Latest news with #UniversityofColorado
Yahoo
a day ago
- Business
- Yahoo
CU Boulder eliminates single-use beverage plastics
DENVER (KDVR) — The University of Colorado Boulder said Thursday that it is eliminating all single-use plastics from its campus beverage services, following a new 10-year pouring rights deal with PepsiCo Beverages. Pepsi initiated a campus-wide transition on July 7 that included re-stocking and/or replacing on-campus vending machines, according to the university, which said cafes and other retail spaces on campus will make the changeover 'as existing products are sold or replaced.' CU students build virtual-reality moon-exploring robot The university said the agreement aligns with its Climate Action Plan and 'supports advocacy from students, staff, faculty and administration.' 'By eliminating single-use plastics from our beverage services, we're not only responding to the values of our campus community – we're building on our legacy as one of the most sustainable campuses in the country,' said CU Boulder Chancellor Justin Schwartz, in a statement. CU Boulder said the agreement with Pepsi has no carve-out clauses or vending exceptions for select plastic-packaged beverages and also requires third-party vendors on campus to comply with the move away from single-use plastics. 'This is more than a contract,' said CU Boulder Vice Chancellor of Sustainability Andrew Mayock, in a statement. 'It's a systems-level change that supports our climate goals and demonstrates how operational decisions can drive meaningful environmental outcomes.' Copyright 2025 Nexstar Media, Inc. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed. Solve the daily Crossword
Scientific American
7 days ago
- Health
- Scientific American
What Would It Take for Bird Flu to Spread among Humans?
H5N1 avian influenza has long been a concerning virus. Since its discovery in 1996 in waterfowl, bird flu has occasionally caused isolated human cases that have quite often been fatal. But last year H5N1 did something strange: it started infecting cattle. The absolute oddity of this leap may have been somewhat lost in the flood of bad news about H5N1, which by 2024 had already caused mass die-offs of seals and other marine mammals and which was simultaneously devastating chicken farms and causing periodic shortages of eggs. But infectious disease specialists were shocked. 'Flu in cows is not really a thing,' says Jenna Guthmiller, a microbiologist and immunologist at the University of Colorado Anschutz Medical Campus. 'If you would ask anybody that studies flu on their 2024 bingo card if they had, you know, mammary infection of dairy cows on there, no one would have.' Influenza hadn't previously been known to infect cattle, much less cause the kind of infections in their udders that have now begun circulating in milking parlors across the country. The continued circulation of H5N1 in cows is one of the biggest concerns experts have about this flu subtype. Though H5N1 hasn't yet spread human-to-human, people can catch the disease from cattle, mostly through close contact with infected milk. And the more it circulates in an animal that humans regularly interact with, the more chances the flu has to stumble on just the right mutation to leap to people and start adapting into something with pandemic potential. On supporting science journalism If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today. 'That's the main thing I worry about in terms of potential human disease,' says Jonathan Runstadler, a professor of infectious disease and global health at the Tufts University Cummings School of Veterinary Medicine. '[It's] increasing that interface and giving the virus the opportunity to establish infection in humans.' Researchers are still trying to catalogue the ways the virus has adapted to spread within cows, seals, cats and hundreds of other mammal species. They're watching for particular mutations and adaptations that might hint that a certain strain of H5N1 could start spreading from person to person. But as the surprise leap into cows shows, flu viruses sometimes do something unexpected and unpredictable. There may be unknown genetic mutations not yet on scientists' watchlists that could change H5N1's behavior overnight. The Leap to Cows The early spring day that H5N1 was first reported to be circulating in dairy cattle was a memorable one for Guthmiller and her colleagues. Guthmiller grew up on a 70-head dairy cattle farm in South Dakota, a biographical tidbit she never expected to overlap with her work as a flu researcher. Flu infecting the udders of cows was such an out-of-left-field idea that when cows started to show signs of sickness (such as poor appetite and discolored milk) in early 2024, veterinarians didn't think to test for influenza at first. It was actually the simultaneous sickening of barn cats, which then tested positive for flu, that led researchers to look for the virus in the cows. Guthmiller and her lab members were already trying to figure out the genetic sequences of the receptor-binding domain (RBD) of the H1N1 seasonal flu that regularly infects humans. The receptor-binding domain is a crucial but delicate fragment of the flu virus that allows it to dock onto and enter specific cells in the body. Mutations within the RBD can enable a virus to lock on to new receptors on new host cell surface. Different species have different types of these receptors, so a genetic switch by the virus can open up new host species for infection. Sometimes, however, a mutation can turn a functional virus into a functionally dead one that's unable to invade any host at all. Guthmiller asked her graduate student Marina Good to pull the genetic sequences for