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A better way to convert dog years to human years – EarthSky

December 1st, 2019 10:41 pm

On the left, a young dog (Jack), and on the right, an old dog (Snoop). Photo by Deborah Byrd.

What does it mean for us humans to age, and what does it mean for your dog to age? Turns out these two processes can be compared, some scientists are now saying, and we dont mean in the sense of the old adage that one dog year equals seven human years. That old saying has been recognized for some time as being, quite clearly, imprecise. If it were true, then like dogs humans should be able to reproduce at age 7. Many of us should live to be 150. Now, however, the tools of science have been applied to the question of true length of dog years. Biologist Tina Wang led new research at Ideker Lab at the UC San Diego School of Medicine. The work has resulted in a better formula for calculating your dogs age in human years. It stems from data on the effects of aging on dogs DNA. It takes breed size into account. The new formula suggests that a 1-year-old dog is closer to age 30 than age 7.

We humans and our dogs (and all other living things) have DNA within our cells, coded with the genetic information, inherited from generations of those who came before us. But aging isnt just about genetics. Its also about a healthy or unhealthy lifestyle, for example, and about whether you contract a disease. Scientists who study aging are now speaking of the effects of these environmental factors in terms of chemical markers on our DNA. These markers specifically methyl groups tag our DNA. According to a emerging theory of aging, its the changing pattern of these tags throughout our lives that determines whether you look and seem young for your age or instead age prematurely. This process the chemical modification of a persons DNA over a lifetime creates what aging researchers call an epigenetic clock

The researchers looked at DNA samples from 104 Labrador retrievers spanning a 16-year age range. They compared changes in their DNA samples against DNA previously collected from 320 humans between the ages of 1 and 103. They specifically looked for similarities in the methylation process between the two sets. Writing in the Washington Post on November 28, 2019, Christopher Ingraham explained that the researchers:

found that the DNA profiles evolved in similar ways across the life span of both [dogs and humans].

UCSDs Trey Ideker, leader of the lab that ran the study, told The Post:

If you look at the methylomes of 2-year-old Labs and you ask what are the closest human methylomes? The answer is that the best matches are in humans about 40 years old. That is just what the data show, no more, no less.

An example of the new dog aging chart using, for the sake of comparison, movie star Tom Hanks is below.

Read more via the Washington Post

EarthSky 2020 lunar calendars are available! They make great gifts. Order now. Going fast!

Wang, Ideker and colleagues illustrated their findings using 2 beloved icons: a Labrador and Tom Hanks. Heres the Washington Posts explanation of this chart: According to the DNA analysis, a 1-year-old Lab is equivalent to a Big-era Hanks, while a 4-year-old mirrors the actors star turn in The Da Vinci Code. By age 9, a Lab has obtained the approximate gravitas of Hanks starring as Ben Bradlee in The Post. Chart via Wang et al. and the Washington Post.

Want the actual formula for adjusting dogs ages to human years? You have to multiply the natural logarithm of the dogs age by 16 and add 31. Thus the formula is:

(human_age = 16ln(dog_age) + 31)

That looks like a complicated formula for most of us. Its the natural logarithm of the dogs real age, multiplied by 16, with 31 added to the total. This natural logarithm calculator might help.

Plus, youll find an easy-to-use dog age calculator in this article by Virginia Morell in Science on November 15, 2019.

Why study dog aging at all? As Morell points out in her article, its not just dogs and humans that undergo DNA methylation as they age. Mice, chimps and wolves have also been shown to have epigenetic clocks. Using dogs to study aging makes sense because dogs live in our homes, and many like their human owners receive once-a-year medical checkups and sometimes hospital treatments. Thus studying aging in dogs is another way of understanding how humans age.

Morell also spoke to Matt Kaeberlein, a biogerontologist at the University of Washington in Seattle, who was not involved with this research but whose lab is conducting a Dog Aging Project (open to all breeds) that includes epigenetic profiles of its canine subjects. He hopes to find out why some dogs develop disease at younger ages or die earlier than normal, whereas others live long, disease-free lives. Kaeberlein told Morell:

We already knew that dogs get the same diseases and functional declines of aging that humans do, and this work provides evidence that similar molecular changes are also occurring during aging.

