AI is whether to <a href="https://collider.com/james-dean-digital-cgi-performance-in-new-movie/">resurrect deceased actors</a> and cast them in new movies. Still, I’m looking forward to seeing more actors de-aged as the technology improves and audiences acclimatise to watching older actors “playing” younger versions of themselves. We are only at the start of Hollywood’s next big adventure.<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/202357/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/ben-mccann-398197">Ben McCann</a>, Associate Professor of French Studies, <a href="https://theconversation.com/institutions/university-of-adelaide-1119">University of Adelaide</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/harrison-ford-is-back-as-an-80-year-old-indiana-jones-and-a-40-something-indy-the-highs-and-lows-of-returning-to-iconic-roles-202357">original article</a>.

Movies

Opioids don’t relieve acute low back or neck pain – and can result in worse pain, new study finds

<a href="https://theconversation.com/profiles/christine-lin-346821">Christine Lin</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/andrew-mclachlan-255312">Andrew McLachlan</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/caitlin-jones-1263090">Caitlin Jones</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/christopher-maher-826241">Christopher Maher</a>, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a> Opioids are the one of the most prescribed pain-relief for people with low back and neck pain. In Australia, around <a href="https://link.springer.com/article/10.1007/s00586-017-5178-4">40% of people</a> with low back and neck pain who present to their GP and <a href="https://qualitysafety.bmj.com/content/28/10/826">70% of people</a> with low back pain who visit a hospital emergency department are prescribed opioids such as oxycodone. But our <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(23)00404-X/fulltext">new study</a>, published today in the Lancet medical journal, found opioids do not relieve “acute” low back or neck pain (lasting up to 12 weeks) and can result in worse pain. Prescribing opioids for low back and neck pain can also cause <a href="https://www.healthdirect.gov.au/taking-opioid-medicines-safely">harms</a> ranging from common side effects – such as nausea, constipation and dizziness – to <a href="https://www.aihw.gov.au/reports/illicit-use-of-drugs/opioid-harm-in-australia/summary">misuse, dependency, poisoning and death</a>. Our findings show opioids should not be recommended for acute low back pain or neck pain. A change in prescribing for low back pain and neck pain is urgently needed in <a href="https://www.tga.gov.au/resources/publication/publications/addressing-prescription-opioid-use-and-misuse-australia">Australia</a> and <a href="https://www.thelancet.com/commissions/opioid-crisis">globally</a> to reduce opioid-related harms. <h2>Comparing opioids to a placebo</h2> In our trial, we randomly allocated 347 people with acute low back pain and neck pain to take either an opioid (oxycodone plus naloxone) or <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/placebo-effect">placebo</a> (a tablet that looked the same but had no active ingredients). Oxycodone is an opioid pain medicine which can be given orally. <a href="https://www.nps.org.au/radar/articles/oxycodone-with-naloxone-controlled-release-tablets-targin-for-chronic-severe-pain">Naloxone</a>, an opioid-reversal drug, reduces the severity of constipation while not disrupting the pain relieving effects of oxycodone. Participants took the opioid or placebo for a maximum of six weeks. People in the both groups also received <a href="https://www.sciencedirect.com/science/article/pii/S1836955321000941">education and advice</a> from their treating doctor. This could be, for example, advice on returning to their normal activities and avoiding bed rest. We assessed their outcomes over a one-year period. <h2>What did we find?</h2> After six weeks of treatment, taking opioids did not result in better pain relief compared to the placebo. Nor were there benefits to other outcomes such as physical function, quality of life, recovery time or work absenteeism. More people in the group treated with opioids experienced nausea, constipation and dizziness than in the placebo group. Results at one year highlight the potential long-term harm of opioids even with short-term use. Compared to the placebo group, people in the opioid group experienced slightly worse pain, and reported a higher risk of <a href="https://academic.oup.com/painmedicine/article/20/1/113/4728236#129780622">opioid misuse</a> (problems with their thinking, mood or behaviour, or using opioids differently from how the medicines were prescribed). More people in the opioid group reported pain at one year: 66 people compared to 50 in the placebo group. <h2>What will this mean for opioid prescribing?</h2> In recent years, international low back pain guidelines have shifted the focus of treatment from drug to non-drug treatment due to <a href="https://www.thelancet.com/article/S0140-6736(18)30489-6/fulltext">evidence</a> of limited treatment benefits and concern of medication-related harm. For acute low back pain, <a href="https://link.springer.com/article/10.1007/s00586-018-5673-2">guidelines</a> recommend patient education and advice, and if required, anti-inflammatory pain medicines such as ibuprofen. Opioids are <a href="https://link.springer.com/article/10.1007/s00586-018-5673-2">recommended only</a> when other treatments haven’t worked or aren’t appropriate. Guidelines for <a href="https://pubmed.ncbi.nlm.nih.gov/33064878/">neck</a> pain similarly discourage the use of opioids. Our latest research clearly demonstrates the benefits of opioids do not outweigh possible harms in people with acute low back pain and neck pain. Instead of advising opioid use for these conditions in selected circumstances, opioids should be discouraged without qualification. <h2>Change is possible</h2> Complex problems such as opioid use need smart solutions, and another study we recently conducted provides convincing data opioid prescribing can be successfully reduced. The <a href="https://qualitysafety.bmj.com/content/30/10/825">study</a> involved four hospital emergency departments, 269 clinicians and 4,625 patients with low back pain. The intervention comprised of: <ul> <li>clinician education about <a href="https://aci.health.nsw.gov.au/networks/musculoskeletal/resources/low-back-pain">evidence-based management</a> of low back pain</li> <li>patient education using posters and handouts to highlight the benefits and harms of opioids</li> <li>providing heat packs and anti-inflammatory pain medicines as alternative pain-management treatments</li> <li>fast-tracking referrals to outpatient clinics to avoid long waiting lists</li> <li>audits and feedback to clinicians on information about opioid prescribing rates.</li> </ul> This intervention reduced opioid prescribing from <a href="https://qualitysafety.bmj.com/content/30/10/825">63% to 51% of low back pain presentations</a>. The <a href="https://emj.bmj.com/content/early/2023/04/02/emermed-2022-212874">reduction was sustained for 30 months</a>. Key to this successful approach is that we worked with clinicians to develop suitable pain-management treatments without opioids that were feasible in their setting. More work is needed to evaluate this and other interventions aimed at reducing opioid prescribing in other settings including GP clinics. A nuanced approach is often necessary to avoid causing <a href="https://theconversation.com/opioid-script-changes-mean-well-but-have-left-some-people-in-chronic-pain-156753">unintended consequences</a> in reducing opioid use. If people with low back pain or neck pain are using opioids, especially at higher doses over an extended period of time, it’s important they seek advice from their doctor or pharmacist before stopping these medicines to avoid <a href="https://www.healthdirect.gov.au/opioid-withdrawal-symptoms">unwanted effects when the medicines are abruptly stopped</a>. Our research provides compelling evidence opioids have a limited role in the management of acute low back and neck pain. The challenge is getting this new information to clinicians and the general public, and to implement this evidence into practice.<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/203244/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/christine-lin-346821">Christine Lin</a>, Professor, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/andrew-mclachlan-255312">Andrew McLachlan</a>, Head of School and Dean of Pharmacy, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>; <a href="https://theconversation.com/profiles/caitlin-jones-1263090">Caitlin Jones</a>, Postdoctoral Research Associate in Musculoskeletal Health, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</a>, and <a href="https://theconversation.com/profiles/christopher-maher-826241">Christopher Maher</a>, Professor, Sydney School of Public Health, <a href="https://theconversation.com/institutions/university-of-sydney-841">University of Sydney</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/opioids-dont-relieve-acute-low-back-or-neck-pain-and-can-result-in-worse-pain-new-study-finds-203244">original article</a>.