the receptor-binding domain of this bizarre cow strain of H5N1. She feared that the mutated form of RBD in this strain could unlock a cell receptor that predominates in the human respiratory tract. In general, flu viruses like to bind to tiny strings of sugars on cell surfaces called sialic acids. These sialic acids are linked together by different kinds of bonds. Avian flu tends to attach to an alpha-2,3 bond. Alpha-2,3 receptors are bountiful in the gastrointestinal tracts of waterfowl and the upper respiratory tracts of chickens. Humans have alpha-2,3 receptors, too, but mostly in the conjunctiva, or lining of the eye, and deep in our lungs. Our upper respiratory tract is largely filled with alpha-2,6, which is the preferred target of the seasonal influenzas that typically circulate in humans. The fact that humans carry alpha-2,3 receptors in the eyes and lower respiratory tract means that we can catch H5N1; currently this appears as mild pink eye or occasionally as a profoundly serious viral pneumonia. Even so, the virus doesn't easily infect the lining of our nose and throat. If it did, humans likely would have spread the disease to one another rapidly via coughing, sneezing and simply breathing. Less than a month after the first public report of H5N1 in a dairy cow in March 2024, Good, Guthmiller and their colleagues discovered a bit of good news that they posted on the preprint site bioRxiv: The flu hadn't made this crucial shift, meaning the circulating strain still preferred alpha-2,3 receptors. (These findings have been replicated multiple times since then, suggesting this is still the case.) What the virus had done, however, was become less choosy about the alpha-2,3-containing sugars it could bind with, Guthmiller says, likely helping enable the sudden spread within cows and other mammals. In some ways, labeling influenza types 'avian' or 'mammalian' can be a little misleading, says Daniel Perez, a professor of poultry medicine at the University of Georgia who studies how viruses leap from animals to humans. Perez and his team have been studying a modified form of H5N1 that is less deadly to animals, and they're finding that the virus's big evolutionary shift has been to replicate more easily in wild bird airways, not just in their gastrointestinal tracts. 'The changes that we're actually seeing in the virus are not necessarily mammalian-adapted mutations,' Perez says. 'What we are seeing is more of these respiratory-adapted mutations that occasionally do help it to replicate better in mammals.' The shift to mammals might have been incidental at first. But now mutations are accumulating in the cattle version of the virus. For instance, they found a mutation in the amino acids at a position in the virus strain's genome called 631, a spot where changes are known to help a virus better interact with mammalian proteins inside the cell. These proteins are involved in the translation of genetic instructions to cellular activity, including the replication of genes that the virus needs to reproduce. 'What we're starting to see are sprinklings of more of these mammalian adaptions happening in the background of this cattle strain,' says Seema Lakdawala, an associate professor of immunology and microbiology at Emory University. As this mammalian spread continues, Lakdawala and other infectious disease researchers worry about further mutations that would help this flu spread even more easily between mammals. This might happen in a slow and stepwise fashion, leading to more animal-human spillovers, followed by household transmission between close contacts and finally to community spread, Lakdawala says. Or it might be quick: another worry is reassortment, the ability of a flu virus to snag genetic material from another flu virus more adept at infecting people. A person who happened to be infected with both avian flu and seasonal flu could be ground zero for this kind of change. 'If this virus continues to circulate in cows and continues to have these sporadic spillover events, eventually it's going to gain segments through reassortment with either a human seasonal strain or a pig strain or another bird strain,' Lakdawala says. If that happens, a pandemic could take off overnight. Flu Red Flags When people are exposed to a high enough viral load of H5N1, they can become infected. There have been 70 known human cases in the U.S., including one death. But to establish itself in a human host, H5N1 would need to do three things, says Richard Webby, the director of the World Health Organization Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds who studies host-microbe interactions at St. Jude Children's Research Hospital. One is to better attach to the receptors found in the human upper respiratory tract, those alpha-2,6 receptors that the virus has not yet unlocked. Fortunately, that seems to be a difficult evolutionary trick for the virus to pull off, Webby says. Perhaps multiple simultaneous evolutionary changes would be needed to make the switch successfully, or maybe receptor binding is so important to a virus's survival, that this part of its genome doesn't mutate so quickly. Whatever the reason, Webby says, 'we haven't really seen any movement there' since H5N1 was discovered. The second change the virus must make is to adapt itself to better interact with the proteins inside human cells. The virus needs these proteins to hijack host cells and replicate, and these proteins in birds and mammals are quite different from each other. There are some changes that researchers suspect would create a strain of H5N1 that is more suited to infecting humans, Webby says. A variant gene sequence in a part of the virus called the PB2-627 domain is known to enable H5N1 to better interact with the human protein ANP32A and more effectively replicate itself. 