Search

How long will you live? New evidence says it’s much more about your choices than your genes

<div class="theconversation-article-body"> One of the most enduring questions humans have is how long we’re going to live. With this comes the question of how much of our lifespan is shaped by our environment and choices, and how much is predetermined by our genes. A study recently published in the prestigious journal <a href="https://www.nature.com/articles/s41591-024-03483-9">Nature Medicine</a> has attempted for the first time to quantify the relative contributions of our environment and lifestyle versus our genetics in how we age and how long we live. The findings were striking, suggesting our environment and lifestyle play a much greater role than our genes in determining our longevity. <h2>What the researchers did</h2> This study used data from the <a href="https://www.ukbiobank.ac.uk/">UK Biobank</a>, a large database in the United Kingdom that contains in-depth health and lifestyle data from roughly 500,000 people. The data available include genetic information, medical records, imaging and information about lifestyle. A separate part of the study used data from a subset of more than 45,000 participants whose blood samples underwent something called “<a href="https://www.nature.com/articles/s41576-022-00511-7">proteomic profiling</a>”. Proteomic profiling is a relatively new technique that looks at how proteins in the body change over time to identify a person’s age at a molecular level. By using this method researchers were able to estimate how quickly an individual’s body was actually ageing. This is called their biological age, as opposed to their chronological age (or years lived). The researchers assessed 164 environmental exposures as well as participants’ genetic markers for disease. Environmental exposures included lifestyle choices (for example, smoking, physical activity), social factors (for example, living conditions, household income, employment status) and early life factors, such as body weight in childhood. They then looked for associations between genetics and environment and 22 major age-related diseases (such as coronary artery disease and type 2 diabetes), mortality and biological ageing (as determined by the proteomic profiling). These analyses allowed the researchers to estimate the relative contributions of environmental factors and genetics to ageing and dying prematurely. <h2>What did they find?</h2> When it came to disease-related mortality, as we would expect, age and sex explained a significant amount (about half) of the variation in how long people lived. The key finding, however, was environmental factors collectively accounted for around 17% of the variation in lifespan, while genetic factors contributed less than 2%. This finding comes down very clearly on the nurture side in the “nature versus nurture” debate. It suggests environmental factors influence health and longevity to a far greater extent than genetics. Not unexpectedly, the study showed a different mix of environmental and genetic influences for different diseases. Environmental factors had the greatest impact on lung, heart and liver disease, while genetics played the biggest role in determining a person’s risk of breast, ovarian and prostate cancers, and dementia. The environmental factors that had the most influence on earlier death and biological ageing included smoking, socioeconomic status, physical activity levels and living conditions. Interestingly, being taller at age ten was found to be associated with a shorter lifespan. Although this may seem surprising, and the reasons are not entirely clear, this aligns with <a href="https://www.sciencedaily.com/releases/2014/05/140509110756.htm">previous research</a> finding taller people are more likely to die earlier. Carrying more weight at age ten and maternal smoking (if your mother smoked in late pregnancy or when you were a newborn) were also found to shorten lifespan. Probably the most surprising finding in this study was a lack of association between diet and markers of biological ageing, as determined by the proteomic profiling. This flies in the face of the extensive body of evidence showing the crucial role of <a href="https://www.nature.com/articles/s43016-023-00868-w">dietary patterns</a> in chronic disease risk and longevity. But there are a number of plausible explanations for this. The first could be a lack of statistical power in the part of the study looking at biological ageing. That is, the number of people studied may have been too small to allow the researchers to see the true impact of diet on ageing. Second, the dietary data in this study, which was self-reported and only measured at one time point, is likely to have been of relatively poor quality, limiting the researchers’ ability to see associations. And third, as the relationship between diet and longevity is likely to be complex, disentangling dietary effects from other lifestyle factors may be difficult. So despite this finding, it’s still safe to say the food we eat is one of the most important pillars of health and longevity. <h2>What other limitations do we need to consider?</h2> Key exposures (such as diet) in this study were only measured at a single point in time, and not tracked over time, introducing potential errors into the results. Also, as this was an observational study, we can’t assume associations found represent causal relationships. For example, just because living with a partner correlated with a longer lifespan, it doesn’t mean this caused a person to live longer. There may be other factors which explain this association. Finally, it’s possible this study may have underestimated the role of genetics in longevity. It’s important to recognise genetics and environment don’t operate in isolation. Rather, health outcomes are shaped by their interplay, and this study may not have fully captured the complexity of these interactions. <h2>The future is (largely) in your hands</h2> It’s worth noting there were a number of factors such as household income, home ownership and employment status associated with diseases of ageing in this study that are not necessarily within a person’s control. This highlights the crucial role of addressing the social determinants of health to ensure everyone has the best possible chance of living a long and healthy life. At the same time, the results offer an empowering message that longevity is largely shaped by the choices we make. This is great news, unless you have good genes and were hoping they would do the heavy lifting. Ultimately, the results of this study reinforce the notion that while we may inherit certain genetic risks, how we eat, move and engage with the world seems to be more important in determining how healthy we are and how long we live.<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/251054/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/hassan-vally-202904">Hassan Vally</a>, Associate Professor, Epidemiology, <a href="https://theconversation.com/institutions/deakin-university-757">Deakin University</a> This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/how-long-will-you-live-new-evidence-says-its-much-more-about-your-choices-than-your-genes-251054">original article</a>. Image: Shutterstock </div>

Caring

Bruce Willis' wife issues amazing reflection on Gene Hackman's passing

As Bruce Willis continues to live with frontotemporal dementia, his wife, Emma Heming Willis, has emerged as a vocal advocate for those who support loved ones with long-term care needs. This week, she reflected on the tragic <a href="https://www.oversixty.com.au/health/caring/gene-hackman-s-cause-of-death-revealed" target="_blank" rel="noopener">deaths of legendary actor Gene Hackman and his wife</a> and caregiver, Betsy Arakawa, in a heartfelt video shared on Instagram. "So this is not something I would normally comment on, but I do really believe that there is some learning in this story," Heming Willis said of Hackman and Arakawa. The couple was found dead in their New Mexico home in late February. According to the New Mexico medical investigator’s office, Arakawa, 65, succumbed to hantavirus, a rare and often fatal disease, while Hackman, 95, passed away days later due to heart disease. Authorities revealed that Hackman had been living with Alzheimer’s disease and may not have realised he was alone after his wife's passing. Heming Willis used the heartbreaking story to highlight a crucial issue: the well-being of caregivers themselves. "It's just made me think of this broader story, and that is that caregivers need care too and that they are vital, and that it is so important that we show up for them so that they can continue to show up for their person," she stated. She further addressed a common misconception about caregivers, saying that many assume they "have it all figured out". "They've got it covered, they're good," she said before clarifying, "I don't subscribe to that. We need to be showing up for them so they can continue to show up for their person." In the caption of her video, Heming Willis reinforced her message: "Caregivers need care too. Period. Full stop. #supportcaregivers." The flood of responses to her post was immediate and heartfelt, as fans and followers shared their experiences for caring for loved ones. "I had the same terrified reaction to Gene Hackman," wrote one reader. "What must he have suffered those last days? And his wife? It’s unfathomable. My father was a dedicated caregiver to my mom. Realising that dementia takes every ounce of patience and energy, my two sisters and I were honoured to take one full day each per week (in addition to afternoon nurses two alternate days) to support my dad’s decision to keep mama at home. She’s been gone three years now and I have never once regretted those special Fridays with her. Your message is so very important." "I’m so glad you said this," wrote another reader. "Because that’s exactly what I was thinking when this happened that his wife was so devoted to him that she didn’t take care of herself and this happens a lot with women a lot! She didn’t have any children, but I’m amazed that no friends checked in on her." Heming Willis speaks from personal experience, having taken on the role of primary caregiver for her husband since his diagnosis. It was announced in 2022 that Bruce Willis would step away from his acting career due to cognitive issues, <a href="https://www.oversixty.com.au/health/caring/cruel-disease-bruce-willis-given-heartbreaking-new-diagnosis" target="_blank" rel="noopener">which were later identified as frontotemporal dementia</a> (FTD), a progressive brain disorder. The couple, who married in 2009, share two daughters, Mabel and Evelyn. Through her platform, Heming Willis remains committed to raising awareness and fostering support for those navigating the complexities of long-term care. Images: Instagram

Caring

Gene Hackman's cause of death revealed

The cause of death of legendary actor Gene Hackman, 95, and his wife Betsy Arakawa, 65, has finally been confirmed, more than a week after they were <a href="https://www.oversixty.com.au/health/caring/sad-new-details-emerge-in-gene-hackman-case" target="_blank" rel="noopener">discovered in their Santa Fe home</a>. The couple was found deceased in their residence on February 26, prompting an investigation by authorities. Dr Heather Jarrell, Chief Medical Examiner for New Mexico, disclosed at a press conference that Hackman succumbed to cardiovascular disease, with advanced Alzheimer’s disease being a significant contributing factor. His wife, Betsy Arakawa, died around seven days earlier from hantavirus pulmonary syndrome, a rare infectious disease contracted through exposure to rodents and their excrement. Authorities found evidence of rodent intrusion in the couple’s home, believed to be the source of Arakawa’s infection. Based on her movements and email communications, Dr Jarrell determined that Arakawa likely passed away on February 11, while Hackman is believed to have died on February 18. Santa Fe County Sheriff Adan Mendoza confirmed that Hackman was likely at home with his deceased wife for seven days before his own death. Dr Jarrell noted that Hackman was in "very poor health", and it was unclear how he managed in his final days without his wife's assistance. Given his advanced Alzheimer’s, Jarrell suggested that it was possible he was unaware that his wife had passed away. “There was no food in his stomach, which means he had not eaten recently, but he had no evidence of dehydration,” she stated. Hantavirus pulmonary syndrome is a severe and often fatal respiratory disease. According to the Mayo Clinic, it begins with flu-like symptoms and rapidly progresses to serious lung and heart complications. The best prevention is avoiding contact with rodents and properly managing rodent-prone areas. Dr Jarrell’s findings confirmed that Hackman had severe heart disease, with evidence of multiple prior heart attacks and chronic high blood pressure. A full-body post-mortem examination showed no signs of trauma. He tested negative for COVID-19, influenza and other respiratory illnesses, as well as hantavirus and carbon monoxide poisoning. Similarly, Arakawa’s autopsy revealed no external or internal trauma. Laboratory tests confirmed the presence of hantavirus, ruling it as the cause of her death. Other tests for respiratory viruses and toxins returned negative results. Dr Jarrell said that there were “no other significant natural disease findings” in either case, and that all medications found in the home were taken as prescribed and did not contribute to their deaths. The tragic passing of Gene Hackman and Betsy Arakawa marks the end of an era for Hollywood, with fans mourning the loss of the two-time Academy Award-winning actor. Hackman, known for his roles in The French Connection, Unforgiven and The Royal Tenenbaums, retired from acting in 2004. The couple had been residing in Santa Fe for many years, enjoying a quiet life away from the public eye. Image: Instagram