Body

Don’t blame women for low libido. Sexual sparks fly when partners do their share of chores – including calling the plumber

When a comic about “mental load” <a href="https://english.emmaclit.com/2017/05/20/you-shouldve-asked/">went viral in 2017</a>, it sparked conversations about the invisible workload women carry. Even when women are in paid employment, they remember their mother-in-law’s birthday, know what’s in the pantry and organise the plumber. This mental load often goes unnoticed. Women also <a href="https://theconversation.com/yet-again-the-census-shows-women-are-doing-more-housework-now-is-the-time-to-invest-in-interventions-185488">continue to do more housework</a> and childcare than their male partners. This burden has been exacerbated over the recent pandemic (homeschooling anyone?), <a href="https://theconversation.com/planning-stress-and-worry-put-the-mental-load-on-mothers-will-2022-be-the-year-they-share-the-burden-172599">leaving women</a> feeling exhausted, anxious and resentful. As sexuality researchers, we wondered, with all this extra work, do women have any energy left for sex? We decided to explore how mental load affects intimate relationships. We focused on female sexual desire, as “low desire” affects <a href="https://www.sciencedirect.com/science/article/abs/pii/S1743609520307566">more than 50% of women</a> and is <a href="https://www.sciencedirect.com/science/article/abs/pii/S0091302217300079">difficult to treat</a>. Our study, published in the <a href="https://www.tandfonline.com/doi/full/10.1080/00224499.2022.2079111">Journal of Sex Research</a>, shows women in equal relationships (in terms of housework and the mental load) are more satisfied with their relationships and, in turn, feel more sexual desire than those in unequal relationships. <h2>How do we define low desire?</h2> Low desire is tricky to explore. More than simply the motivation to have sex, women describe sexual desire as a state-of-being and a need for closeness. Adding to this complexity is the fluctuating nature of female desire that changes in response to life experiences and the <a href="https://www.bbc.com/future/article/20160630-the-enduring-enigma-of-female-desire">quality of relationships</a>. Relationships are especially important to female desire: relationship dissatisfaction is a <a href="https://pubmed.ncbi.nlm.nih.gov/18410300/">top risk factor</a> for low desire in women, even more than the physiological impacts of age and menopause. Clearly, relationship factors are critical to understanding female sexual desire. As a way of addressing the complexity of female desire, a <a href="https://link.springer.com/article/10.1007/s10508-018-1212-9">recent theory</a> proposed two different types of desire: dyadic desire is the sexual desire one feels for another, whereas solo desire is about individual feelings. Not surprisingly, dyadic desire is intertwined with the dynamics of the relationship, while solo desire is more amorphous and involves feeling good about yourself as a sexual being (feeling sexy), without needing validation from another. <h2>Assessing the link</h2> Our research acknowledged the nuances of women’s desire and its strong connection to relationship quality by exploring how fairness in relationships might affect desire. The research involved asking 299 Australian women aged 18 to 39 questions about desire and relationships. These questions included assessments of housework, mental load – such as who organised social activities and made financial arrangements – and who had more leisure time. We compared three groups: <ul> <li>relationships where women perceived the work as equally shared equal (the “equal work” group)</li> <li>when the woman felt she did more work (the “women’s work” group)</li> <li>when women thought that their partner contributed more (the “partner’s work” group).</li> </ul> We then explored how these differences in relationship equity impacted female sexual desire. <h2>What we found</h2> The findings were stark. Women who rated their relationships as equal also reported greater relationship satisfaction and higher dyadic desire (intertwined with the dynamics of the relationship) than other women in the study. Unfortunately (and perhaps, tellingly), the partner’s work group was too small to draw any substantial conclusions. However, for the women’s work group it was clear their dyadic desire was diminished. This group was also less satisfied in their relationships overall. We found something interesting when turning our attention to women’s solo desire. While it seems logical that relationship inequities might affect all aspects of women’s sexuality, our results showed that fairness did not significantly impact solo desire. This suggests women’s low desire isn’t an internal sexual problem to be treated with <a href="https://www.insider.com/guides/health/yoni-eggs#:%7E:text=Yoni%20eggs%20are%20egg%2Dshaped,bacterial%20infections%20and%20intense%20pain.">mindfulness apps and jade eggs</a>, but rather one that needs effort from both partners. Other relationship factors are involved. We found children increased the workload for women, leading to lower relationship equity and consequently, lower sexual desire. Relationship length also played a role. Research shows long-term relationships are <a href="https://link.springer.com/article/10.1007/s10508-018-1175-x">associated with</a> decreasing desire for women, and this is often attributed to the tedium of over-familiarity (think of the bored, sexless <a href="https://www.youtube.com/watch?v=kBq-Nyo0lQg">wives in 90s sitcoms</a>). However our research indicates relationship boredom is not the reason, with the increasing inequity over the course of a relationship often the cause of women’s disinterest in sex. The longer some relationships continue, the more unfair they become, lowering women’s desire. This may be because women take on managing their partner’s relationships, as well as their own (“It’s time we had your best friend over for dinner”). And while domestic housework may start as equally shared, over time, women <a href="https://www.abs.gov.au/media-centre/media-releases/women-spent-more-time-men-unpaid-work-may">tend to do more</a> household tasks. <h2>What about same-sex couples?</h2> Same-sex couples have <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/fare.12293">more equitable relationships</a>. However, we found the same link between equity and desire for women in same-sex relationships, although it was much stronger for heteronormative couples. A sense of fairness within a relationship is fundamental to all women’s satisfaction and sexual desire. <h2>What happens next?</h2> Our findings suggest one response to low desire in women could be to address the amount of work women have to take on in relationships. The link between relationship satisfaction and female sexual desire has been firmly established in <a href="https://link.springer.com/article/10.1007/s10508-018-1175-x">previous research</a> but our findings explain how this dynamic works: women’s sense of fairness within a relationship forecasts their contentment, which has repercussions on their desire for their partner. To translate our results into clinical practice, we could run trials to confirm if lowering women’s mental load results in greater sexual desire. We could have a “housework and mental load ban” for a sample of women reporting low sexual desire and record if there are changes in their reported levels of desire. Or perhaps women’s sexual partners could do the dishes tonight and see what happens. Image credit: Shutterstock This article originally appeared on <a href="https://theconversation.com/dont-blame-women-for-low-libido-sexual-sparks-fly-when-partners-do-their-share-of-chores-including-calling-the-plumber-185401" target="_blank" rel="noopener">The Conversation</a>.