'It's a change the virus can make pretty easily when it does start to replicate in a mammal system, unlike the receptor change,' Webby says. Finally, an adapted avian flu would need to evade our innate immune system, the body's nonspecific defenses against new invaders. Human influenzas, for example, are adept at evading human antiviral proteins called Mx GTPases, while H5N1 is not. There are other considerations as well, including how long the virus can survive outside the body, which determines how easily it can transmit. The cattle strain of H5N1 is very stable in milk, Lakdawala and her team have found. For a virus to transmit between people, though, it needs to be stable in human mucus or saliva. Seasonal influenzas that infect humans are expelled into the world in tiny globules of spit or snot, and those secretions protect the virus as it travels between hosts, Lakdawala says. 'Novel viruses that come in may not have that same kind of protection,' she says. On the other hand, if dairy workers continue to catch H5N1 pink eye from milking cows, there is a risk of further adaptation—in all of these ways. Being able to recognize alpha-2,3 alone seems sufficient for the virus to keep spreading in cows, Guthmiller says, so there doesn't seem to be much evolutionary pressure for the virus to recognize alpha-2,6 receptors in the cow mammary glands, Guthmiller says. But the human nose, connected to the eye lining by the tear ducts, could be fertile ground for H5N1 if it could unlock those ample receptors. Each time the virus spreads from a cow to a person, it gets another shot at this evolutionary opportunity. The virus may or may not take it. It may or may not be able to. One complication to this story, Guthmiller says, is that though the nose is probably the first place in the body that the immune system encounters most viruses, researchers know little about the immune response in the nasal tissue. It's a labyrinth of folded mucosa, and unlike blood, it's not easy to get samples of the actual tissue from a person who is sick or recovered. Guthmiller's lab is now studying internal nose samples from people who have had this tissue surgically removed for unrelated medical reasons. They're mapping the cell types found in the layers of tissue, trying to understand how the nose responds to new incursions by unfamiliar viral visitors. The Future of Flu The CDC ended its emergency response to avian flu in early July, citing a decline in animal cases and the absence of human cases since February 2025. Avian flu is somewhat seasonal, with peaks in fall and spring as wild birds migrate. But evolution happens over longer time scales. The 2009 H1N1 pandemic, known as the 'swine flu' pandemic, was caused by a new H1N1 flu strain that had emerged from a mix of several pig flus, a human flu and an avian flu. Oddly, people older than age 60 had some preexisting immunity to this new Frankenstein's monster of a virus, which turned out to be because it shared similarity with the descendants of the devastating 1918 pandemic flu. These long-ago flu lineages had been in circulation when people aged 60-plus in 2009 were kids but had been replaced by H2N2 viruses in 1957. Pig versions had persisted, however, gradually evolving and swapping bits of genes with avian and human flus. Before the 2009 virus had emerged, a handful of farm workers had been infected with these 'triple-reassorted' viruses, but these infections didn't go on to infect others. Then, 'all of a sudden, the North American pig lineage grabbed two segments from the Eurasian pig lineages, probably somewhere in [Mexico], and that virus started to spill over,' Lakdawala says. A new human pandemic, which may have killed around half a million people worldwide, was born. Fortunately, there are already approved human vaccines for H5N1, Perez says. These are based on older strains, but the vaccines would probably still protect against severe disease should the virus start spreading human-to-human. Preexisting vaccine know-how and newer technologies such as those used to create mRNA vaccines would also allow for the quick development of updated vaccines, he says. Whether H5N1 causes the next flu pandemic, it's safe to say one will come. There have been four flu pandemics since 1918, and today's high-density agricultural practices provide prime hunting ground for viruses. On poultry farms, nearly 175 million birds have been affected since 2022, according to the U.S. Department of Agriculture. Egg-laying operations have been dense for decades, but similar practices are spreading to other types of animal husbandry. Small farms with a few dozen cows, like the one Guthmiller grew up on, were once common. Now farms with at least 1,000 cows comprise more than 55 percent of the dairy herds in the U.S., according to the USDA. This density, along with the practice of moving cows between herds, means that viral spillovers that might have once died out on a small farm in South Dakota can now spread far and wide. In that sense, rather than a revolutionary understanding of influenza, Perez says, the best course of action might be a rethinking of agricultural practices. Humans are increasing the size of farms without increasing farm hygiene, which sets the stage for the emergence of new pathogens. 'Yes, we can keep making better vaccines faster,' he says. But an ounce of prevention is worth a pound of cure. 'It would be much easier if we created the conditions of raising animals in a way that actually prevents emergence of disease instead of promoting them,' Perez says. 'The best vaccine is the one we don't have to use.'