Caring

Sad new details emerge in Gene Hackman case

Authorities in New Mexico have shared a grim new update on the shocking deaths of Gene Hackman and his wife. New information has suggested that the Hollywood actor, 95, and his wife, 63, had passed away in their home nine days before their bodies were found. The bodies of the deceased couple, who were married for 24 years, were found by a maintenance worker who spotted their bodies through a window. Authorities are yet to determine a cause of death for both Hackman and Arakawa but have repeatedly ruled out foul play. In an investigation update on Friday, Santa Fe County Sheriff Adan Mendoza said a pathologist had advised that tests for carbon monoxide poisoning were negative. Mendoza also said the pathologist was given an insight into Hackman's last moments due to the activity in his pacemaker. "An initial interrogation was conducted of Mr Hackman's pacemaker. This revealed that his last event was recorded on February 17th, 2025," he told reporters. "It is a good assumption that was his last day of life." However it remains unclear whether Hackman, who was found in the kitchen of the home, or Arakawa, who was located in a bathroom, died first. One of the couple's dogs was also located deceased in the bathroom, while two other dogs were found alive at the property. Alongside Arakawa's body, police found an orange prescription pill bottle in the bathroom and pills scattered across the floor. While a toxicology report has been requested on the pills, as well as other medications found inside the house, the report could take months to be completed. The discovery of the pills was described as "something of concern", with Mendoza telling NBC News: "That's obviously very important evidence at the scene". Hackman appeared in more than 80 films throughout his career, as well as on television and the stage after his breakout role as the brother of bank robber Clyde Barrow in 1967's Bonnie and Clyde, earning him his first Oscar nomination. He won an Oscar for best actor in 1972 for his portrayal of detective Popeye Doyle in The French Connection, and in 1993 won an Oscar for best supporting actor for Unforgiven. Image credits: MediaPunch/Shutterstock Editorial

Caring

Got no COVID-19 symptoms? A gene mutation might be the reason

<div> <div class="copy"> A global study has unearthed a possible genetic reason why some people infected with the virus that causes COVID-19 show no symptoms. Human leukocyte antigens – or HLAs – are important genes that support immune function in the human body, particularly in identifying viral pathogens. And a particular variation in the HLA-B complex has been found to at least double the likelihood that a person infected with SARS-CoV-2 will be asymptomatic. For people who inherit a copy of the HLA-B15 variant from one parent, there was a 2.4 times greater chance of avoiding symptoms. Homozygous carriers — born with copies of the variant from each parent — were 8.5 times more likely to avoid symptoms. It’s a somewhat common variant among certain ethnicities – about 1 in 10 people with European ancestry are potential carriers – but having the gene is not a guaranteed protector against coronavirus symptoms. The findings, <a href="https://doi.org/10.1038/s41586-023-06331-x" target="_blank" rel="noreferrer noopener" data-type="URL" data-id="https://doi.org/10.1038/s41586-023-06331-x">published</a> in Nature, have emerged from a joint study between researchers at the University of California San Fransisco and Australian institutions including Latrobe University, Monash University and the QIMR Berghofer Centre. The research came about almost by accident. <div class="in-content-area content-third content-right"><a href="https://cosmosmagazine.com/health/covid/link-between-blood-type-and-risk-of-covid-19-infection/"> </a></div> Co-lead authors Professor Stephanie Gras from Latrobe and Jill Hollenbach from UCSF first met at a research conference in May 2022 and pooled their resources to track the association of possible gene variations with COVID-19 symptoms. Their teams narrowed a group of 30,000 people with high-quality HLA data to a cohort of about 1,500 unvaccinated people who tested positive for the virus. They then focussed on five locations of interest in the HLA genes while monitoring the emergence of symptoms to determine which variants, if any, might have a greater linkage to being COVID asymptomatic. “The [SARS-CoV-2] virus gets inside cells and ‘presents’ some small part of the virus on the surface via the HLA molecule,” Gras explains. “Those act as a red flag for T cells. The cell sends the signal to the T cell that it has been infected with the virus, and the T cells get activated and kill that [infected] cell. “HLA-B15 can actually present a small part of the spike protein that is very similar between SARS-CoV-2 and seasonal coronaviruses… [that] circulate every year in the population and give us the common cold during winter most of the time. They share some similarities.” The understanding provides a possible application for future treatments. Now an association between the variant and asymptomatic cases has been identified, the Gras and Hollenbach teams have begun to study the interaction between HLA-B15 and the SARS-CoV-2 spike protein at the atomic level. That research is already underway, including at the Australian Synchrotron at the Australian Nuclear Science and Technology Organisation. “We’re doing atomic-level models of proteins to understand the interaction,” Gras says. “We want to compare the T cells within people who are asymptomatic with HLA-B15 and people who are not asymptomatic with HLA-B15. Actually, HLA-B15 is not a magic bullet, you can have it and still have severe COVID.” Image credits: Getty Images </div> <div id="contributors"> <a href="https://cosmosmagazine.com/health/covid/got-no-covid-19-symptoms-a-gene-mutation-might-be-the-reason/">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/matthew-agius">Matthew Ward Agius</a>. </div> </div>

Body

“Irwin genes are strong”: Bindi shares adorable candid snap

Bindi Irwin has delighted fans after sharing a sweet snap of her two-year-old daughter, Grace Warrior cuddling a giant tortoise. The wildlife warrior took to Instagram to share the sweet snap with a comparison photo of herself hugging a giant tortoise when she was around Grace’s age. “Holding my newborn daughter wondering if she’ll love wildlife like I did” she captioned one of the photos in the Reel. The next two photos showed comparison photos of the mother-daughter duo which showed that the apple doesn’t fall far from the tree. “Our Grace Warrior, the Wildlife Warrior," she captioned the post. <blockquote class="instagram-media" style="background: #FFF; border: 0; border-radius: 3px; box-shadow: 0 0 1px 0 rgba(0,0,0,0.5),0 1px 10px 0 rgba(0,0,0,0.15); margin: 1px; max-width: 540px; min-width: 326px; padding: 0; width: calc(100% - 2px);" data-instgrm-captioned="" data-instgrm-permalink="https://www.instagram.com/reel/Cs4wPGzBjZZ/?utm_source=ig_embed&utm_campaign=loading" data-instgrm-version="14"> <div style="padding: 16px;"> <div style="display: flex; flex-direction: row; align-items: center;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 40px; margin-right: 14px; width: 40px;"> </div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 100px;"> </div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 60px;"> </div> </div> </div> <div style="padding: 19% 0;"> </div> <div style="display: block; height: 50px; margin: 0 auto 12px; width: 50px;"> </div> <div style="padding-top: 8px;"> <div style="color: #3897f0; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: 550; line-height: 18px;">View this post on Instagram</div> </div> <div style="padding: 12.5% 0;"> </div> <div style="display: flex; flex-direction: row; margin-bottom: 14px; align-items: center;"> <div> <div style="background-color: #f4f4f4; border-radius: 50%; height: 12.5px; width: 12.5px; transform: translateX(0px) translateY(7px);"> </div> <div style="background-color: #f4f4f4; height: 12.5px; transform: rotate(-45deg) translateX(3px) translateY(1px); width: 12.5px; flex-grow: 0; margin-right: 14px; margin-left: 2px;"> </div> <div style="background-color: #f4f4f4; border-radius: 50%; height: 12.5px; width: 12.5px; transform: translateX(9px) translateY(-18px);"> </div> </div> <div style="margin-left: 8px;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 20px; width: 20px;"> </div> <div style="width: 0; height: 0; border-top: 2px solid transparent; border-left: 6px solid #f4f4f4; border-bottom: 2px solid transparent; transform: translateX(16px) translateY(-4px) rotate(30deg);"> </div> </div> <div style="margin-left: auto;"> <div style="width: 0px; border-top: 8px solid #F4F4F4; border-right: 8px solid transparent; transform: translateY(16px);"> </div> <div style="background-color: #f4f4f4; flex-grow: 0; height: 12px; width: 16px; transform: translateY(-4px);"> </div> <div style="width: 0; height: 0; border-top: 8px solid #F4F4F4; border-left: 8px solid transparent; transform: translateY(-4px) translateX(8px);"> </div> </div> </div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center; margin-bottom: 24px;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 224px;"> </div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 144px;"> </div> </div> <p style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; line-height: 17px; margin-bottom: 0; margin-top: 8px; overflow: hidden; padding: 8px 0 7px; text-align: center; text-overflow: ellipsis; white-space: nowrap;"><a style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: normal; line-height: 17px; text-decoration: none;" href="https://www.instagram.com/reel/Cs4wPGzBjZZ/?utm_source=ig_embed&utm_campaign=loading" target="_blank" rel="noopener">A post shared by Bindi Irwin (@bindisueirwin)</a> </div> </blockquote> The adorable photo has been praised by fans who commented how proud Steve Irwin would be of his daughter and granddaughter. "It’s in the Irwin blood! You guys have the most beautiful connection with wildlife and each other! Steve Irwin genes are strong!” wrote one fan. "Your dad is probably so so proud looking down,” commented a second person. "This gives me happy goosebumps babe,” wrote a third. Images: Instagram