Relationships

The verdict: Full fat versus low fat milk

The idea of full low milk being healthier for us began circulating in the 1950s. It was shown that saturated fat increased blood cholesterol levels, with certain statistical evidence leading to the assumption it resulted in higher rates of heart disease and obesity. This idea is not totally wrong. Full fat milk does indeed have a high saturated fat content, about 65 percent in fact. <a href="http://www.simoneaustin.com/" target="_blank" rel="noopener">Simone Austin</a>, accredited practising dietitian and spokesperson for the <a href="http://daa.asn.au/" target="_blank" rel="noopener">Dietitians Association of Australia</a> addresses the claims that saturated fat should be avoided when it comes to weight management. “We are still recommending saturated fat should be kept to a minimum as there is still a link between saturated and plasma cholesterol levels, however full cream milk is only 4% total fat and is therefore not a high fat product, depending on quantity of course.” Health and nutrition coach and whole foods chef, Lee Holmes, believes that low-fat milk is a great option for those trying to lose weight. Even though the fat is skimmed, the milk itself still contains an abundance of calcium and protein, and these are essential to weight loss. “Low-fat milk is better for overall weight control and maintenance as it only contains 0.15% fat as opposed to full-cream milk which contains 3.8% fat” she explains. The New Zealand Ministry of Health recommends enjoying mostly low and reduced fat milk and milk products, as it can reduce the total daily kilojoule intake to aid with weight management. This is generally believed to lead to weight loss and reduced risk of heart disease. However, Simone explains why it is not quite that straight forward. “Fat can give some feeling of satiety. If you are having less milk overall, and it is more filling to have full cream milk, then this might decrease overall volume of food consumed and therefore not be detrimental”. This approach is supported by recent research conducted by <a href="../%20http:/www.ncbi.nlm.nih.gov/pubmed/26746178">Swedish researchers</a>, looking at the dairy consumption of a group of middle aged men. If found that those who ate full fat dairy products were less likely to become obese over a period of 12 years, compare with men who rarely ate high- fat diary. This is because the weight-loss effect of reducing saturated fat depends on what replaces it in the diet, which is usually sugar and carbohydrates. Unfortunately, most of us are susceptible to consciously or unconsciously replacing a larger reduction in calories with something else. So, if you drink low-fat varieties of milk in order to reduce calorie intake, you must ensure you are not making up these calories elsewhere for this approach to be effective. However, in your quest for a slimmer waist line, it is important not to overlook other important health factors. Milk is a primary source of nutrients, and according to both Simone and the <a href="http://ro.uow.edu.au/cgi/viewcontent.cgi?article=2032&context=sspapers" target="_blank" rel="noopener">ABS</a>, most over-60s simply aren’t getting what they need. “In New Zealand the annual per capita consumption of milk has declined by 30% in the last 20 years, and 20% of the New Zealand population has an inadequate intake of calcium”. Simone stresses that simply aiming to meet serves is the priority. “Milk also provides a valuable source of protein and as we age our efficiency at using protein reduces, so we need to have a little more”. Lee Holmes echoes this, stating that ideally, people over 60 years of age should be having two to three glasses of cow’s milk daily to absorb the necessary amounts of calcium. If you don’t want to consume that much milk, are lactose intolerant or prefer to opt for non-cow’s milk (such as almond) you need to make these nutrients up elsewhere. “You may want to consider a quality, natural supplement to ensure you are giving your body all the nutrients it needs." So whether it be low-fat or full-fat, say cheers to milk and manage your weight loss in accordance with other health factors. Image: Getty Images