Yahoo
14-07-2025
- Health
- Yahoo
Deion Sanders Snaps Over Reporter's Question About His Health, Refuses to Take Question
University of Colorado football coach Deion Sanders shot down a question about his health from a reporter with The Athletic, accusing the outlet of publishing 'bull-junk.' Speaking at Big 12 Media Days at The Star in Frisco, Texas, the NFL Hall of Famer refused to discuss his undisclosed medical issues. Advertisement 'Coach, what have been the challenges of your health issues, and what does an average day look like for you?' asked reporter David Ubben. Sanders was quick and terse with his response. 'Athletic, sometimes y'all be on that bull-junk, so I'm really not gonna tell you much. You know that. But I'm not here to talk about my health,' he fired back. 'I'm here to talk about my team.' Deion Sanders' Health Issues Remain a Mystery As Sportsnaut readers are well aware, Deion Sanders was absent from the team's annual summer football camps last month, with reports suggesting the 57-year-old coach was dealing with an unspecified health issue and had been recovering. Advertisement His eldest son, Deion Sanders Jr., shared in a YouTube livestream on June 8th that his father was 'feeling well' but did not provide details or a timeline for his ailment. 'Coach Prime' hinted at health struggles on a May 30 podcast with former NFL player Asante Samuel, mentioning a 14-pound weight loss and describing his condition as being at 'a whole other level.' 'What I'm dealing with right now is a whole other level,' Sanders told Samuel. 'I'm coming back, but I needed this. I needed this exchange because I haven't had any energy.' For whatever reason, and as is his right, the Buffaloes coach has been unwilling to detail what led to his drastic weight loss and lethargy. Advertisement And he didn't appreciate even being asked about it. RELATED: Coach Prime Sidelined – Deion Sanders Misses Colorado Camps Due to Health Concerns Not His First or Worst Run-in With a Reporter Despite initially bristling at the question, Sanders was quick to flash a smile and pivot to what a day looks like for him on the range. 'Average day? I'm looking good. I'm living lovely. God has truly blessed me,' he replied to Ubben. 'Not a care in the world. Not a want or desire in the world. Thank you, sir.' 'Neon' Deion certainly looks healthy and seems pretty happy about his current state, based on that answer. That's all anybody can really hope for. Advertisement This interaction was tame compared to one of Sander's most infamous run-ins with a reporter. You may recall Deion dumping ice water on late sports broadcaster Tim McCarver – repeatedly – when the latter criticized him for abandoning the Atlanta Braves in the middle of a playoff series to play for the Falcons. Last season, a reporter from The Denver Post was banned due to negative coverage of the Buffaloes. Ubben should feel fortunate by comparison. Cleveland Browns rookie quarterback Shedeur Sanders, Deion's son, believes that 99% of the criticism he has faced is actually directed at his father because of his past behavior. Also Read:: Scout Confirms Why Shedeur Sanders Cratered During the NFL Draft: 'Very Polarizing Guy' Advertisement Related Headlines
Axios
09-07-2025
- Axios
Megan Trussell's family question investigation