Family & Pets

KISS concert halted as Gene Simmons falls ill on stage

KISS singer Gene Simmons gave fans - and bandmates - a fright when dehydration got the better of him live on stage, and the group were forced to bring their entire concert to a halt. In a video from the event, KISS’ Paul Stanley can be seen addressing the crowd, telling them that “we’re gonna have to stop to take care of him. Because we love him, right?” He goes on to call for a cheer for Simmons, with the 73-year-old catching his breath on a chair on stage - the same chair that he remained in for the rest of the show, after a five minute break to assure he was well enough to continue. <blockquote class="twitter-tweet"> Gene Simmons, baixista e vocalista do Kiss, passa mal e show é brevemente interrompido na Arena da Amazônia. <a href="https://t.co/nphJEj1PQo">pic.twitter.com/nphJEj1PQo</a> — A Crítica (@ACritica) <a href="https://twitter.com/ACritica/status/1646372105523478529?ref_src=twsrc%5Etfw">April 13, 2023</a></blockquote> And while fans were concerned for the singer, he later took to social media to assure them that he was “fine” and looking forward to the band’s next stadium performance. “I’m fine. Yesterday at Manaus Stadium in Brazil, [I] experienced weakness because of dehydration,” he explained. “We stopped for about five minutes, I drank some water, and then all was well. Nothing serious.” “Brazil is hotter than hell!!” one fan responded, “so glad you're okay and I can't wait to see you in São Paulo! Take care, god of thunder!!” “Even the God of Thunder needs hydration,” another agreed. “Good to hear you're doing well.” <blockquote class="twitter-tweet"> Hey everybody, thanks for the good wishes. I’m fine. Yesterday at Manaus Stadium in Brazil, experienced weakness because of dehydration. We stopped for about five minutes, I drank some water, and then all was well. Nothing serious. Tomorrow, Bogota Stadium. See you there! — Gene Simmons (@genesimmons) <a href="https://twitter.com/genesimmons/status/1646530305791266818?ref_src=twsrc%5Etfw">April 13, 2023</a></blockquote> And as news broke around the world of what had gone down in Brazil, Simmons returned with another round of assurances, writing that it was “not a big deal” while again thanking everyone for their well wishes. “Last night we played Amazon jungle Stadium/Brazil. Humidity and temperature were sky high. I was dehydrated and was forced to sit for a song,” he said. “We got back on stage in 5 minutes & finished the show.” It was enough for his fans, who were quick to share their delight that their star was okay, as well as voicing their excitement for upcoming shows - with a good portion of requests for the singer to take care of himself, and avoid a repeat performance. “Happy to hear you're doing better,” one wrote. “Even more happy it wasn’t anything serious.Ya'll take care.” “Frankly, I don’t know [how] you do it every night. You’re amazing!” another declared. Meanwhile, some could see the humour in it all now that their fears had been put to rest, with one joking “and who says playing music couldn't be dangerous”. Images: Twitter

Caring

Super rare pic of unrecognisable Gene Hackman

For the first time in a long time, legendary actor Gene Hackman has been spotted out and about at the age of 93. The icon had been reclusive in recent years, and these are the first photos of him snapped in a very long time. The Superman star still seemed fit and looked quite healthy in the snaps taken in Santa Fe, New Mexico. The retired actor was spotted enjoying a fast food lunch at a parking lot after going through the Wendy’s drive-thru. He is still sporting his signature moustache in the rare sighting. <blockquote class="twitter-tweet"> New photos of Hollywood Legend Gene Hackman have been released. He is currently 93-years-old. These are the first photos of him in years. <a href="https://t.co/5pn1wXN81w">pic.twitter.com/5pn1wXN81w</a> — Daily Loud (@DailyLoud) <a href="https://twitter.com/DailyLoud/status/1633270131324223489?ref_src=twsrc%5Etfw">March 8, 2023</a></blockquote> Hackman’s last movie role was with Ray Romano and Christine Baranski in the 2004 comedy Welcome To Mooseport. In July 2004, Hackman was interviewed by Larry King, where he announced there were no new film projects lined-up and believed his acting career was over. Years later, the star confirmed his retirement while promoting his third novel Escape From Andersonville, back in 2008. In an interview with CQ in 2011, he was asked if he would ever come out of retirement to do another film, and he responded, “If I could do it in my own house, maybe, without them disturbing anything and just one or two people.” CQ also asked him, “how do you want to be remembered?" “As someone who tried to portray what was given to them in an honest fashion. I don't know, beyond that. I don't think about that often, to be honest. I'm at an age where I should think about it.” He said with a laugh. Hackman has long been one of the most highly regarded film actors of all time, leading his Mississippi Burning director Alan Parker to state that “he is incapable of bad work. Every director has a shortlist of actors he’d die to work with, and I’ll bet Gene’s on every one.” The thespian really made waves when he was nominated for an Oscar for the Best Supporting Actor category for the 1970s film I Never Sang For My Father. A year later, he became a leading man in incredible fashion, winning the Academy Award for Best Actor in his New York City Detective Jimmy 'Popeye' Doyle in The French Connection (1971). Hackman’s career only went up from there, with countless awards under his belt, including two Oscars, two BAFTA awards and two Golden Globes. Image credit: Getty

Movies

Chris Hemsworth’s Alzheimer’s gene doesn’t guarantee he’ll develop dementia

Chris Hemsworth, famous for his role as the god Thor in Marvel Cinematic Universe movies, has announced he will be <a href="https://www.theguardian.com/film/2022/nov/21/chris-hemsworth-to-take-time-off-from-acting-after-discovering-alzheimers-risk" target="_blank" rel="noopener">taking a break</a> from acting after being told he has two copies of the <a href="https://www.nia.nih.gov/news/study-reveals-how-apoe4-gene-may-increase-risk-dementia" target="_blank" rel="noopener">APOE4 gene</a>, increasing his risk of Alzheimer’s. Having one copy of the <a href="https://www.science.org/doi/abs/10.1126/science.8346443" target="_blank" rel="noopener">APOE4 gene</a> increases your risk for Alzheimer’s 2-3 times. Two copies increases your risk 10-15 times. But the key here is “risk”. Having one or more copies of the gene doesn’t guarantee Chris or anyone else in a similar situation will go on to develop Alzheimer’s, the most common form of dementia. Sharing the news Hemsworth’s willingness to share his concerns about developing Alzheimer’s with millions should be applauded. It’s a reminder to all of us to keep an eye on our health and reduce our risk of future illness. Alzheimer’s, and dementia more broadly, is <a href="https://www.dementiastatistics.org/statistics/global-prevalence/" target="_blank" rel="noopener">set to challenge</a> health-care systems worldwide. In Australia alone there are <a href="https://www.dementia.org.au/statistics" target="_blank" rel="noopener">up to</a> 500,000 people with dementia, supported by almost 1.6 million carers. By 2036, about <a href="https://www.dementia.org.au/sites/default/files/NATIONAL/documents/The-economic-cost-of-dementia-in-Australia-2016-to-2056.pdf" target="_blank" rel="noopener">450 people</a> are predicted to be diagnosed daily. So understanding how APOE4 alters the risk for the major cause of dementia may be pivotal in preventing cases. But not all people with the APOE4 gene go on to develop Alzheimer’s. This means that there may be a combination of environmental factors interplaying with the gene that lead some people to develop Alzheimer’s, while others do not. What’s APOE4 got to do with Alzheimer’s? Most Australians have APOE3 or APOE2 genes. In Caucasians it’s only <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5531868/" target="_blank" rel="noopener">about 15%</a>, like Hemsworth, who have inherited an APOE4 gene. The APOE gene types are best known for their role in modulating the metabolism of lipids (fats), such as cholesterol and triglycerides. They code for synthesis of different versions of the protein APOE, with subtle differences in structure. The APOE proteins become an integral part of lipoproteins in the blood. These are the fat-carrying particles your GP measures to consider your risk of heart disease. APOE proteins have a similar function in the brain, to modulate lipid levels. But in the context of Alzheimer’s, researchers study it for its effect on the integrity of brain cells. Accumulating evidence <a href="https://www.sciencedirect.com/science/article/pii/S0197458022000550" target="_blank" rel="noopener">suggests</a> APOE4, is associated with brain inflammation and cellular damage. <blockquote class="twitter-tweet"> APOE4 is the strongest genetic risk factor for Alzheimer’s disease. A study in <a href="https://twitter.com/Nature?ref_src=twsrc%5Etfw">@Nature</a> establishes a functional link between APOE4, cholesterol, myelination and memory, offering therapeutic opportunities for Alzheimer’s disease. <a href="https://t.co/bNsmDVPfFW">https://t.co/bNsmDVPfFW</a> <a href="https://t.co/58odE1JASl">pic.twitter.com/58odE1JASl</a> — Nature Portfolio (@NaturePortfolio) <a href="https://twitter.com/NaturePortfolio/status/1594762841487249410?ref_src=twsrc%5Etfw">November 21, 2022</a></blockquote> Can we prevent Alzheimer’s? 1. Look after your capillaries Damaged and leaky blood vessels (capillaries) in the brain lead to inflammation, the death of brain cells and cognitive impairment. In fact, in Alzheimer’s, damaged capillaries are the earliest sign of the type of brain damage that causes disease. The protein encoded by the APOE4 gene may be less able to support healthy capillaries in the brain. <a href="https://www.sciencedirect.com/science/article/abs/pii/S0163782709000563" target="_blank" rel="noopener">We suggested</a> APOE4 increases the abundance of specific complexes of lipoproteins and proteins in blood that silently damage brain capillaries, causing them to leak. We also see more brain capillary leakage in mice fed Western-style diets richer in saturated fats. The relationship between how the APOE proteins mediate lipid metabolism and capillary health in humans is poorly understood. But we have 60 years of research knowledge to say with confidence that eating foods good for the heart should also be good for the brain. This is particularly relevant for people with the APOE4 gene. So if you have the APOE4 gene and want to minimise your risk of Alzheimer’s, a healthy diet is a good place to start. <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img src="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=316&fit=crop&dpr=1 600w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=316&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=316&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=397&fit=crop&dpr=1 754w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=397&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=397&fit=crop&dpr=3 2262w" alt="Capillaries" /></a><figcaption>Looking after your capillaries with a healthy diet is a good place to start. <a class="source" href="https://www.shutterstock.com/image-illustration/system-many-small-capillaries-branch-out-1745173364" target="_blank" rel="noopener">Shutterstock</a></figcaption></figure> 2. Give your brain a break Reducing unnecessary stimuli to “give your brain a rest” may have big impact over decades of your life. The latter may be a more important consideration if you have the APOE4 gene. That’s because the APOE gene is also linked to how the brain uses energy, which may lead to more <a href="https://www.frontiersin.org/articles/10.3389/fnmol.2018.00216/full" target="_blank" rel="noopener">oxidative stress and damage</a>. While we’ve yet to collect robust data in humans, take a digital detox now and again, plan some down time, and avoid unnecessary stress if you can. Should we test for the APOE4 gene? Some people might be tempted to get tested for the APOE4 gene, especially if there’s a family history of Alzheimer’s. But unless genetic testing is going to change your treatment (for instance, by taking certain medications to slow progression of brain damage), or your behaviour to minimise your risk Alzheimer’s, then testing is not justified. We can’t change the genes our parents gifted us, but we can change our environment. Poor diet, every drop of alcohol you drink, obesity and diabetes, high blood pressure and sedentary behaviour <a href="https://www.dementia.org.au/risk-reduction" target="_blank" rel="noopener">all contribute, over time</a>, to poorer vascular health and increase your risk of dementia. We’re still learning about how these risk factors for Alzheimer’s interact with the APOE4 gene. But there is no reason we shouldn’t all take greater responsibility for minimising our risk of dementia now, whether we have the APOE4 gene or not.<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/195094/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> Writen by John Mamo. Republished with permission from <a href="https://theconversation.com/chris-hemsworths-alzheimers-gene-doesnt-guarantee-hell-develop-dementia-heres-what-we-can-all-do-to-reduce-our-risk-195094" target="_blank" rel="noopener">The Conversation</a>. Image: Instagram