Its a beautiful demonstration of the conserved features of the epigenetic age clocks shared by dogs and humans.

Read more via Science

Heres Jack again when he was 6 or 7 months old. He grew fast! According to the new formula devised by UC San Diego aging researchers, he would have been in his late teens or early 20s when this photo was taken.

Bottom line: A team of researchers on aging at the University of California San Diego performed a genetic analysis of dogs and humans and discovered that compared with humans dogs age faster at first. They reach the equivalent of human middle age after only a few years.

Source: Quantitative translation of dog-to-human aging by conserved remodeling of epigenetic networks

Via the Washington Post

Via Science

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Emerging science gives Norcod a path to further expansion – The Fish Site

December 1st, 2019 10:41 pm

While robust market fundamentals point to a bright future for responsible aquaculture generally, in Norway massively improved biological material is paving the way for a rebound in cod farming in particular.

There has been very limited activity in cod production globally in recent years but that is about to change as pioneering aquaculture venture Norcod's plans to establish cod farming on an industrial scale gather momentum. Led by personnel with deep industry experience, Norcod is convinced that cod has the potential to be a significant contributor to the Norwegian economy. Quality biomass is the critical input factor.

Stemfish with poor biology and first-generation fry of inconsistent quality were partly to blame for the biomass loss seen during the last foray into cod farming between 2004 and 2012. Since then quantum leaps in biology have radically changed the landscape, with an estimated half-a-billion Norwegian kroner invested in two cod breeding programs that have been working quietly in the background in the belief that the tide would again turn.

Aquaculture-focused national research institute Nofima's breeding programme kicked off in 2002 with the goal to evolve economically important characteristics and disease resistance. Commercial hatchery player Havlandet Marin Yngel AS followed suit a year later. Their far-sighted commitment has seen the biological challenges of stagnant growth, susceptibility to infection and high escape figures systematically overcome.

Dramatically increased survival rate and quality of fry has been achieved through careful selection of eggs post fertilisation. The development of stemfish feed with minimal contamination has also boosted egg quality. Detailed comparative studies also showed that using eggs from four-year-old fish produce the best outcomes, according to Nofima.

Fish have been selected and developed for faster growth, higher harvest yield and higher resistance, while new feeds have been developed that support optimal growth and intestinal health. Farmed cod now grows up to 35 percent to 40 percent faster than fish in the wild.

Faster growth has always been the highest priority and has been the focus of the cod breeding programme. Breeding has led to a growth increase of 9 percent to 10 percent per generation, or around 3 percent per year about the same as for farmed salmon, says Atle Mortensen, senior scientist at Nofima.

Data from the stemfish produced for Norcod shows a dramatic 40 percent increase in survival rate for fish below 5 grams, up from 10 percent a decade ago. Successfully selecting for smaller heads has also been a game changer in boosting yield. In wild cod the much larger head can account for 40 percent of body weight.

Today's sixth generation of stem fish is a highly stable product and a completely different fish to 15 years ago, says Norcod managing director Rune Eriksen. Havlandet is now at capacity to deliver around three million fry, at 2-3 grams each, per annum. A kick-off batch of 260,000 fry from Nofima is already in production for Norcod and slated to go into the sea at the company's two facilities northwest of Trondheim imminently.

While growth was the holy grail, selecting specifically for other characteristics typically reduced the growth rate. Targeted breeding for disease resistance was unavoidable until the arrival of new and effective vaccines on the market. With these now available, the bacterial infections vibrosis and atypical furunculosis no longer pose a threat to farmed cod.

As per today there are no virus diseases that create problems for farmed cod. Both cod lice and sea lice affect cod but do not harm the fish like salmon lice do. Intestinal obstruction has very occasionally caused mortality in the sea phase. Compared to farmed salmon the health status of farmed cod is extremely good, says Mortensen.