Food & Wine

Magda Szubanski calls for "fat" people to be protected from online hate speech

Magda Szubanski has called for vilification rules to be put in place for "fat people" online, only to be blasted by her following. The comedian shared the controversial tweet in which she wondered why "fat" people are not "protected" from hate speech online. She wrote, "It's interesting to me that you are banned from attacking just about every identity on Twitter except being fat. Why are we not protected from vilification?" Szubanski was then blasted by several heartless online users, as she received comments such as, "Have another Snickers bar. Sounds like your blood sugar is low," and "Lose some weight then." Despite receiving plenty of support from fans, the controversial tweet saw more personal attacks. "Ever see any obese old people? No, because they all die young. If you are going to do that to yourself, then you will have to accept noticing," another wrote. "Because you choose to be fat," yet another wrote. Magda was only too happy to call out the backlash, as she accused the online users of dumping their "toxic self-loathing" onto her, as they believe she "wouldn't fight back". "It's pretty clear from the response to my tweet that some people hate fat people because their own hearts are so full of hate that they need to dump all their toxic self-loathing onto someone who they think won't fight back." "Well, not this little fat duck. She got teeth," she wrote. She also went on to say that the online trolls proved her point entirely as many commenters defended her, saying it would go a long way if we were all a little nicer to each other online. Image credits: Getty Images

Body

Airline responds to "fat-shaming" onboard comments

Dr Sydney Watson – a US-based Australian journalist and political commentator – took to Twitter on October 11 to complain about being sat between two obese people on an American Airlines flight. Her mid-flight comments caused an immediate furore as she posted that “I am currently - literally - WEDGED between two OBESE people on my flight,” along with a photo of her personal space being invaded. “This is absolutely NOT acceptable or okay. If fat people want to be fat, fine. But it is something else entirely when I'm stuck between you, with your arm rolls on my body, for 3 hours. “I don't care if this is mean. My entire body is currently being touched against my wishes. I can't even put the arm rests down on either side because there's no f***ing room. “I'm sick of acting like fatness to this extent is normal. Let me assure you, it is not. “If you need a seat belt extender, you are TOO FAT TO BE ON A PLANE. “Buy two seats or don't fly.” <blockquote class="twitter-tweet"> I am currently - literally - WEDGED between two OBESE people on my flight. This is absolutely NOT acceptable or okay. If fat people want to be fat, fine. But it is something else entirely when I'm stuck between you, with your arm rolls on my body, for 3 hours. <a href="https://t.co/9uIqcpJO8I">pic.twitter.com/9uIqcpJO8I</a> — Dr. Sydney Watson (@SydneyLWatson) <a href="https://twitter.com/SydneyLWatson/status/1579609743244800006?ref_src=twsrc%5Etfw">October 10, 2022</a></blockquote> Dr Watson said she asked the passenger on her right if he wanted to move to sit next to his sister to which he declined. She continued the rest of her flight sitting uncomfortably with no air hostess offering to switch her seat. Her complaint went viral with the official American Airlines Twitter account responding to Dr Watson saying: “Our passengers come in all different sizes and shapes. We're sorry you were uncomfortable on your flight.” This however was not enough for Dr Watson who eventually found out that “what happened to me went against American Airlines own policies regarding overweight passengers.” A few days later after her initial flight, an American Airlines worker got in contact with Dr Watson apologising for the inconvenience and offered her a $150 Trip Credit. “I'd rather take the $150 American Airlines offered me as a refund and give it to someone who needs a PT or a gym membership,” she tweeted in response. Still furious at what occurred on the flight, Dr Watson said she has no regrets over being in the news for fat shaming. “I'm not sorry. I meant everything I said. Justifying obesity is NOT OKAY,” she said. “And, rock on to anyone trying to lose weight and change their lives. I believe in you.” Images: Twitter/Instagram

Travel Trouble

Fat Bear Winner: ‘747’ lays b-ruin to rivals despite fishy voting

After eating lots of tasty fish in preparation for the northern hemisphere’s winter, Brown bear 747 has been crowned the winner of the annual Fat Bear Week. The initiative, run by the US National Parks Service and multimedia organisation explore, gives the public a chance to vote for the biggest brown bear in Alaska’s Katmai National Park. Over one week, people cast their votes for eight nominated bears that have been gorging on river salmon in the lead up to their hibernation. After a summer of catching and eating fish – usually salmon – in the Brooks River, the bears reach peak size in early to mid-October. Shortly, they’ll go into a five-to-eight-month slumber, emerging after the coldest part of the Alaskan winter. The initiative shines a light on the behaviours and survival methods of the species which resides across northern hemisphere continents towards the Arctic Circle. Although brown bears are now extinct in much of central and southern Europe, some still persist in Romania and the Balkan states, and they remain across Russia, Alaska, Canada, the Himalayas and Tibetan plateau. It is also an important indicator species for other wildlife due to their wide habitat range, and play important ecological roles as seed dispersers, and lower-level species managers through predation. Get stuffed! Cheating claims in lead up to Fat Bear final Prior to the grand final between 747 and brown bear 901, a shocking case of voting fraud left organisers decidedly grizzly. A spam attack of votes during the semi-finals threatened to derail 747’s quest for a second Fat Bear crown. Fortunately, organisers were hot onto the bogus bruin ballots. <div class="newsletter-box"> <div id="wpcf7-f6-p218507-o1" class="wpcf7" dir="ltr" lang="en-US" role="form"> </div> </div> “Like bears stuff their face with fish, your ballot box, too, has been stuffed,” Katmai organisers said on Monday. “It appears someone has decided to spam the Fat Bear Week poll, but fortunately it is easy for us to tell which votes are fraudulent. We have discarded the fake votes.” Publicly voted animal awareness competitions are notoriously prone to phony voting. The Guardian Australia Bird of the Year competition infamously saw a case of dodgy democracy in 2019 when a case of automated voting was detected by the <a href="https://www.theguardian.com/news/datablog/2019/nov/11/voter-detected-in-guardians-australian-bird-of-the-year-poll" target="_blank" rel="noopener">avian electoral commission.</a> Cosmos’ own Australian Mammal of the Year competition <a href="https://cosmosmagazine.com/nature/amoty/too-much-love-for-the-mammals/" target="_blank" rel="noopener">was this year hit</a> by a bout of egregious electioneering when hundreds of spam votes were cast for some animals vying for the crown. Fortunately, as with Fat Bear Week, spotting and omitting a bad ballot is a straightforward task of, usually, spotting unusual voting patterns. <img src="https://oversixtydev.blob.core.windows.net/media/2022/10/fat-bear-2022-1.jpg" alt="" width="1200" height="675" /> 2022 Fat Bear Week winner ‘747’ hunts for a tasty fish. Image: Courtesy L. Law via Katmai National Park. 747 does it again Brown bear 747 – aptly named after a jumbo jet – claimed victory with 68,105 votes to rival 901’s 56,875. It was 747’s second premiership, having previously claimed the title in 2020. ‘480 Otis’ holds the record of four titles – exactly half the number of Fat Bear Weeks held. “Though he may be blissfully unaware of his two titles, the gains are real,” say the Fat Bear Week organisers. “In the bear world, fat is fit and these chunky contenders have been working tirelessly to pack on the pounds necessary for survival.” A record 1.027 million votes were cast in the 2022 edition of the event. <img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=218507&title=Fat+Bear+Winner%3A+%26%238216%3B747%26%238217%3B+lays+b-ruin+to+rivals+despite+fishy+voting" width="1" height="1" /> <div id="contributors"> <a href="https://cosmosmagazine.com/nature/fat-bear-voting-winner/" target="_blank" rel="noopener">This article</a> was originally published on <a href="https://cosmosmagazine.com" target="_blank" rel="noopener">Cosmos Magazine</a> and was written by Cosmos. Image: Courtesy L. Law via Katmai National Park. </div>