Mind

Evidence that human evolution driven by major environmental pressures discovered

The genes of ancient humans might have changed substantially due to environmental pressures and change, say an international team of researchers. A widely held belief related to human evolution is that our ancient ancestors’ ability to fashion tools, shelter, and use advanced communication skills may have helped to shield them from large environmental impacts such as changing climate, disease and exposure to other events affecting mortality. But research led out of Australian Centre for Ancient DNA at the University of Adelaide suggests that beneficial genes may have played a more important role in preserving our ancestors. Until now, the sudden increase in frequency of these genes in human groups was masked by the exchange of DNA between people during reproduction. Now, analyses of more than one thousand ancient genomes dating as far back as 45,000 years ago have found historic signals showing genetic adaptation was more common than previously thought. The study of evolutionary events, says the study’s co-lead author Dr Yassine Souilmi, has increased substantially in recent years, as these are the points where human genetics take historic turns. “Evolutionary events [are] exactly what shape our genetic diversity today,” Souilmi tells Cosmos. “That’s what makes us vulnerable to certain diseases [and] resistant to others. “Having a good understanding of evolution, we can have a better understanding of who we are.” Previous research by the Centre has uncovered a range of evolutionary trends, from historic climate change causing the demise of ancestral lions and bears, to the first interactions between humans and coronaviruses 20,000 years ago. And the broader field of research into ancient DNA has shed light on important moments in human history. Only recently did analyses of ancient genes uncover locations on the human genome associated with surviving Yersinia pestis – the bacterium that causes the bubonic plague. <h2>Single events probably triggered selection</h2> This study, published in Nature Ecology and Evolution, has similarly found environmental events might have been more influential on evolution among Eurasian groups. Such events might lead to a point of natural selection. Take, for instance, the emergence of a pathogen. If such a disease could kill people, those who managed to survive and continue reproducing would pass down favourable traits to subsequent generations. “Natural selection acts in two different mechanisms,” says Souilmi. “It only cares about whether you’re procreating successfully… when it acts, it’s either killing a lot of people, [preventing] some people from reproducing successfully, or some people are just not finding mates because they have some sort of ailment that’s not allowing them to mate successfully, or might make them undesirable. “What we’re finding is that the signal of natural selection we detected in this [research] was likely a single event, because the signal is clustered in time in a very early migration out of Africa. “Not all of the [events] we detected occurred at the same time, but the bulk of them did.” <h2>A mirror to the present</h2> This ‘agnostic’ study did not seek to identify the external pressures leading to the selection events indicated in these ancient genes, but future research by the team will seek to uncover that information. Studies like this, or those into specific pressures like the influence of the Black Death or coronaviruses on humans, show the impact of environmental change on our genetics. Souilmi says this is both insightful and cautionary, as environmental change in the present could be studied by humans in the future. He speculates that changes in the Earth’s climate, or the emergence of new pathogens, likely imposed selection pressures on ancient groups, whether through forcing shortages or changes to food supply or imposing physiological stressors. “Very likely, it’s the environment, the temperature, the weather patterns, that would have somewhat impacted the dietary regime of our ancestors out of Africa, and pathogens would have driven this [genetic] adaptation, which has shaped our genetic diversity now,” Souilmi says. “The direct lesson, socially, now, is that if we’re ever faced with events that are similar to that, we are not as immune to extreme episodes of adaptation where a lot of people might die, or be unable to reproduce. “Unless we do something to counteract the environmental changes, or viruses, bacterial or other pandemics, it could be a bad thing.” This article originally appeared on <a href="https://cosmosmagazine.com/science/human-evolution-driven-by-environment/" target="_blank" rel="noopener">cosmosmagazine.com</a> and was written by Matthew Agius. Image: Shutterstock

Body

Excelling as a musician takes practice and requires opportunities – not just lucky genes

What makes talented musicians so good at what they do? There’s plenty of evidence that people can be born that way. Research findings suggest that about <a href="https://doi.org/10.1136/jmg.2007.056366">half of musical ability is inherited</a>. Even if that’s true, it doesn’t mean you must have musical talent in your genes to excel on the bass, oboe or drums. And even if you’re fortunate enough to belong to a family that includes musicians, you would still need to study, practice and get expert guidance to play well. As a <a href="https://scholar.google.com/citations?user=34DZlUIAAAAJ&hl=en&oi=ao">music professor and conductor</a>, I’ve seen the role that practice and experience play in propelling musicians toward mastery and success. There are some factors that help a musician get started – and heredity could be one of them. But musical skill is ultimately a complex interplay between <a href="https://doi.org/10.1177%2F0022429416680096">lots of practice and high-quality instruction</a>. <h2>The role genes can play</h2> Of course many great musicians, including some who are world famous, are related to other musical stars. Liza Minnelli, the famed actress, singer and dancer, is one of the late entertainer <a href="https://hollywoodlife.com/feature/judy-garland-kids-4728886/">Judy Garland’s three children</a>. <a href="https://people.com/music/jon-batiste-everything-to-know">Jon Batiste</a> – “The Late Show” bandleader, pianist and composer who has won Emmy, Oscar and Golden Globe awards – has at least 25 musicians in his family. Saxophonist Branford, trumpeter Wynton, trombonist Delfeayo and drummer Jason Marsalis are the <a href="https://www.npr.org/sections/coronavirus-live-updates/2020/04/02/825717204/ellis-marsalis-patriarch-of-new-orleans-most-famous-musical-family-has-died">sons of pianist Ellis Marsalis</a>. Singer and pianist <a href="https://www.notablebiographies.com/news/Ge-La/Jones-Norah.html">Norah Jones</a> is the daughter of Indian sitar player <a href="https://www.vogue.in/culture-and-living/content/norah-jones-on-her-relationship-with-pandit-ravi-shankar-september-2020-cover-interview-hope">Ravi Shankar</a>, though Jones had little contact with her renowned father while growing up. Absolute pitch, also known as perfect pitch, is the ability to recognize and name any note you hear anywhere. Researchers have found that it <a href="https://doi.org/10.1086/301704">may be hereditary</a>. But do you need it to be a great musician? Not really. <h2>Most people are born with some musical ability</h2> I define musical ability as the possession of talent or potential – the means to achieve something musical. Then there’s skill, which I define as what you attain by working at it. You need at least some basic musical ability to acquire musical skills. Unless you can hear and discern pitches and rhythms, you can’t reproduce them. But people may overestimate the role of genetics because, with very rare exceptions, <a href="https://www.apa.org/monitor/feb05/absolute">almost everyone can perceive pitches</a> and rhythms. My research regarding children’s musicality suggests measures of singing skills are <a href="https://doi.org/10.1177/0022429416666054">normally distributed</a> in the population. That is, pitch ability follows a <a href="https://www.investopedia.com/terms/b/bell-curve.asp">bell curve</a>: Most people are average singers. Not many are way below average or excellent. My team’s most recent research suggests that this distribution is <a href="https://doi.org/10.1177/00224294211032160">true for rhythm</a> in addition to pitch. Not surprisingly, some musical skills are correlated. The more training you have on specific musical skills, the <a href="https://doi.org/10.1177/00224294211011962">better you’ll test on certain others</a>. This is probably because musical experience enhances other musical abilities. To sum it up, an emerging body of research indicates that practice doesn’t make perfect. But for most people, it helps a lot. <h2>Lessons and practice are essential</h2> What about people who say they they can’t keep a beat? It turns out that they almost always can track a steady beat to music. They just haven’t done it enough. Indeed, the last time I gave a nonbeliever our lab’s test for rhythm perception, she performed excellently. For that and for singing, some people just need <a href="https://www.nytimes.com/2020/01/21/magazine/how-to-sing-in-tune.html">a little help</a> to move past assumptions they lack talent: You can’t say you’re incapable of something if you haven’t spent time trying. Some researchers and <a href="https://strategiesforinfluence.com/malcolm-gladwell-10000-hour-rule/">journalists have promoted</a> the idea it takes <a href="https://doi.org/10.1037/0033-295X.100.3.363">10,000 hours of practice or training to master</a> a new skill. Innate ability puts people at different starting lines toward musical mastery. But once you’ve started to study an instrument or singing style, skill development depends on many other factors. Getting lessons, practicing often and being in a musical family may make those more likely. For example, Lizzo, a hip-hop superstar and classically trained flute player, had the luck to <a href="https://www.thefamouspeople.com/profiles/lizzo-44986.php">grow up in family of music lovers</a>. They all had their own taste in music. Her success is a microcosm of why a well-rounded musical education for young people matters. The singers in the choir I lead at Penn State have a range of experience, from a little to a lot. Yet soon after they join it, they develop the ability to <a href="https://doi.org/10.1177/87551233211040726">pick a good key and starting pitch</a> as they get to know their own voices. Practicing more doesn’t change your baseline potential, it just changes what you can presently do. That is, if you practice a specific song over and over again, eventually you’re going to get better at it. Jonathon Heyward, the Baltimore Symphony’s new conductor, who has <a href="https://www.nytimes.com/2022/07/21/arts/music/jonathon-heyward-baltimore-symphony-orchestra.html">no musicians in his family</a>, has worked really hard to excel. He started taking cello lessons at age 10 and hasn’t stopped since, playing and practicing and studying. <h2>Privilege can play a role</h2> Socioeconomic factors can also enter the equation. While conducting research, I’ve seen high-income college students from high-income families, with more years of musical experience, perform better than their classmates who have lower-income backgrounds and had fewer opportunities. Genes can give someone a head start. At the same time, having a quiet space where you can practice on an acoustic instrument or a digital workstation might make a more decisive difference for the musical prospects of most children. The same goes for having money for private lessons or access to free classes. Even so, many of the best musicians, including jazz greats <a href="https://www.louisarmstronghouse.org/biography/">Louis Armstrong</a> and <a href="https://www.pbs.org/wnet/americanmasters/billie-holiday-about-the-singer/68/">Billie Holiday</a>, grew up facing many hardships. With the right conditions for practice and gaining experience, who knows where the next Liza or Lizzo will come from. Image credits: Getty Images This article originally appeared on <a href="https://theconversation.com/excelling-as-a-musician-takes-practice-and-requires-opportunities-not-just-lucky-genes-186693" target="_blank" rel="noopener">The Conversation</a>.