The fish now show significant domestication, especially calm behaviour in the sea phase, swimming as a school in rings around the net much like salmon. That is astonishing given that selection was not made based on behaviour characteristics, says Mortensen. Not surprisingly, healthy, happy fish adapted to confinement grow faster. The high level of escape in the past was caused by the cod chewing holes in the nets. Today's tame fish display little desire to escape, while new standards and net technologies have also mitigated this tendency. Norcod's facilities are state of the art, optimising technical developments in equipment and feeding systems achieved in salmon farming in recent years.

Cannibalism is a peculiar trait of cod under stress but this problem has been virtually eradicated in the sixth generation of tame fish by means of improved feed and better feed distribution, allowing even growth across the population. Better growth, improved feed and optimal utilisation of feed also make it much easier to satisfy year-round demand.

Breeding has traditionally featured a combination of individual and family-based selection, with family selection ensuring diversity in the broodstock. The advent of molecular genetics, where information from the entire genome can be used for much greater precision in selecting for positive characteristics, promises even faster progress in the future.

Norcod stands to reap the rewards of these biological breakthroughs as a first mover. The quality of its cod is unmatched and unique globally. Initiating such a breeding project from scratch that could guarantee such strong characteristics would require a huge investment of time and money. But consumers want cod right now. Wild stocks are under pressure with limitations in capture quotas squeezing supply. Demand can only be met with cost-effective farming. Norcod's timing is on target to satisfy a market hungry for stable deliveries of fresh cod 12 months of the year.

Ensuring the welfare of the cod themselves throughout the production cycle also remains top priority. We should always remember that these are living creatures that should be handled with care and respect. No question, Eriksen says.

The production process from fry to plate takes between 23 to 26 months. Norcod has its sights set on sales of 9,000 tonnes of cod in 2021, rising to a total of 10 facilities with an output of 25,000 tonnes in 2025. We believe we have a very solid business case, says Eriksen. The market is waiting.

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Student life through the screen – The Gateway Online

December 1st, 2019 10:41 pm

Most of us on the University of Alberta campus have grown up intertwined with the internet. We are digital natives; social interaction on the web is just as natural as in-person communication to us. An essential part of our self-understanding as U of A students, then, comes not just from us interacting in physical space taking classes, participating in extracurriculars, and partying with our pals but also in the digital space of social media.

While the U of A has a plethora of social media pages dedicated to official campus organizations and events, there are a few private U of A pages that serve several purposes: asking questions about registration; sharing unique campus experiences; and even laughing at the U of A itself. How do all these pages operate differently, and how do they create a sense of identity on campus?

A block away from the Enbridge Centre, Im grabbing coffee with Ross Lockwood, the man who started one of the biggest U of A social media pages out there. Sitting at a table on a patio enclosed by office buildings, we sip coffee and talk about the origins of Overheard at the University of Alberta.

Overheard was started by Lockwood and a few friends back in 2007, back when Lockwood was in his third year of a physics degree and before Facebook allowed photo posts. Inspired by the blog Overheard in New York and the quote wall tradition in Lister, Lockwood says that the group mostly just wanted a fun space for U of A students to talk about the weird and wacky stuff theyd heard on campus.

[Overheard] was initially a small group, so maybe like five people had access to it, he says. But we made it public and more people found it useful its a good platform for discussions and things like that.

Due to its public status, the group began to grow very quickly. Overheard now has over 20,000 members, with posts being made daily. Overheard posts are supposed to tackle interesting, odd, or hilarious things overheard or seen on campus. Often this takes the form of text posts recalling snippets of conversation heard in a library; other times its bizarre photos of campus happenings.

If Overheard didnt exist, where would these people be expressing themselves, and where would that expression be appreciated?

Lockwood says that one of the reasons the group is great for U of A students is because it allows people to make connections that they may not have the chance to make in person. He cites Ray Dagg, a custodian at the University Station LRT stop, as one of the prime examples. Dagg, who has become a beloved figure in the group, often posts nature photos from around campus, which get a sizable amount of attention.