Family & Pets

Ultra-processed foods: it’s not just their low nutritional value that’s a concern

In countries such as the UK, US and Canada, ultra-processed foods now account for <a href="https://pubmed.ncbi.nlm.nih.gov/30744710/">50% or more</a> of calories consumed. This is concerning, given that these foods have been linked to a number of different health conditions, including a greater risk of <a href="https://pubmed.ncbi.nlm.nih.gov/33167080/">obesity</a> and various chronic diseases such as <a href="https://nutritionj.biomedcentral.com/articles/10.1186/s12937-020-00604-1">cardiovascular disease</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/35896436/">dementia</a>. Ultra-processed foods are <a href="https://pubmed.ncbi.nlm.nih.gov/30744710/">concoctions of various industrial ingredients</a> (such as emulsifiers, thickeners and artificial flavours), amalgamated into food products by a series of manufacturing processes. Sugary drinks and many breakfast cereals are ultra-processed foods, as are more recent innovations, such as so-called <a href="https://www.sciencedirect.com/science/article/pii/S2213453019301144,">“plant-based” burgers</a>, which are typically made of protein isolates and other chemicals to make the products palatable. The intense industrial processes used to produced ultra-processed foods destroy the <a href="https://pubmed.ncbi.nlm.nih.gov/35067754/">natural structure</a> of the food ingredients and strip away many beneficial nutrients such as fibre, vitamins, minerals and phytochemicals. Many of us are well aware that ultra-processed foods are harmful for our health. But it’s been unclear if this is simply because these foods are of poor nutritional value. Now, two new studies have shown that poor nutrition may not be enough to explain their health risks. This suggests that other factors may be needed to fully explain their health risks. <h2>The role of inflammation</h2> The <a href="https://www.bmj.com/content/378/bmj-2022-070688">first study</a>, which looked at over 20,000 health Italian adults, found that participants who consumed the highest number of ultra-processed foods had an increased risk of dying prematurely from any cause. The <a href="https://www.bmj.com/content/378/bmj-2021-068921">second study</a>, which looked at over 50,000 US male health professionals, found high consumption of ultra-processed foods was associated with a greater risk of colon cancer. What’s most interesting about these studies is that the health risks from eating a diet high in ultra-processed foods remained even after they had accounted for the poor nutritional quality of their diets. This suggests that <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8747015/">other factors</a> contribute to the harms caused by ultra-processed foods. It also implies that getting the right nutrients elsewhere in the diet may not be enough to cancel out the risk of disease from consuming ultra-processed foods. Similarly, attempts by the food industry to improve the nutritional value of ultra-processed foods by adding a few more vitamins may be side-stepping a more fundamental problem with these foods. So what factors may explain why ultra-processed foods are so harmful to our health? The Italian study found that inflammatory markers – such as a higher white blood cell count – were higher in groups that ate the most ultra-processed foods. Our bodies may trigger an inflammatory response for any number of reasons – for example, if we catch a cold or get cut. The body responds by sending signals to our immune cells (such as white blood cells) to attack any invading pathogens (such as bacteria or viruses). Usually, our inflammatory response resolves quite quickly, but some people may develop chronic inflammation throughout their body. This can cause tissue damage, and is involved in many chronic diseases – such as <a href="https://pubmed.ncbi.nlm.nih.gov/25859884/">cancer</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/28744020/">cardiovascular disease</a>. Many studies have found that poor diets can increase inflammation in the body, and that this is linked to <a href="https://pubmed.ncbi.nlm.nih.gov/28744020/">higher risk</a> of chronic diseases. Given that signs of inflammation were seen in participants of the Italian study who ate the most ultra-processed foods, this could suggest that inflammation may contribute to why ultra-processed foods increase disease risk. Some food additives common in ultra-processed foods (such as emulsifiers and artificial sweeteners) also increase inflammation in the gut by causing <a href="https://pubmed.ncbi.nlm.nih.gov/29899036/">changes to the gut microbiome</a>. <figure class="align-center ">Some researchers have theorised that ultra-processed foods increase inflammation because they are recognised by the body as foreign – much like an invading bacteria. So the body mounts an inflammatory response, which has been dubbed “<a href="https://pubmed.ncbi.nlm.nih.gov/24939238/">fast food fever</a>”. This increases inflammation throughout the body as a result.</figure> Although the US colon cancer study did not establish if inflammation increased in the men consuming the most ultra-processed foods, inflammation is strongly linked with an <a href="https://pubmed.ncbi.nlm.nih.gov/27821485/">increased risk of colon cancer</a>. Research shows that other mechanisms – such as <a href="https://www.bmj.com/content/378/bmj-2022-070688">impaired kidney function</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/19502515/">toxins in packaging</a> – may also explain why ultra-processed foods cause so many dangerous health problems. Since inflammatory responses are hard-wired in our bodies, the best way to prevent this from happening is by not eating ultra-processed foods at all. Some plant-based diets high in natural, unprocessed foods (such as the <a href="https://pubmed.ncbi.nlm.nih.gov/36039924/">Mediterranean diet</a>) have also been shown to be anti-inflammatory. This may also explain why plant-based diets free from ultra-processed foods can help ward off <a href="https://pubmed.ncbi.nlm.nih.gov/26148921/">chronic diseases</a>. It’s currently not known to what extent an anti-inflammatory diet can help counteract the effects of ultra-processed foods. Simply reducing your intake of ultra-processed foods may be a challenge. Ultra-processed foods are designed to be hyper-palatable – and together with persuasive marketing, this can make resisting them an enormous challenge for <a href="https://pubmed.ncbi.nlm.nih.gov/33153827/">some people</a>. These foods are also not labelled as such on food packaging. The best way to identify them is by looking at their ingredients. Typically, things such as emulsifiers, thickeners, protein isolates and other industrial-sounding products are a sign it’s an ultra-processed food. But making meals from scratch using natural foods is the best way to avoid the harms of ultra-processed foods.<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/189918/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/richard-hoffman-221275">Richard Hoffman</a>, Associate lecturer, Nutritional Biochemistry, <a href="https://theconversation.com/institutions/university-of-hertfordshire-799">University of Hertfordshire</a> This article is republished from <a href="https://theconversation.com">The Conversation</a>. Read the <a href="https://theconversation.com/ultra-processed-foods-its-not-just-their-low-nutritional-value-thats-a-concern-189918">original article</a>.