Music

Surprise discovery shows you may inherit more from your mum than you think

What if we could inherit more than our parents’ genes? What if we could inherit the ability to turn genes on and off? These possibilities have come to light after our <a href="https://www.nature.com/articles/s41467-022-32057-x" target="_blank" rel="noopener">recent study</a>, published in Nature Communications. We found information in addition to our genes was passed down from mum to offspring to affect how their skeleton develops. That’s the “epigenetic” information that’s normally reset between generations. Our research was in mice, the first case of its kind in mammals where a long-lasting epigenetic effect from the mother’s egg is carried down to the next generation. This has lifelong consequences for that generation’s health. However, we cannot be certain the equivalent epigenetic changes are also inherited in humans, including the implications for how our skeleton develops and potential impact on diseases. <h2>Hold up, what’s epigenetics again?</h2> Our genes (packages of DNA) tell our body to make certain proteins. But our cells also need instructions to know whether a gene should be used (switched on) or not (switched off). These instructions come in the form of chemical or “epigenetic” tags (small molecules) that sit on top of the DNA. You accumulate these tags throughout your life. Think of how punctuation marks help a reader understand a sentence. Epigenetic tags allow the cell to understand a DNA sequence. Without these epigenetic tags, the cell might make a protein at the wrong time or not at all. Timing is crucial in how embryos develop. If certain genes are expressed (switched on to produce a protein) too early or too late, an embryo will not develop properly. <h2>What did we find?</h2> We were interested in understanding the function of a protein in mouse eggs (ova) called SMCHD1. By removing SMCHD1 from mouse eggs, we found mice that developed from eggs lacking SMCHD1 had an altered skeleton, with some vertebrae in the spine being disrupted. This could only be explained by an epigenetic change due to the loss of SMCHD1 in the egg. In particular, we looked at a set of genes known as Hox genes. These encode a series of proteins known to control how mammals’ skeletons develop. Hox genes are found in all animals, from flies to humans, and are crucial for setting up our spine. Evolution has finely tuned the timing of the expression of Hox genes during embryonic development to ensure the skeleton is assembled correctly. <blockquote class="twitter-tweet"> Happy to share that my first first author paper is out in <a href="https://twitter.com/NatureComms?ref_src=twsrc%5Etfw">@NatureComms</a> showing that maternal SMCHD1 regulates Hox genes in the mouse embryo! Thanks to my PhD supervisors <a href="https://twitter.com/BlewittMarnie?ref_src=twsrc%5Etfw">@BlewittMarnie</a> <a href="https://twitter.com/Eddy_McGlinn?ref_src=twsrc%5Etfw">@Eddy_McGlinn</a> <a href="https://twitter.com/hashtag/Epigenetics?src=hash&ref_src=twsrc%5Etfw">#Epigenetics</a> <a href="https://twitter.com/hashtag/InHoxWeTrust?src=hash&ref_src=twsrc%5Etfw">#InHoxWeTrust</a> <a href="https://t.co/taYQmt1NAU">https://t.co/taYQmt1NAU</a> 1/n — Natalia Benetti (@nataliabenetti_) <a href="https://twitter.com/nataliabenetti_/status/1551709619361239040?ref_src=twsrc%5Etfw">July 25, 2022</a></blockquote> Our study showed that epigenetic tags established by the mother’s SMCHD1 in her egg can impact how these Hox genes are expressed in her offspring. The findings are a big surprise because almost all epigenetic tags in the egg are erased shortly after conception. Think of this a bit like a factory reset. This means it’s unusual to have epigenetic information from the mother’s egg carried on to her offspring to shape how they grow. <h2>What does this mean for us?</h2> Our findings suggest even the genes you don’t inherit from your mother can still influence your development. This may have implications for the children of women with variants in their SMCHD1 gene. Variations in SMCHD1 cause human diseases such as a form of <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/muscular-dystrophy" target="_blank" rel="noopener">muscular dystrophy</a>. In the future, SMCHD1 might be a target for new medicines to alter how the protein functions and help patients with diseases caused by variations in SMCHD1. So it’s important to understand what consequences the disruption of SMCHD1 in the egg might have on future generations. <h2>How about other diseases?</h2> Scientists are now beginning to understand that the epigenetic tags added to our genes are sensitive to changes in the environment. This can mean environmental variations, such as our diet or level of physical activity, can affect how our genes are expressed. However, these changes do not alter the DNA itself. The epigenetic state undergoes the most changes when the egg is developing and during very early embryonic development, due to the “factory reset” between generations. This means the embryo is more vulnerable to epigenetic, including environmental, changes during this developmental window. As we discover more cases where epigenetic information is inherited from the mother, there may be instances where the diet or other environmental changes the mother experiences could impact the next generation. Given that scientists can now study what happens in a single egg, we are well placed to determine how that might happen and work out what exactly we could be inheriting. This article originally appeared in The Conversation. Image: Shutterstock

Body

Keeping to the beat controlled by 69 genes – not just our feet

Are you a dancing queen or do you have two left feet? Turns out that keeping to the beat is partly to do with our <a class="spai-bg-prepared" href="https://www.nature.com/articles/news.2007.359" target="_blank" rel="noreferrer noopener">genetics</a>. An international team of researchers conducted a study on the genetic variation of 606,825 individuals, all of whom completed a musical ability questionnaire (including “Can you clap in time with a musical beat?”), with some also participating in beat synchronisation experiments including telling rhythms apart (Phenotype Experiment 1) and tapping in time with music (Phenotype Experiment 2). Of the participants, 91.57% said yes to the question, “Can you clap in time with a musical beat?” Those who said yes also scored higher in the rhythm perception and tapping synchrony experiments. Looking at the genetic variation, 69 genes showed significant difference between the rhythmic and arhythmic participants, with VRK2 being the most strongly associated. This gene has been linked previously to behavioural and psychiatric traits (including depression, schizophrenia and developmental delay), suggesting a biological link between beat synchronisation and neurodevelopment. <div class="newsletter-box spai-bg-prepared"> <div id="wpcf7-f6-p195164-o1" class="wpcf7 spai-bg-prepared" dir="ltr" lang="en-US" role="form"> <form class="wpcf7-form mailchimp-ext-0.5.62 spai-bg-prepared init" action="/science/biology/keeping-the-beat-genetics/#wpcf7-f6-p195164-o1" method="post" novalidate="novalidate" data-status="init"> <input class="wpcf7-form-control wpcf7-text referer-page spai-bg-prepared" name="referer-page" type="hidden" value="https://cosmosmagazine.com/people/" data-value="https://cosmosmagazine.com/people/" aria-invalid="false" /> </form> </div> </div> Several physiology traits also seemed to be linked to beat synchronisation, including processing speed, grid strength, usual walking pace, and peak respiratory flow. These may be linked to the evolution of language and sociality through music in early humans. For modern humans, our ability to keep the beat may help to predict developmental speech-language disorders, and serve as a mechanism for <a class="spai-bg-prepared" href="https://www.frontiersin.org/articles/10.3389/fnhum.2021.789467/full" target="_blank" rel="noreferrer noopener">rhythm-based rehabilitation</a>, including for <a class="spai-bg-prepared" href="https://cosmosmagazine.com/science/biology/bilingual-patients-recover-better-from-stroke/" target="_blank" rel="noreferrer noopener">stroke</a> and <a class="spai-bg-prepared" href="https://www.nature.com/articles/s41598-017-16232-5" target="_blank" rel="noreferrer noopener">Parkinson’s disease</a>. This study has been <a class="spai-bg-prepared" href="https://doi.org/10.1038/s41562-022-01359-x" target="_blank" rel="noreferrer noopener">published</a> in Nature Human Behaviour. <figure class="wp-block-embed is-type-video is-provider-youtube wp-block-embed-youtube wp-embed-aspect-16-9 wp-has-aspect-ratio spai-bg-prepared"> <div class="wp-block-embed__wrapper spai-bg-prepared"> <div class="entry-content-asset spai-bg-prepared"> <div class="embed-wrapper spai-bg-prepared"> <div class="inner spai-bg-prepared"><iframe class="spai-bg-prepared" title="The Go-Go's - We Got The Beat (Official Music Video)" src="https://www.youtube.com/embed/f55KlPe81Yw?feature=oembed" width="500" height="281" frameborder="0" allowfullscreen="allowfullscreen"></iframe></div> </div> </div> </div> </figure> We got the beat… well maybe some of us!  <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=195164&title=Keeping+to+the+beat+controlled+by+69+genes+%E2%80%93+not+just+our+feet" width="1" height="1" />  <div id="contributors"> <a href="https://cosmosmagazine.com/science/biology/keeping-the-beat-genetics/" 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 <a href="https://cosmosmagazine.com/contributor/qamariya-nasrullah" target="_blank" rel="noopener">Qamariya Nasrullah</a>. Qamariya Nasrullah holds a PhD in evolutionary development from Monash University and an Honours degree in palaeontology from Flinders University. Image: Getty Images </div>