I think for a lot of people, being able to develop a community without face-to-face interaction is really good, he says. My question is, if Overheard didnt exist, where would these people be expressing themselves, and where would that expression be appreciated?

With the expansion of the group and Facebook adding new features over the years, the strictness of this doctrine has changed a bit. But its core philosophy has remained the same: make posts that are relevant to the U of A community.

Overheard has always [been about] whats relevant to the university community, Lockwood says. Memes might be funny for a subset of people, they might be annoying for another subset, but we really go for, does this contribute anything of value to the community at large?

This value is not just humorous or light-hearted anymore; at times, Overheard has been at the centre of more serious campus going-ons. One such event happened on October 21 2016, when multiple Overheard members began posting anecdotes about a man contemplating jumping off the sixth floor of CCIS (the man was later taken to hospital without injury). The incident, which was still ongoing when the first posts were made, sparked rampant discussion around the mans motivations, if he was safe, and how mental health is dealt with on campus. For Lockwood and the admin team at Overheard, this was a moment when they realized they needed to step up. They decided to include several campus and Edmonton mental health and distress line services on their page.

We were like, if its something that happens on campus and this person didnt have access to resources, we need to be the place where those resources exist, Lockwood says. Where else would somebody look for help? One of the first places that people get introduced to digitally [at] university, is Overheard.

A year before the CCIS incident, an Overheard post was made about Evan Tran, a U of A student who died by suicide. Tran was well-known on campus; he was a moderator on the Facebook page University of Alberta Compliments, volunteered with the Dean of Students office for their mental health initiatives, was a member of Students Council and General Faculties Council, and volunteered for various student groups. The post mentioning Tran has over 1,900 likes. Commenters are gave their condolences, offered solidarity with Trans family and other students on campus, and shared links to campus resources.

For Overheard admin and recent U of A engineering graduate Subhashis Chikoritaborty, this is one of his favorite moments hes seen on the page.

The amount of support I saw from faculty, [Trans] friends, and everyone who was close was absolutely incredible, he tells me.

Posts like these, and the reactions theyve garnered, seem to represent the other side of the discussion space that Overheard is attempting to foster: one thats not just about funny happenings, but also about vulnerable campus moments and the issues that affect all U of A students.

We want to create a discussion space where people should feel free to discuss [serious] things, [and] I think Overheard can provide that kind of space because its high-traffic, Chikoritaborty says. If you can share something like that [or] something vulnerable, we try to create a space where people can share those thoughts and feel a bit of comfort.

Moving on from Facebook, we come to reddit. More specifically, we come to r/uAlberta, the de-facto subreddit for the U of A community. Founded in 2011 and just over 13,500 members strong, the subreddit is a place for students to ask questions about anything related to their degree, including the quality of certain profs, how to register in certain courses, and what program is best to enroll in. Users have created lengthy guides for various programs and have told varied stories about their U of A experiences; some incredible successes, and some failures as well.

u/firesofpompeii, one of the admins of the subreddit and recent graduate from molecular genetics, says that the subreddit is set apart from other social media sites due to two things: its emphasis on anonymity, and its focus on user engagement.

With reddit in general, anyone can post at any time, [and] although there are users who are more well-known, its not like there are popular users who a lot of people follow, he says. [Everyone is] at an equal playing field, which you dont always get with other social media platforms.

The subreddit is not just a place to ask questions. Much like Overheard, r/ualberta has become a locus for campus discussion; unlike Overheard, however, the subreddits user anonymity has led to the rise and fall of several trollish characters.

If you were to sort of say something in a kind of normal way, often it doesnt get much traction on those sites, but if you say it in a more extreme way, you might get more of a reaction.