Food & Wine

Low iron is a health risk made worse by COVID

“Beauty is an iron mine,” once remarked the Australian mining magnate, Gina Reinhart. She was talking about a precious resource, but iron is also profoundly <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464783/" target="_blank" rel="noopener">important to living organisms</a>: from bacteria and fungi, to mammals like us. Iron acts as a key to numerous metabolic functions within our bodies. But iron deficiency remains as <a href="https://cdn.who.int/media/docs/default-source/nutritionlibrary/focusing-on-anaemia_970a28fe-a055-4e63-b3ba-11be7b940b16.pdf?sfvrsn=9ab36bdb_6&download=true" target="_blank" rel="noopener">one of the top global health risks</a> recognised by the World Health Organization (WHO). Iron deficiency has become the most prevalent micronutrient disorder worldwide, and COVID may be worsening the problem. <h2>Iron is hard to get</h2> The type of iron we mine is different from the “free-form” iron that can be used biologically. Free-form iron has a propensity to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842161/" target="_blank" rel="noopener">jump between two chemical states</a>, allowing it to bind to various molecules, and participate in all sorts of essential reactions within our bodies. But we see a different story again during food digestion. Inside our upper small intestine where iron is most effectively absorbed, free-form iron tends to bind to oxygen, other minerals and food components. This often results in rock-like, insoluble clumps (which are like the ones we mine!). These are too big to pass through or between our cells. This means that even when we consume enough iron, <a href="https://www.ncbi.nlm.nih.gov/books/NBK448204/#:%7E:text=Heme%20iron%2C%20derived%20from%20hemoglobin,and%20is%20less%20well%20absorbed." target="_blank" rel="noopener">typically only ~15–35% of it is absorbed</a>. It also means iron availability can be <a href="https://ift.onlinelibrary.wiley.com/doi/10.1111/1541-4337.12669" target="_blank" rel="noopener">improved, or inhibited</a> depending on how we eat it or what we eat it with. For example, heme iron from animal flesh has a <a href="https://omlc.org/spectra/hemoglobin/hemestruct/heme-struct.gif" target="_blank" rel="noopener">cage-like structure</a>, which carries the iron in a soluble form that prevents it from clumping during absorption. In many Western countries, heme iron only accounts for <a href="https://academic.oup.com/metallomics/article/3/2/103/6016197?login=true#219037456" target="_blank" rel="noopener">10% of the iron eaten, but two thirds</a> of the total iron absorbed. <h2>More of us are at risk of deficiency</h2> Getting sufficient iron sounds like simple maths: we want to add enough to our dietary intake to make up for the iron being lost from the body, such as through faeces, skin shedding, menstruation (for women) and sweat. But the two sides of the equation can change depending on who and where we are throughout our lifetime. Generally, iron deficiency occurs when our body’s stores of iron are depleted from not having consumed or absorbed enough iron to meet our needs. This can happen when people restrict their diets, such as for religious, social or medical reasons. Some people also have a tough time keeping up when their iron needs increase, such as <a href="https://www.nature.com/articles/s41430-019-0400-6" target="_blank" rel="noopener">pregnant women</a> and <a href="https://academic.oup.com/ajcn/article/106/suppl_6/1681S/4823199" target="_blank" rel="noopener">growing children</a>. But iron deficiency can also happen when the body has enough iron, <a href="https://onlinelibrary.wiley.com/doi/10.1111/bjh.12311" target="_blank" rel="noopener">but can’t effectively transport it into cells</a>. This is common in those with both acute and chronic infections, heart and autoimmune conditions, and cancers. In these cases, the underlying disease needs to be treated first, rather than improving iron intake. The table below summarises some common causes of iron deficiency. Sometimes multiple causes may occur simultaneously – for example, for many elite athletes (<a href="https://link.springer.com/article/10.1007/s00421-019-04157-y" target="_blank" rel="noopener">35% of women and 11% of men</a>), iron deficiency results from reduced absorption due to inflammation, on top of increased loss through sweat and breakdown of blood cells. <h2>COVID hasn’t helped</h2> The ongoing COVID epidemic has also introduced multiple risk factors for iron deficiency. We know severe infection with SARS-CoV-2 (the virus that causes COVID) may change the way some people <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8305218/" target="_blank" rel="noopener">metabolise iron</a>, leading to lower iron levels up to two months after infection. This <a href="https://onlinelibrary.wiley.com/doi/10.1002/jmv.26774" target="_blank" rel="noopener">contributes to symptoms</a> commonly reported after infection, such as fatigue and lethargy. Recovery from the pandemic itself has also exacerbated <a href="https://www.oecd.org/coronavirus/policy-responses/food-supply-chains-and-covid-19-impacts-and-policy-lessons-71b57aea/" target="_blank" rel="noopener">food supply issues</a>, as well as the <a href="https://blogs.worldbank.org/developmenttalk/global-income-inequality-and-covid-19-pandemic-three-charts" target="_blank" rel="noopener">rising global income inequality</a>. This means more people face barriers to food security – and the nutrient-dense foods that help boost our iron intake like red meat or leafy greens may be unavailable or unaffordable for them. <h2>Before you pick up a pill</h2> It may be tempting to pick up one of the many widely available iron supplements to attempt to boost your intake. However, we have to keep in mind that conventional iron supplementation is <a href="https://www.tandfonline.com/doi/full/10.1185/03007995.2012.761599" target="_blank" rel="noopener">associated with some negative side effects</a>. These include damage to our gut lining, nausea, diarrhoea and constipation. Iron supplementation has also been linked to changes in the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400826/" target="_blank" rel="noopener">gut microbiome</a>, a critical determinant of health. The WHO has recommended <a href="https://cdn.who.int/media/docs/default-source/micronutrients/gff-part-1-en.pdf?sfvrsn=afc1c426_2" target="_blank" rel="noopener">two other approaches</a>: diet diversification and food fortification. <a href="https://cdn.who.int/media/docs/default-source/anaemia/areacop-webinar---24-september-2020/areacop-webinar-nancyaburto-presentation.pdf?sfvrsn=7abd1427_4" target="_blank" rel="noopener">Diet diversification</a> is exactly as it sounds: having a diet with a variety of wholefoods such as fruits and vegetables, grains and legumes, meat, dairy, and nuts and seeds. This approach not only ensures sufficient levels of iron are found in the foods we eat, but also that they come with different forms or “vehicles” to improve absorption. This approach works <a href="https://apps.who.int/iris/bitstream/handle/10665/349086/WHO-EURO-2021-4007-43766-61591-eng.pdf?sequence=1&isAllowed=y" target="_blank" rel="noopener">even with plant-based foods</a>. Food fortification, where iron is added to processed foods, is also a fairly safe yet accessible option due to its lower dose. In Australia, iron is commonly fortified in products such as bread, cereals and ready-to-drink mixes. It can be challenging to get the iron into our body and where it’s needed. But before turning to supplements, we must remind ourselves that food sources should always be first-in-line. In cases of diagnosed deficiencies, your healthcare professional will provide you with further information where supplements are necessary. This article originally appeared on <a href="https://theconversation.com/low-iron-is-a-health-risk-made-worse-by-covid-how-to-get-more-without-reaching-for-supplements-185020" target="_blank" rel="noopener">The Conversation</a>. Image: Shutterstock