Body

Feel connected to nature? It might be in your genes

<div><div class="copy">Have you ever wondered why some people turn to wild places for solace, while others shudder at the thought of the untamed? Why some people’s idea of a great weekend away involves pitching a tent in a muddy field full of creepy crawlies, while others think camping is a lesser form of torture?According to a <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3001500" target="_blank" rel="noreferrer noopener">new study</a> published in PLOS Biology, the answer may be at least partially written into our genes.In a collaboration with researchers from the National University of Singapore, the University of Queensland’s Professor Richard Fuller compared data from more than 1,000 sets of identical twins to find out how genetics may influence our relationship with nature.“We compared twins who had been raised together with twins raised apart, in an attempt to demonstrate genetic heritability of two traits: how strongly they feel connected to nature, and the amount of time a person spends in nature,” Fuller says.Their approach to the question, using identical twins, allowed them to tease apart the strength of genetic versus environmental influences.Fuller says the team were “truly surprised” by their results, finding that nature-loving behaviours were heritable between 34 and 48% of the time.“This means there may be innate genetic differences among people’s psychological connection with natural environments and how they experience them,” says Fuller.“Our results help to explain why some people have a stronger desire than others to be in nature.”A genetic component to the relationship between humans and the biosphere has long been speculated, often under the moniker of the “<a href="https://www.frontiersin.org/articles/10.3389/fpsyg.2021.700709/full" target="_blank" rel="noreferrer noopener">biophilia hypothesis</a>”, but this is the first time it has been convincingly demonstrated.The current research builds genetic insight into our knowledge of nature-lust, which has previously been understood primarily through the lens of geographical circumstances. The new results suggest that while some of us may be genetically predisposed to connect with our wild side more than others, our circumstances still have a heady influence.“Our results reinforced previous findings that a person’s environment is the predominant driver behind their enjoyment of nature,” Professor Fuller said.“But the new information on the role of genetics in shaping our relationship with nature is a significant discovery.”Lead author Dr Chia-chen Chang from the National University of Singapore believes the insight from this study may help to better inform efforts to bring people closer to nature, an issue that is becoming increasingly important as the impact of growing urbanisation on mental health becomes clearer.“We know that more and more people today are living in urban environments, and this is usually associated with more mental health issues,” she says.“This includes lower levels of subjective wellbeing, a higher risk of psychiatric disorders, or increased depression and anxiety.”Chang says the process of connecting urban dwellers with the natural environment can prove challenging in our highly developed city-scapes, but that the benefits make the effort worthwhile.“Spending a little time at home in the garden can be a great way to experience some nature, but this can’t always be achieved, especially for those in urban areas,” she says.“Increasing accessibility to nature for urban residents through projects such as communal gardens will be hugely beneficial and will play an important part in improving people’s wellbeing overall.”The results also add to a growing body of research that relies on insights from the study of twins, with the current study involving participants from <a href="https://twinsuk.ac.uk/" target="_blank" rel="noreferrer noopener">TwinsUK</a>: the United Kingdom’s largest adult twin registry and most clinically detailed twin study in the world.TwinsUK, which has more than 14,000 registered twin participants, has been instrumental in progressing understanding of how genetic variation relates to human health and disease, with data underpinning 76 individual studies and over 800 publications to date.Image credits: Getty Images <img id="cosmos-post-tracker" style="height: 1px!important;width: 1px!important;border: 0!important" src="https://syndication.cosmosmagazine.com/?id=181148&title=Feel+connected+to+nature%3F+It+might+be+in+your+genes" width="1" height="1" data-spai-target="src" data-spai-orig="" data-spai-exclude="nocdn" /> </div><div id="contributors">This article was originally published on <a href="https://cosmosmagazine.com/health/body-and-mind/genetic-basis-for-biophilia/" target="_blank" rel="noopener">cosmosmagazine.com</a> and was written by Jamie Priest. </div></div>

Mind

Feel connected to nature? It might be in your genes

Have you ever wondered why some people turn to wild places for solace, while others shudder at the thought of the untamed? Why some people’s idea of a great weekend away involves pitching a tent in a muddy field full of creepy crawlies, while others think camping is a lesser form of torture?<div class="copy">According to a <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3001500" target="_blank" rel="noreferrer noopener">new study</a> published in PLOS Biology, the answer may be at least partially written into our genes.In a collaboration with researchers from the National University of Singapore, the University of Queensland’s Professor Richard Fuller compared data from more than 1,000 sets of identical twins to find out how genetics may influence our relationship with nature.“We compared twins who had been raised together with twins raised apart, in an attempt to demonstrate genetic heritability of two traits: how strongly they feel connected to nature, and the amount of time a person spends in nature,” Fuller says.Their approach to the question, using identical twins, allowed them to tease apart the strength of genetic versus environmental influences.Fuller says the team were “truly surprised” by their results, finding that nature-loving behaviours were heritable between 34 and 48% of the time.“This means there may be innate genetic differences among people’s psychological connection with natural environments and how they experience them,” says Fuller.“Our results help to explain why some people have a stronger desire than others to be in nature.”A genetic component to the relationship between humans and the biosphere has long been speculated, often under the moniker of the “<a href="https://www.frontiersin.org/articles/10.3389/fpsyg.2021.700709/full" target="_blank" rel="noreferrer noopener">biophilia hypothesis</a>”, but this is the first time it has been convincingly demonstrated.The current research builds genetic insight into our knowledge of nature-lust, which has previously been understood primarily through the lens of geographical circumstances. The new results suggest that while some of us may be genetically predisposed to connect with our wild side more than others, our circumstances still have a heady influence.<div class="newsletter-box"><div id="wpcf7-f6-p181148-o1" class="wpcf7" dir="ltr" lang="en-US" role="form"></div></div>“Our results reinforced previous findings that a person’s environment is the predominant driver behind their enjoyment of nature,” Professor Fuller said.“But the new information on the role of genetics in shaping our relationship with nature is a significant discovery.”Lead author Dr Chia-chen Chang from the National University of Singapore believes the insight from this study may help to better inform efforts to bring people closer to nature, an issue that is becoming increasingly important as the impact of growing urbanisation on mental health becomes clearer.“We know that more and more people today are living in urban environments, and this is usually associated with more mental health issues,” she says.“This includes lower levels of subjective wellbeing, a higher risk of psychiatric disorders, or increased depression and anxiety.”Chang says the process of connecting urban dwellers with the natural environment can prove challenging in our highly developed city-scapes, but that the benefits make the effort worthwhile.“Spending a little time at home in the garden can be a great way to experience some nature, but this can’t always be achieved, especially for those in urban areas,” she says.“Increasing accessibility to nature for urban residents through projects such as communal gardens will be hugely beneficial and will play an important part in improving people’s wellbeing overall.”The results also add to a growing body of research that relies on insights from the study of twins, with the current study involving participants from <a href="https://twinsuk.ac.uk/" target="_blank" rel="noreferrer noopener">TwinsUK</a>: the United Kingdom’s largest adult twin registry and most clinically detailed twin study in the world.TwinsUK, which has more than 14,000 registered twin participants, has been instrumental in progressing understanding of how genetic variation relates to human health and disease, with data underpinning 76 individual studies and over 800 publications to date. <img id="cosmos-post-tracker" style="height: 1px!important;width: 1px!important;border: 0!important" src="https://syndication.cosmosmagazine.com/?id=181148&title=Feel+connected+to+nature%3F+It+might+be+in+your+genes" width="1" height="1" data-spai-target="src" data-spai-orig="" data-spai-exclude="nocdn" /> </div><div id="contributors"><a href="https://cosmosmagazine.com/health/body-and-mind/genetic-basis-for-biophilia/" 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 <a href="https://cosmosmagazine.com/contributor/jamie-priest" target="_blank" rel="noopener">Jamie Priest</a>. Jamie Priest is a science journalist at Cosmos. She has a Bachelor of Science in Marine Biology from the University of Adelaide.Image: Getty Images</div>

Body

Some endangered species can no longer survive in the wild. So should we alter their genes?