The parents of Megan Trussell, the University of Colorado student found dead in February in Boulder Canyon, believe investigators were too quick to rule their daughter's death a suicide and have launched an independent investigation in the hope of getting the case reexamined. Catch up quick: Trussell, 18, was last seen leaving the CU Boulder campus on the night of Feb. 9. She was found dead near the 40-mile marker on Boulder Canyon Drive on Feb. 15. The Boulder County Coroner's Office ruled in May that Trussell, who was prescribed Adderall in 2019, died from "toxic effects of amphetamine, and exposure to a cold environment." The death was ruled a suicide based on "toxicology results and the presence of undigested prescription medication" among other factors, the coroner's office stated. Yes, but: Independent coroners told the Boulder Reporting Lab that the sheer number of pills did support the suicide finding. Driving the news: Trussell's parents requested further testing of the undigested medication in her stomach, and they said last week the coroner's office agreed. The family also gave out care packages in Central Park last Friday to see if anyone in the unhoused community had information that could be relevant to the case. Friction point: Trussell's father, Joe, told Axios Boulder he felt investigators were quick to rule the case a suicide "because that was the easiest conclusion for them to come to." He added: "I was expecting a narrative of some sort, a story … We got none of that. They basically just said, 'Suicide, any questions?'" "They had no sense of urgency, and I felt they had no curiosity," Trussell's mother Vanessa Diaz told us. The other side: Boulder County Sheriff Curtis Johnson released a statement saying that "detectives and deputies conducted a thorough investigation of Megan's death based on the available evidence." "This was a tragic situation," Johnson stated, adding officials with both the sheriff's and coroner's offices met several times with the family attorney to discuss the case. Trussell's parents described their daughter, a film major and bass player, as a laid-back, unique, upbeat and friendly person who "packed a lot into 18 years." "She was cool; she was my little soulmate," Joe Trussell said. Between the lines: Joe Trussell said his daughter had no history of self-harm nor history of suicidal thoughts they knew of. No suicide note was found. Trussell's parents said even if their daughter was suicidal, the location and method "didn't make sense." The sheriff's office called the area where Trussell was found " hard-to-reach terrain," and her parents said Trussell was neither a hiker nor a cyclist and would have had no reason to know about the area. Joe Trussell said a friend who lives in Boulder and rides his bike in the canyon regularly went to the site and told them, "I had no idea this culvert existed. … Nothing will ever convince me that your daughter walked up here." The parents told Axios Boulder that other evidence pointed to foul play. Diaz said the pathologist was too quick to attribute facial and head injuries to the terrain and not a possible assault. Trussell was found with only one shoe, but damage on the exposed sock was to the heel, not the sole, which Diaz felt indicated Trussell had been dragged. Trussell's purse was found by a community member near the 39.6-mile marker of U.S. 36 along the bike path, several miles from her body. Her phone was sold at a Boulder grocery store on March 2 by a man experiencing homelessness who said he'd received it from another unhoused person. What they're saying: Trussell's parents said community members have shared their outrage at the ruling and the perceived lack of investigation. Joe Trussell said searching for the answer "doesn't bring Megan back," but it's a matter of community safety. "Grief is going to be with me the rest of my life," he said. "But as long as it takes, we're going to keep doing this." What's next: Though the case is closed, the sheriff's office told Axios Boulder it would reopen the investigation if new evidence warrants doing so. The Trussell family said they are looking at hiring a private investigator and getting an autopsy review as they continue their "grassroots" effort to reopen the case. Diaz has taken leave as an elementary school teacher to investigate, poring over a binder full of reports and getting billed $700 for requesting video evidence.