Body

“What a low act!": Daniel Morcombe's parents outraged at upcoming film

The devastated parents of murdered Queensland boy Daniel Morcombe have blasted an upcoming film about their son’s death. Daniel Morcombe was only 13 years old when he was abducted and murdered on Queensland’s Sunshine Coast in December, 2003. In August 2011, Brett Peter Cowan was arrested and later found guilty of Daniel’s murder. Now parents Denise and Bruce Morcombe have come out attacking the film The Stranger, which tells the story of an undercover detective trying to catch a killer in Australia. The Stranger premiered at Cannes earlier this year and will play at the Melbourne International Film Festival in August. A statement from the Morcombe’s was shared on the Daniel Morcombe Foundation Facebook page calling the film a “low act” and have asked people not to watch it. <blockquote class="twitter-tweet"> The movie “The Stranger” is not supported by the Morcombe family. Individuals who make money on a heinous crime are parasites. They are callously disrespectful to Daniel, the DMF & the Morcombe family. We find the making of the movie morally corrupt and cruel. Shame on you. <a href="https://t.co/9FEFAp5g0G">pic.twitter.com/9FEFAp5g0G</a> — Denise Morcombe OAM (@DeniseMorcombe) <a href="https://twitter.com/DeniseMorcombe/status/1547358728286261248?ref_src=twsrc%5Etfw">July 13, 2022</a></blockquote> “What a low act! I won’t be going to watch this movie. I won’t be recommending anyone go. The movie is not supported or sanctioned in any way by the Morcombe family,” the statement read. “It’s appalling storyline ignores our family‘s pain and chooses to profit from 13-year-old Daniel Morcombe. “Next year will mark 20 years since we lost Daniel. The passage of time does not make it any easier. Personally, I find the making of this movie morally corrupt and a cruel, callous, selfish cash grab by all involved. Shame on you. “I recommend the public stay away from it and either save their money or consider donating it to the Daniel Morcombe Foundation.” Mrs Morcombe took it further and called the movie makers “parasites” for disrespecting her son. <blockquote class="twitter-tweet"> We are not amused! How can anyone give oxygen to a crime that is so, so evil? Connections of the movie have blood on their hands. — Bruce Morcombe (@BruceMorcombe) <a href="https://twitter.com/BruceMorcombe/status/1547361223804481536?ref_src=twsrc%5Etfw">July 13, 2022</a></blockquote> “The movie ‘The Stranger’ is not supported by the Morcombe family. Individuals who make money on a heinous crime are parasites,” she wrote. “They are callously disrespectful to Daniel, the DMF & the Morcombe family. We find the making of the movie morally corrupt and cruel. Shame on you.” Mr Morcombe responded to his wife’s tweet saying: “We are not amused! How can anyone give oxygen to a crime that is so, so evil? Connections of the movie have blood on their hands.” Director Thomas M Wright said he made the film to share a different perspective of the story because he could not “presume” what the family was going through. “One reason I chose not to show the child or family (in The Stranger) was to make a film with a clear moral perspective,” he previously said. “I couldn’t presume to know anything of the experience of that family. But I could see that there was a story about empathy and making meaning in the wake of violence, not violence itself.” According to Hollywood reporter, “the film offers a fictionalised portrait of the massive undercover operation that cracked the infamous cold case of 13-year-old Daniel Morcombe, who went missing in 2003.” Images: Daniel Morcombe Foundation