Around the world, populations of many beloved species are declining at increasing rates. According to one <a href="https://www.theguardian.com/environment/2020/sep/30/world-plant-species-risk-extinction-fungi-earth">grim projection</a>, as many as 40% of the world’s species may be extinct by 2050. Alarmingly, many of these declines are caused by threats for which few solutions exist. Numerous species now depend on conservation breeding programs for their survival. But these programs typically do not encourage species to adapt and survive in the wild alongside intractable threats such as climate change and disease. This means some species can no longer exist in the wild, which causes major downstream effects on the ecosystem. Consider, for example, how a coral reef would struggle to function without corals. What if there was another way? My colleagues and I have developed an intervention method that aims to give endangered species the genetic features they need to survive in the wild. <img src="https://images.theconversation.com/files/411140/original/file-20210714-13-1bf7ccv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" alt="bleached coral with fish" /> Genetically altering coral may help them survive in a warmer world. Rick Stuart-Smith <h2>Bringing theory into practice</h2> Over generations, natural selection enables species to adapt to threats. But in many instances today, the speed at which threats are developing is outpacing species’ ability to adapt. This problem is especially apparent in wildlife threatened by newly emerging infectious diseases such as chytridiomycosis in amphibians, and in climate-affected species such as corals. The toolkit my colleagues and I developed is called “targeted genetic intervention” or TGI. It works by increasing the occurrence or frequency of genetic features that impact an organism’s fitness in the presence of the threat. We outline the method in a recent <a href="https://www.sciencedirect.com/science/article/abs/pii/S0169534721003384">research paper</a>. The toolkit involves <a href="https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/artificial-selection">artificial selection</a> and <a href="https://www.frontiersin.org/articles/10.3389/fbioe.2019.00175/full">synthetic biology</a>. These tools are well established in agriculture and medicine but relatively untested as conservation tools. We explain them in more detail below. Many tools in our TGI toolkit have been discussed in theory in conservation literature in recent decades. But rapid developments in genome sequencing and synthetic biology mean some are now possible in practice. The developments have made it easier to understand the genetic basis of features which enable a species to adapt, and to manipulate them. <img src="https://images.theconversation.com/files/442166/original/file-20220124-19-xc82dx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" alt="frog on wet rock" /> Some animal species cannot adapt in time to survive threats such as disease. Shutterstock <h2>What is artificial selection?</h2> Humans have long used artificial (or phenotypic) selection to promote desirable characteristics in animals and plants raised for companionship or food. This genetic alteration has led to organisms, such as domestic dogs and maize, that are dramatically different from their wild progenitors. Traditional artificial selection can lead to outcomes, such as high inbreeding rates, that affect the health and resilience of the organism and are undesirable for conservation. If you’ve ever owned a purebred dog, you might be aware of some of these genetic disorders. And when it comes to conservation, determining which individuals from a species are resistant to, say, a deadly pathogen would involve exposing the animal to the threat – clearly not in the interests of species preservation. Scientists in the livestock industry have developed a new approach to circumvent these problems. Called genomic selection, it combines data from laboratory work (such as a disease trial) with the genetic information of the animals to predict which individuals bear genetic features conducive to adaptation. These individuals are then chosen for breeding. Over subsequent generations, a population’s ability to survive alongside pervasive threats increases. Genomic selection has led to disease-resistant salmon and livestock that produce more milk and better tolerate heat. But it is yet to be tested in conservation. <img src="https://images.theconversation.com/files/442161/original/file-20220124-27-11vyq0z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" alt="cows in green field" /> Artificial selection has been used to develop traits that humans desire in livestock. Shutterstock <h2>What is synthetic biology?</h2> <a href="https://www.genome.gov/about-genomics/policy-issues/Synthetic-Biology">Synthetic biology</a> is a toolkit for promoting change in organisms. It includes methods such as transgenesis and gene editing, which can be used to introduce lost or novel genes or tweak specific genetic features. Recent synthetic biology tools such as <a href="https://medlineplus.gov/genetics/understanding/genomicresearch/genomeediting/">CRISPR-Cas9</a> have created a buzz in the medical world, and are also starting to gain the <a href="https://portals.iucn.org/library/node/48408">attention</a> of conservation biologists. Such tools can accurately tweak targeted genetic features in an individual organism – making it more able to adapt – while leaving the rest of the genome untouched. The genetic modifications are then passed on to subsequent generations. The method reduces the likelihood of unintended genetic changes that can occur with artificial selection. Synthetic biology methods are currently being trialled for conservation in multiple species around the world. These include the <a href="https://www.esf.edu/chestnut/resistance.htm">chestnut tree</a> and black-footed <a href="https://neo.life/2021/05/cloning-wildlife-and-editing-their-genes-to-protect-them-and-us/">ferrets</a> in the United States, and <a href="https://theconversation.com/gene-editing-is-revealing-how-corals-respond-to-warming-waters-it-could-transform-how-we-manage-our-reefs-143444">corals</a> in Australia. I am working with researchers at the University of Melbourne to develop TGI approaches in Australian frogs. We are trialling these approaches in the iconic southern corroboree frog, and plan to extend them to other species if they prove effective. Worldwide, the disease chytridiomycosis is devastating frog populations. Caused by the fungal pathogen Batrachochytrium dendrobatidis, it has led to the extinction of about <a href="https://www.nationalgeographic.com/animals/article/amphibian-apocalypse-frogs-salamanders-worst-chytrid-fungus">90 frog species</a> and declines in as many as 500 others. Many frog species now rely on conservation breeding for their continued survival. No effective solution for restoring chytrid-susceptible frogs to the wild exists, because the fungus cannot be eradicated. <img src="https://images.theconversation.com/files/442155/original/file-20220124-23-cebr8a.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" alt="gloved hand removed portion of DNA strand" /> CRISPR technology could potentially be used to edit the genes of endangered species. Shutterstock <h2>Looking ahead</h2> As with many conservation approaches, targeted genetic intervention is likely to involve trade-offs. For example, genetic features that make a species resistant to one disease may make it more susceptible to another. But the rapid rate of species declines means we should trial such potential solutions before it’s too late. The longer species are absent from an ecosystem, the greater the chance of irreversible environmental changes. Any genetic intervention of this type should involve all stakeholders, including Indigenous peoples and local communities. And caution should be taken to ensure species are fit for release and pose no risk to the environment. By bringing the concept of TGI to the attention of the public, government, and other scientists, we hope we will spur discussion and encourage research on its risks and benefits.<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; text-shadow: none !important;" src="https://counter.theconversation.com/content/175226/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/tiffany-kosch-1304685">Tiffany Kosch</a>, Research Fellow, <a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a> 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/some-endangered-species-can-no-longer-survive-in-the-wild-so-should-we-alter-their-genes-175226">original article</a>. Image: Melbourne Zoo

Travel Trouble

Willy Wonka star reveals Gene Wilder’s “favourite brat”

A child star who had the opportunity to work alongside the infamous Gene Wilder has spoken out on the experience, 50 years since its first premier date. Charlie and the Chocolate Factory hit movie screens 50 years ago on June 30, 1971 and achieved rapid success almost overnight. The film went on to become a phenomenon that was registered in the United States National Film Registry by the Library of Congress for being deemed “culturally, historically or aesthetically significant”. The child actors Peter Ostrum, Julie Dawn Cole, Michael Bollner, Paris Themmen and Denise Nickerson – who played Charlie Bucket, Veruca Salt, Augustus Gloop, Mike Teavee and Violet Beauregarde – all came together for a virtual reunion in honour of the film’s anniversary. <img style="width: 500px; height: 281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7842239/willy-wonka.jpg" alt="" data-udi="umb://media/b9da36eca8c24fbeb170655d6cf92150" /> Image: Yahoo The actors all had the opportunity to co-star together, and even got to explore the imagined Wonka Chocolate Factory. The cast recounted such fond memories of exploring the film sets in Bavarian Germany and working with Gene Wilder. Themmen admitted that he was indeed a “notorious troublemaker on the set.” So much so that even Wilder called him “a handful”. “I can corroborate that,” the actor, who played the television-obsessed rascal Mike Teavee, admitted. “I was younger than the others. I was 11, they were 13 and was naturally just sort of more high-spirited and rambunctious.” <img style="width: 500px; height: 281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7842237/willy-wonka-1.jpg" alt="" data-udi="umb://media/a8d501bcedd64f7b97dd573169a7717a" /> Image: Yahoo The now-62-year-old opened up about one brief moment he shared with Wilder, in 1976 during a fundraiser screening for the film Silver Streak at the Avon Theatre in Stamford, Connecticut. “I sat at the back of the room and he gave his commentary and then I went up to the front of the room afterwards with my poster in hand,” Themmen relived with a smile. “I said, ‘Hi, Gene, how you doing? I’m Paris Themmen, I was Mike Teavee in Willy Wonka.” “And he said, ‘Oh you were a brat!’ And I flashed all the way back 50 years, or 40 years at that time, and said, ‘Well, I’m 50-something now and maybe not as much of a brat.’ And he signed my poster, ‘To my favourite brat.’” Wilder died in 2016 at the age of 83 after a long vibrant career. Cole, who played Veruca Salt, said: “I think people kind of want us to tell you that he was like Willy Wonka offset, but he wasn’t. “He was such a lovely, kind man, very unassuming,” she said. “He was just down to earth, not pretentious, he was just a wonderful person to be around and to work with,” said Ostrum, who played Charlie Bucket.

Movies

China's failed gene edited baby experiment proves we're not ready for human embryo modification

More than a year ago, the world was shocked by Chinese biophysicist He Jiankui’s attempt to use CRISPR technology to modify human embryos and make them resistant to HIV, which led to the birth of twins Lulu and Nana. Now, crucial details have been revealed in a recent <a href="https://www.technologyreview.com/s/614764/chinas-crispr-babies-read-exclusive-excerpts-he-jiankui-paper/">release of excerpts</a> from the study, which have triggered a series of concerns about how Lulu and Nana’s genome was modified. How CRISPR works CRISPR is a technique that allows scientists to make precise edits to any DNA by altering its sequence. When using CRISPR, you may be trying to “knock out” a gene by rendering it inactive, or trying to achieve specific modifications, such as introducing or removing a desired piece of DNA. Gene editing with the CRISPR system relies on an association of two molecules. One is a protein, called Cas9, that is responsible for “cutting” the DNA. The other molecule is a short RNA (ribonucleic acid) molecule which works as a “guide” that brings Cas9 to the position where it is supposed to cut. The system also needs help from the cells being edited. DNA damage is frequent, so cells regularly have to repair the DNA lesions. The associated repair mechanisms are what introduce the deletions, insertions or modifications when performing gene editing. How the genomes of Lulu and Nana were modified He Jiankui and his colleagues were targeting a gene called CCR5, which is necessary for the HIV virus to enter into white blood cells (<a href="https://www.medicalnewstoday.com/articles/320987.php">lymphocytes</a>) and infect our body. One variant of CCR5, called CCR5 Δ32, is missing a particular string of 32 “letters” of DNA code. This variant naturally occurs in the human population, and results in a high level of resistance to the most common type of HIV virus. The team wanted to recreate this mutation using CRISPR on human embryos, in a bid to render them resistant to HIV infection. But this did not go as planned, and there are several ways they may have failed. First, despite claiming in the abstract of their unpublished article that they reproduced the human CCR5 mutation, in reality the team tried to modify CCR5 close to the Δ32 mutation. As a result, they generated different mutations, of which the effects are unknown. It may or may not confer HIV resistance, and may or may not have other consequences. Worryingly, they did not test any of this, and went ahead with implanting the embryos. This is unjustifiable. The mosaic effect A second source of errors could have been that the editing was not perfectly efficient. This means that not all cells in the embryos were necessarily edited. When an organism has a mixture of edited and unedited cells, it is called a “mosaic”. While the available data are still limited, it seems that both Lulu and Nana are mosaic. This makes it even less likely that the gene-edited babies would be resistant to HIV infection. The risk of mosaicism should have been another reason not to implant the embryos. Moreover, editing can have unintended impacts elsewhere in the genome. When designing a CRISPR experiment, you choose the “guide” RNA so that its sequence is unique to the gene you are targeting. However, “off-target” cuts can still happen elsewhere in the genome, at places that have a similar sequence. He Jiankui and his team tested cells from the edited embryos, and reported only one off-target modification. However, that testing required sampling the cells, which were therefore no longer part of the embryos - which continued developing. Thus, the remaining cells in the embryos had not been tested, and may have had different off-target modifications. This is not the team’s fault, as there will always be limitations in detecting off-target and mosaicism, and we can only get a partial picture. However, that partial picture should have made them pause. A bad idea to begin Above, we have described several risks associated with the modifications made on the embryos, which could be passed on to future generations. Embryo editing is only ethically justifiable in cases where the benefits clearly outweigh the risks. Technical issues aside, the researchers did not even address an unmet medical need. While the twins’ father was HIV-positive, there is already a well-established way to prevent an HIV-positive father from infecting embryos. This “<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4779710/">sperm washing</a>” method was actually used by the team. The only benefit of the attempted gene modification, if proven, would have been a reduced risk of HIV infection for the twins later in life. But there are safer existing ways to control the risk of infection, such as condoms and mandatory testing of blood donations. Implications for gene editing as a field Gene editing has endless applications. It can be used to <a href="https://www.nature.com/articles/d41586-019-02770-7">make plants such as the Cavendish banana more resistant to devastating diseases</a>. It can play an important role in the adaptation to climate change. In health, we are already seeing <a href="https://www.npr.org/sections/health-shots/2019/11/19/780510277/gene-edited-supercells-make-progress-in-fight-against-sickle-cell-disease">promising results</a> with the editing of somatic cells (that is, non-heritable modifications of the patient’s own cells) in beta thalassemia and sickle cell disease. However, we are just not ready for human embryo editing. Our techniques are not mature enough, and no case has been made for a widespread need that other techniques, such as preimplantation genetic testing, could not address. There is also much work still needed on governance. There have been individual calls for a moratorium on embryo editing, and expert panels from the <a href="https://www.nature.com/articles/d41586-019-00942-z">World Health Organisation</a> to <a href="https://en.unesco.org/news/unesco-panel-experts-calls-ban-editing-human-dna-avoid-unethical-tampering-hereditary-traits">UNESCO</a>. Yet, no consensus has emerged. It is important these discussions move <a href="https://www.nature.com/articles/d41586-019-03525-0">in unison</a> to a second phase, where other stakeholders, such as patient groups, are more broadly consulted (and informed). Engagement with the public is also crucial. Correction: this article originally described RNA (ribonucleic acid) as a protein, rather than a molecule.<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; text-shadow: none !important;" src="https://counter.theconversation.com/content/128454/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/dimitri-perrin-392467">Dimitri Perrin</a>, Senior Lecturer, <a href="http://theconversation.com/institutions/queensland-university-of-technology-847">Queensland University of Technology</a> and <a href="https://theconversation.com/profiles/gaetan-burgio-202386">Gaetan Burgio</a>, Geneticist and Group Leader, The John Curtin School of Medical Research, <a href="http://theconversation.com/institutions/australian-national-university-877">Australian National University</a> This article is republished from <a href="http://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/chinas-failed-gene-edited-baby-experiment-proves-were-not-ready-for-human-embryo-modification-128454">original article</a>.