Yahoo
03-07-2025
- Health
- Yahoo
New Research Suggests Intelligence Can Be Predicted as Early as 7 Months Old
Fact checked by Sarah ScottA new study found that some kids may show signs of intelligence as babies Experts say parents shouldn't let the study worry them—intelligence also depends on environment and parental involvement Intelligence is more than just IQ, and there are ways for parents to cultivate intelligence throughout their child's lifeNew parents are notorious for looking for early signs of their infant's intelligence—a babbled first word, waving or blowing kisses, a spark of recognition when they see a familiar face. Most of the time it's just an attempt to prove their baby is just as special as their parents know they are—but it might actually be possible to predict a person's adult IQ in infancy? A new study from the University of Colorado Boulder suggests your baby will show signs of intelligence just as early as new parents are convinced they can. In fact, researchers found that it may be possible to predict how well a person will perform on a cognitive test in their 30s as early as 7 months old. So, how exactly can a baby's brain reveal its future potential? To find out, University of Colorado Boulder researchers recruited 500 families with twins (both fraternal and identical). They followed participants at 7 and 9 months, then at age 1, and every year until age 17, continuing every five years into their 30s. Analyzing the decades of data collected from their participants, the goal was to better understand how genes and environment interact to shape a child's development. By studying twins, researchers could determine the distinct roles that genes and shared environment play. Since identical twins share 100% of their genes while fraternal twins share only about 50% (like regular siblings), comparing their IQ similarities allowed researchers to infer how much of cognitive ability is due to genetics versus shared environmental factors. Daniel Gustavson, PhD, an assistant research professor at the University of Colorado Boulder and lead author on the study, says a shared environment includes 'all the aspects of their home, neighborhood, school environments.' The study found that early on, the environment (before age three) can have a measurable and lasting impact on a person's cognitive ability later in life, accounting for around 10% of individual differences in IQ, Dr. Gustavson notes. To test infant cognition, researchers used seven measures, including the 'novelty preference' task that assessed how long infants spend looking at a new toy versus a familiar one, vocalizations (babbling sounds made by the infant), visual expectation (tracking an object), tester ratings (attentiveness, activity, mood), and the Bayley Scales of Infant and Toddler Development. While these specific infant tests (at seven to nine months) predicted only a small percentage of an adult's IQ, the study found that by age three, the yearly follow-ups could predict 20% of what Dr. Gustavson calls 'across-person differences' in IQ. This prediction rapidly increased between ages seven and 16, a period when he says genetics 'really start to take hold.' Although the genes we inherit significantly contribute to our IQ, Dr. Gustavson wants parents to know that heritability doesn't mean 'we can't change who we're going to become.' There are always ways to intervene and learn new skills. The study emphasizes that early environment matters, but it doesn't specify how parents can best nurture cognitive growth. To bridge that gap, we spoke with Sara Douglas, PsyD, Ed.M, a psychologist specializing in neuropsychological evaluations, and pediatrician Heather Gosnell, MD, to offer helpful suggestions. IQ is often viewed as a singular number, but Dr. Douglas says it's essential to look at IQ as one's capacity 'within multiple traits and features.' Here are some simple strategies for holistically nurturing cognitive development in young kids. Viewed this way, a stimulating environment can provide exposure that enhances these traits. Dr. Douglas suggests allowing an infant 'to spend time feeling different textures, seeing different patterns, hearing different notes, [and] interacting with different people.' She adds it's a good idea to 'provide different opportunities for novel experiences. If possible, provide different experiences in the different weeks of development, so young kids have the opportunity both to learn the first [skill], and expand their interest to the next.' Parent-child interaction is also key, says Dr. Gosnell, because 'simple routines like reading, talking, and playing have a powerful impact on brain development and set the foundation for learning.' She recommends reading twenty minutes a day to your infant and continuing this routine through childhood as it supports at-home brain development. You can also narrate your day to help build language skills. And if possible, avoid screen time before 18 months. Once introduced, she says to choose quality programming, watch together, and limit screen time to one hour a day. Remember that this study does not indicate that intelligence is a binary—it's not the case that either they show signs of intelligence early on and will grow upto intelligent, or they don't, and they won't. Intelligence can develop over time, starting with parents who use some of the strategies outlined above. And it doesn't help to stress out over these milestones that will vary from child to child anyway. 'Don't worry if your baby isn't 'advanced' in every area or if they miss one milestone, as uneven development is completely typical,' says Dr. Gosnell. Late talking and short attention spans are also not a cause for concern. 'Most late talkers catch up by age 4 to 7, especially when they understand well, are developing normally in other areas, and receive speech therapy if needed,' Gosnell states. 'Toddlers naturally have very brief focus periods, which is normal and, on their own, don't predict future attention problems.'That said, if you're worried about developmental delays, early intervention will give your child the best chance to reach their full potential. Dr. Gosnell advises talking with your pediatrician if your child isn't 'picking up new skills or seems to be losing abilities they once had.'And remember—IQ and intelligence isn't everything, and definitely does not indicate that your child will be a good person or a productive member of society. 'There are personality traits (like kindness, empathy, genuineness, being a good listener),' says Dr. Douglas, 'that are not factored into intelligence testing that are, in many regards, more important than cognitive traits that are measured.' Read the original article on Parents