Movies

Low-cost gel film pulls clean drinking water from desert air, raising hopes of quenching the world’s driest communities

One in three people lives in <a class="spai-bg-prepared" href="https://www.un.org/en/events/desertification_decade/whynow.shtml" target="_blank" rel="noreferrer noopener">drylands</a>, areas covering more than 40% of the Earth’s surface that experience significant water shortages. Scientists and engineers have now developed a new material that could help people living in these areas access <a class="spai-bg-prepared" href="https://cosmosmagazine.com/earth/water/an-answer-to-the-clean-water-crisis/" target="_blank" rel="noreferrer noopener">clean drinking water</a> by capturing it right out of the atmosphere, according to a new study in Nature Communications. They’ve developed a gel film that costs just $2 per kilogram to produce and can pull water from the air in even the driest climates; 1kg of it can produce more than 6 litres per day in less than 15% relative humidity (RH), and 13 litres in areas with up to 30% RH. Relative humidity is the ratio of the current absolute humidity to the highest possible absolute humidity. So a 100% RH means that the air is completely saturated with water vapour and cannot hold any more. People tend to feel most comfortable between 30% and 50%, and arid climates have less than 30% RH. These results are promising, as previous attempts to pull water from the desert air have typically been energy-intensive and not very efficient. “This new work is about practical solutions that people can use to get water in the hottest, driest places on Earth,” says senior author Guihua Yu, professor of Materials Science and Mechanical Engineering at the University of Texas in Austin, US. “This could allow millions of people without consistent access to drinking water to have simple, water-generating devices at home that they can easily operate.” <div class="newsletter-box spai-bg-prepared"> <div id="wpcf7-f6-p192317-o1" class="wpcf7 spai-bg-prepared" dir="ltr" lang="en-US" role="form"> <form class="wpcf7-form mailchimp-ext-0.5.61 spai-bg-prepared resetting" action="/technology/gel-film-desert-drinking-water/#wpcf7-f6-p192317-o1" method="post" novalidate="novalidate" data-status="resetting"> <input class="wpcf7-form-control wpcf7-text referer-page spai-bg-prepared" name="referer-page" type="hidden" value="https://cosmosmagazine.com/technology/" data-value="https://cosmosmagazine.com/technology/" aria-invalid="false" /> </form> </div> </div> The gel is made with <a class="spai-bg-prepared" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hydroxypropyl-cellulose" target="_blank" rel="noreferrer noopener">hydroxypropyl cellulose</a> (HPC) which is produced from cellulose, and a common kitchen ingredient called <a class="spai-bg-prepared" href="https://www.sciencedirect.com/science/article/abs/pii/S0141813016310339" target="_blank" rel="noreferrer noopener">konjac glucomannan</a>, as well as lithium chloride salt (LiCl). It forms a hydrophilic (water attracting) porous film with a large surface area that collects the water vapour from air. “The gel takes two minutes to set simply. Then, it just needs to be freeze dried, and it can be peeled off the mould and used immediately after that,” explains Weixin Guan, a doctoral student on Yu’s team and a lead researcher of the work. And, because the cellulose is thermo-responsive, it becomes hydrophobic (water repelling) when heated which allows the collected water to be released within 10 minutes through mild heating at 60 °C. This means that the overall energy needed to produce the water is minimised. The film is also flexible, can be moulded into a variety of shapes and sizes, and producing it requires only the gel precursor – which includes all the relevant ingredients poured into a mould. “This is not something you need an advanced degree to use,” says lead author Youhong “Nancy” Guo, a former doctoral student in Yu’s lab and now a postdoctoral researcher at the Massachusetts Institute of Technology. “It’s straightforward enough that anyone can make it at home if they have the materials.” And because it’s so simple, the authors say the challenges of scaling the technology up and achieving mass usage are reduced.  <img id="cosmos-post-tracker" class="spai-bg-prepared" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=192317&title=Low-cost+gel+film+pulls+clean+drinking+water+from+desert+air%2C+raising+hopes+of+quenching+the+world%E2%80%99s+driest+communities" width="1" height="1" />  <div id="contributors"> <a href="https://cosmosmagazine.com/technology/gel-film-desert-drinking-water/">This article</a> was originally published on <a href="https://cosmosmagazine.com">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/imma-perfetto">Imma Perfetto</a>. Imma Perfetto is a science writer at Cosmos. She has a Bachelor of Science with Honours in Science Communication from the University of Adelaide. Image: The University of Texas at Austin/Cockrell School of Engineering </div>

Technology

Over 60

News

Shop

Catalogues

Travel

Health

Lifestyle

Finance

Entertainment

Property

Information

Keep up to date

Search

Walking can prevent low back pain, a new study shows

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

Alzheimer’s may have once spread from person to person, but the risk of that happening today is incredibly low

Can I actually target areas to lose fat, like my belly?

6 signs you’re low in iron

What is cognitive functional therapy? How can it reduce low back pain and get you moving?

Censorship or sensible: is it bad to listen to Fat Bottomed Girls with your kids?

Rob Lowe's West Wing confession

Weight loss: why you don’t just lose fat when you’re on a diet

Harrison Ford is back as an 80-year-old Indiana Jones – and a 40-something Indy. The highs (and lows) of returning to iconic roles

Opioids don’t relieve acute low back or neck pain – and can result in worse pain, new study finds

Don’t blame women for low libido. Sexual sparks fly when partners do their share of chores – including calling the plumber

The verdict: Full fat versus low fat milk

Magda Szubanski calls for "fat" people to be protected from online hate speech

Airline responds to "fat-shaming" onboard comments

Fat Bear Winner: ‘747’ lays b-ruin to rivals despite fishy voting

Ultra-processed foods: it’s not just their low nutritional value that’s a concern

Low iron is a health risk made worse by COVID

“What a low act!": Daniel Morcombe's parents outraged at upcoming film

Low-cost gel film pulls clean drinking water from desert air, raising hopes of quenching the world’s driest communities