Theres been a few notorious users on the subreddit who have drawn the ire of many of the subreddits frequenters. The most notorious of them all, however, was u/unsunghero. They initially drew the ire of the subreddit by starting a thread called Am I too Competitive?. In the thread, they detailed how they would scout out classes considered GPA boosters and ask the professors to curve the class average down, all because they [wanted] to protect the sanctity of the A grade.

u/unsunghero would continue to troll the subreddit and share many controversial opinions, and soon the moderators of r/uAlberta were getting complaints. They couldnt do much, however, because u/unsunghero technically wasnt violating the rules of the subreddit. As long as a user is being civil in expressing their opinion, even if it is one that many people disagree with, the moderators let their posts stand.

Weve had a lot of users complain about them, thats why weve had to tell them that until theyre attacking other subscribers then theres nothing we can really do about it, u/firesofpompeii says. We definitely dont want to censor people.

To anyone whos spent anytime online, this kind of behaviour isnt unusual. Johnathan Cohn, an assistant professor in the department of English at the U of A whose research focuses on critical internet studies and digital culture, says that digital spaces often lend themselves to this kind of behaviour. This is both because theyre a relatively safe space to perform different identities and figure out who you are, and because these sites encourage more extreme modes of behaviour.

If you were to sort of say something in a kind of normal way, often it doesnt get much traction on those sites, but if you say it in a more extreme way, you might get more of a reaction, Cohn says. So it also sort of encourages people who are more extreme, in one way or another, to interact more, and it discourages people who maybe dont like that kind of interaction.

Trolls arent the only thing that the subreddit occasionally fosters. It has broken out into meme territory as well, creating lore that has arguably given the community its own identity and history beyond being a forum for student questions.

The most recent example of such territory is the Ghoul Wars, a saga that began on January 24 2019 with a post by u/lividnaynay that spoke of an experience they had with a particularly unhygienic student. Three days later, u/RogerMooreIsMyDad made a post stating I swear im (sic) going to buy a costco pack of deodorant and hand it out to all the little engg ghouls running around DICE.

That was enough to set off a dramatized war between the Ghouls and the Resistance. Posts were made detailing battle plans for the war, casualty reports, and the development of ghoul-repellant technology. Dozens upon dozens of these posts sprung up; it felt like an augmented reality game had suddenly began on the subreddit.

When I ask u/firesofpompeii about the Ghoul War, he simply laughs; I can practically hear his head shake over the phone.

That kinda made me feel really old, cause I had no idea what was going on, he says. I was just kind of a bystander to that.

In his five years as admin, this isnt the first time u/firesofpompeii has seen events like the Ghoul War arise. Back in 2016, r/uAlberta and r/UCalgary had a meme war, flaming each other in various memes over a period of a few months. Events like this are apparently cyclical on the subreddit; they come and go, cementing themselves as defining moments in the development of the rhetoric and identity of the subreddit.

With each of these cycles, r/uAlberta slowly becomes its own community apart from the physical U of A.

The term meme was first coined by Richard Dawkins in his book The Selfish Gene. For Dawkins, memes are like genes of culture; they are ideas and concepts that spread in communities and get passed down over time. A memes fidelity how well it can retain its original idea as it spreads varies depending on the specificity of the idea. Oftentimes memes with community-specific ideas dont travel very far, whiles memes with more generalizable ideas do.

This can be seen in the different content U of A-related Instagram meme pages put out. Some pages like @ualberta_memes stick very close to U of A material, with past topics including Konz (a short-lived and universally hated pizza place in the Students Union Building), the UASU, and other U of A happenings. Other pages, like @uofaenggmemes seem to take general engineering student memes and put a U of A label on them.

[More generalized memes] translate very broadly but are very weak in their transmission, Cohn says. They can be rethought and reused in a lot of ways, but the original meaning or community [from whence the meme came] gets lost very quickly.

@ualberta_memes is the biggest U of A Instagram meme page, having gained over 6,600 followers since its start on February 4 2019. The admin of the page a third-year kinesiology student who wishes to remain anonymous tells me over the phone that he started the page as a way to kill boredom. He posted a few memes on that fateful day, and the response he received encouraged him to continue.

We can either come to school and just clock-in clock-out, or you can look at everything around you and kind of care a little more than you usually do.