Technology

Gene Kelly’s wife reveals another side to the Hollywood icon

When she first met him in 1985, she had no idea who he was – but Patricia Ward Kelly was soon to develop a special insight into Hollywood legend Gene Kelly both as an artist and a person. Patricia, then 26, was working on a documentary about the Smithsonian museum when she was introduced to the then-73-year-old Gene, who was tapped as the television special’s host. After she was made aware of his fame, Patricia took out videos from the store and carried out a marathon viewing. What she watched – from Singin’ in the Rain to Brigadoon – left her mouth “agape”. The two soon became closer and bonded over the poetry of William Butler Yeats. Before long, Gene invited her to California to become his biographer, and their working relationship turned into a romance. Gene and Patricia tied the knot in 1990. Throughout the decade they spent together, Patricia documented her partner’s words – be it in writing or tape recording – nearly every day, and in the process, grew a greater appreciation of the seemingly “two-dimensional” man that the audience knew and loved. “People have no idea of the magnitude of him,” she told Over60. “He looks great up on-screen dancing, [but] many people don’t realise he created what you’re seeing, that he directed and choreographed it, and that’s really what he wanted to be known for … for being behind the camera, and for changing the look of dance on film.” <div class="embed-responsive embed-responsive-16by9"><iframe class="embed-responsive-item" src="https://www.youtube.com/embed/x7CIgWZTdgw"></iframe></div> Gene, she said, had some personal favourites from his impressive filmography. The first and most widely known was the 1949 musical On the Town, which Gene took part in co-directing and choreographing. “He would often say that because it broke new ground by shooting the opening number on location,” she said. “That just had not been done in that way, and that really influenced the French New Wave filmmakers like François Truffaut.” However, Gene also had a lesser-known pick – a work that grew out of his childhood interests. According to Patricia, Gene revealed in private that he really enjoyed The Three Musketeers because swordplay and acrobatics were some of “what he loved as a little boy growing up”. Gene died in 1996 at the age of 83 following a series of strokes – but Patricia has been determined to keep his legacy and memory alive. In 2012, Patricia launched Gene Kelly: The Legacy and has since toured with it around the world. Patricia said a “show” is not quite the right word to describe the program. “I often refer to it as a kind of an experience. It begins the minute the door is open,” she said. In the “one-woman presentation”, set to tour Australia next year, Patricia is set to share some stories, film clips, previously unreleased recordings, personal memorabilia, and insights culled from hours of interviews and conversations with her husband. “It’s like we’re sitting in the living room having a chat, and I’m bringing these things out,” she said. “Even though it’s a very large venue, people [will] just feel like we’re in this very intimate setting.” Gene Kelly: The Legacy is coming to Australia in February 2020.

Movies

Why some animals have different coloured eyes

Some dogs have two different coloured eyes. Do other animals (besides people) and, if so, why? – George, aged ten, Hethersett, UK. Some dogs are born with one brown eye and one blue eye, which can look very strange, since we’re used to seeing dogs with two brown eyes. This is sometimes called “<a href="https://books.google.co.uk/books?id=pjJKkwJbLBQC&pg=PA211&lpg=PA211&dq=heterochromia+wall+eye&source=bl&ots=QERmm7E3NI&sig=ACfU3U3XvEL1ro-jPAjO3iVmnkAFHukTNg&hl=en&sa=X&ved=2ahUKEwiZntXElZbjAhU8UBUIHVrwBXUQ6AEwF3oECAkQAQ#v=onepage&q=heterochromia%20wall%20eye&f=false">wall eye</a>”, and it’s caused by certain genes that are passed down from parents to offspring. If you look closely, you’ll also see that dogs with two different coloured eyes have unusually coloured coats, too. Their coats might be dappled or streaked with white. This is because the genes for eye colour and coat colour are <a href="https://www.ias.ac.in/article/fulltext/jgen/052/02/0425-0440">closely connected</a>. The parents themselves may not show any sign of these unusual coat or eye colours. But usually there’s at least one dog on both sides of the family tree that has the unusual colouring. That’s how the mother and father can both pass on the genes that give some of their puppies the unusual colouring. By now, you might be wondering – what are <a href="https://kids.britannica.com/kids/article/gene/603646">genes</a>? Let me explain: every living thing is made up of cells. Each cell contains all the information needed to tell the body what to look like and how to work. Every little bit of information is called a “gene”, and there are lots and lots of genes which decide nearly every aspect of how we are. Passed down from parents For example, there are <a href="https://www.sciencedaily.com/terms/human_genome.htm">around 25,000 genes</a> in human cells, which can decide everything from our height, to our hair colour or how likely we are to get certain diseases. The genes are made up of DNA, and held together on stringy structures called “chromosomes” in the centre of the cell. <a href="https://images.theconversation.com/files/282211/original/file-20190702-126364-gkw5od.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img src="https://images.theconversation.com/files/282211/original/file-20190702-126364-gkw5od.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" alt="" /></a> See inside a cell, where genes are made of DNA. <a href="https://en.wikipedia.org/wiki/Chromosome#/media/File:Eukaryote_DNA-en.svg" class="source">Wikimedia Commons/Magnus Manske.</a>, <a href="http://creativecommons.org/licenses/by-sa/4.0/" class="license">CC BY-SA</a> Because every mammal comes from two parents, it has two copies of every gene – one from the mother and one from the father. Each copy may be telling the body to do something different. For example, the mother’s gene might be saying “dark hair” while the father’s says “fair hair”. In that case, the mother’s gene will win and their baby will have dark hair, because the dark hair gene is dominant over the fair hair gene. The baby will only have fair hair if both parents pass on the gene for fair hair. The genes for wall eye and streaky coat are similar to the fair haired gene, in this way. An animal will only have those features if that specific gene is passed down from both parents. When the mother and father carry the gene, but don’t have wall eye themselves, then some of their offspring will have it, though not all of them. Wall eye woes Wall eye is also sometimes seen in rabbits, cats, cattle, sheep and horses. Horses that have one blue eye usually have black and white patches on their coat – they are called “piebald” or “pinto” or “paint”. Some of these horses even have two blue eyes (one of mine does!), which makes them look even more unusual. Humans can also have one blue eye and another of a different colour, like brown or green. This often goes with a white streak in the front of their hair. Sometimes, having wall eye can cause problems. For dogs, the eye that is blue often has problems that <a href="https://www.ias.ac.in/article/fulltext/jgen/052/02/0425-0440">can affect its sight</a>. For this reason, breeders don’t let two dogs with wall eye and streaky coat have puppies together. If they do, then the puppies will often be blind and sometimes deaf as well. In horses, wall eye does not seem to cause problems with vision, though having two blue eyes can be <a href="https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1002653&type=printable">associated with deafness</a>. Some cats and humans who have it can also have trouble hearing, and humans whose parents both have wall eye may be unable to speak or hear. <a href="https://theconversation.com/profiles/jan-hoole-384563">Jan Hoole</a>, Lecturer in Biology, <a href="http://theconversation.com/institutions/keele-university-1012">Keele University</a> This article is republished from <a href="http://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/curious-kids-why-do-some-animals-have-two-different-coloured-eyes-119727">original article</a>.

Family & Pets

News

Shop

Catalogues

Contests

Entertainment

Travel

Health

Lifestyle

Finance

Property

Games

Information

Keep up to date

Search

How long will you live? New evidence says it’s much more about your choices than your genes

Bruce Willis' wife issues amazing reflection on Gene Hackman's passing

Gene Hackman's cause of death revealed

Sad new details emerge in Gene Hackman case

Got no COVID-19 symptoms? A gene mutation might be the reason

“Irwin genes are strong”: Bindi shares adorable candid snap

KISS concert halted as Gene Simmons falls ill on stage

Super rare pic of unrecognisable Gene Hackman

Chris Hemsworth’s Alzheimer’s gene doesn’t guarantee he’ll develop dementia

Evidence that human evolution driven by major environmental pressures discovered

Excelling as a musician takes practice and requires opportunities – not just lucky genes

Surprise discovery shows you may inherit more from your mum than you think

Keeping to the beat controlled by 69 genes – not just our feet

Feel connected to nature? It might be in your genes

Feel connected to nature? It might be in your genes

Some endangered species can no longer survive in the wild. So should we alter their genes?

Willy Wonka star reveals Gene Wilder’s “favourite brat”

China's failed gene edited baby experiment proves we're not ready for human embryo modification

Gene Kelly’s wife reveals another side to the Hollywood icon

Why some animals have different coloured eyes

Our Partners