@ualberta_memes sources his content from a variety of places. Typically he makes the memes himself and posts them directly to his page, but he also will post submissions and take ideas for memes. The core of his content, in typical internet meme fashion, pokes fun at a group; namely, the various faculties on campus.

A lot of it is just to show that we all have faults and we can all kind of make fun of ourselves to a certain level, he says.

@ualberta_memes feels personally that the U of A lacks a strong sense of culture, given how large the school is and that people from all over the world attend it. Through making posts that highlight universal U of A experiences like the disaster that was Konz or Listers dodgeball culture @ualberta_memes hopes to help students feel more connected to their campus.

You get people [starting] to care a little more about the small things that you see on campus, he says. Thats kind of important because we can either come to school and just clock-in clock-out, or you can look at everything around you and kind of care a little more than you usually do.

In this way, students are able to feel more attached to their campus and to each other in more tangible ways; instead of simply proclaiming Im a U of A student because I go to the U of A, students can begin to point out the multitude of small, specific details that make up their campus experience.

Another account, @ualbertameme, started just a month after @ualberta_memes. The main admin of the page a third-year science student who also wished to remain anonymous was inspired to start his page in a similar way to @ualberta_memes.

When sourcing posts for the page, @ualbertameme looks for universal U of A experiences that are easily translatable into memes. The page is run by a small team of about five people, all of whom work on different aspects of the page; some post content, others check analytics, and others handle responding to DMs and comments from followers.

Some of the feedback that @ualbertameme has gotten from his followers is that his pages memes help boost student morale, especially during exam season. In a way, being able to laugh about the experience of being a U of A student helps to bring people together and make student life a little easier.

University is supposed to be a relatively fun experience, although it can get really difficult at times, he says. I guess seeing things like memes kind of helps alleviate the pressure or the anxiety that comes with university.

What makes an Instagram meme page different from hanging out on Overheard or r/uAlberta? Both page admins have different answers. For @ualberta_memes, its having an anonymous admin post all the memes. He can post memes on behalf of people who are afraid of judgement, and can also act as a scapegoat in case someone gets upset about their faculty being made fun of.

The whole anonymous aspect of me posting, I think, gives people more comfort to comment what they want, he says. It doesnt have to feel like whoever is posting it might be made fun of or might be judged by their friends or something.

Its easy on these sites to feel like you have nothing to contribute and that therefore youre not part of the community, but thats the normal situation.

For @ualbertameme, its the relaxed nature of Instagram pages, which dont have to have as strict of accountability measures as other platforms.

Certain pages like Overheard, they have to appear [to have] a certain level of responsibility and accountability, he says. On meme pages, people can post whatever they want and there wouldnt really be any repercussions unless its a very serious thing.

***

If theres one thing all of these pages try to do, its capture fragments of the U of A student experience and provide a space for them to be disseminated and discussed. With their varying degrees of anonymity, subject matter, and unique rhetoric and rules, each page fills a different niche.

Many of us may feel out of place on these pages; we may lurk instead of post, feeling out of place or feeling like we lack something to contribute. But as Cohn said before, most people who post on these pages are on the hyper end of extroverted, and they likely only make up a small percentage of the group.

If youre someone in these groups who doesnt post much and you feel sort of marginal, you are actually the norm, he says. Its easy on these sites to feel like you have nothing to contribute and that therefore youre not part of the community, but thats the normal situation.

Lurker or poster, we all can feel more connected to our campus through these pages. They bring us together in times of need, alleviate exam pain, foster discussion about issues on campus, and help us begin to love the little things about being a U of A student.

These pages, arguably, are just as integral to being a U of A student as going to class.

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Humans Co-Evolved with Immune-Related Diseasesand It’s Still Happening – Lab Manager Magazine

December 1st, 2019 10:41 pm

Credit: iStock

Some of the same mutations allowing humans to fend off deadly infections also make us more prone to certain inflammatory and autoimmune diseases, such as Crohn's disease. In a review published November 27 in the journalTrends in Immunology, researchers describe how ancestral origins impact the likelihood that people of African or Eurasian descent might develop immune-related diseases. The authors also share evidence that the human immune system is still evolving depending on a person's location or lifestyle.

"In the past, people's lifespans were much shorter, so some of these inflammatory and autoimmune diseases that can appear in the second half of life were not so relevant," says first author Jorge Dominguez-Andres (@dominjor), a postdoctoral researcher at Radboud Institute for Molecular Life Science in the Netherlands. "Now that we live so much longer, we can see the consequences of infections that happened to our ancestors."

One of the body's best defenses against infectious diseases is inflammation. Dominguez-Andres and senior author Mihai Netea, a Radboud University immunologist and evolutionary biologist, compiled data from genetics, immunology, microbiology, and virology studies and identified how the DNA from people within different communities commonly infected with bacterial or viral diseases was altered, subsequently allowing for inflammation. While these changes made it more difficult for certain pathogens to infect these communities, they were also associated with the emergenceover timeof new inflammatory diseases such as Crohn's disease, Lupus, and inflammatory bowel disease.

"There seems to be a balance. Humans evolve to build defenses against diseases, but we are not able to stop disease from happening, so the benefit we obtain on one hand also makes us more sensitive to new diseases on the other hand," says Dominguez-Andres. "Today, we are suffering or benefiting from defenses built into our DNA by our ancestors' immune systems fighting off infections or growing accustomed to new lifestyles."

For example, the malaria parasite Plasmodium sp. has infected African populations for millions of years. Because of this, evolutionary processes have selected people with DNA that favors resistance to infections by causing more inflammation in the body. In doing so, this has also contributed to making modern Africans prone to developing cardiovascular diseases, such as atherosclerosis, later in life.

Dominguez-Andres and Netea also write about how the early-human ancestors of Eurasians lived in regions still inhabited by Neanderthals and interbred. Today, people with remainders of Neanderthal DNA can be more resistant against HIV-1 and 'staph' infections, but are also more likely to develop allergies, asthma, and hay fever.

The negative side effects of changes in each population's immune systems are a relatively recent finding. "We know a few things about what is happening at the genetic level in our ancestry, but we need more powerful technology. So, next generation sequencing is bursting now and allowing us to study the interplay between DNA and host responses at much deeper levels," says Dominguez-Andres. "So, we are obtaining a much more comprehensive point of view."

These technologies are also revealing how our immune systems are evolving in real time because of modern lifestyle changes. African tribes that still engage in hunting have greater bacterial gut diversity than urbanized African-Americans that eat store-bought foods. Also, changes in hygiene patterns seen in the last two centuries have improved sanitation, drinking water, and garbage collection, and have led to reduced exposure to infectious pathogens relative to previous times. As humans move toward processed foods and stricter hygiene standards, their bodies adapt by developing what researchers call "diseases of civilization," such as type 2 diabetes.

Moving forward, Dominguez-Andres and Netea will expand their research to communities that fall outside African and Eurasian populations. "So far, all of the studies we went through are focused on populations with European and African descent, but they must also be extended to indigenous and other populations to improve the representation of human genetic diversity," says Dominguez-Andres. "Lifestyles and ecologic natures can really differ and influence immune responses. So, more work needs to be done."

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Longevity Linked to Proteins That Calm Overexcited Neurons – Quanta Magazine

November 30th, 2019 6:46 pm

A thousand seemingly insignificant things change as an organism ages. Beyond the obvious signs like graying hair and memory problems are myriad shifts both subtler andmore consequential: Metabolic processes run less smoothly; neurons respond less swiftly; the replication of DNA grows faultier.

But while bodies mayseem to just gradually wear out, many researchers believe instead that aging is controlled at the cellular and biochemical level. They find evidence for this in the throngof biological mechanisms that are linked to aging but also conserved across species as distantly related as roundworms and humans. Whole subfields of research have grown up around biologists attempts to understand the relationships among the core genes involved in aging, which seem to connect highly disparate biological functions, like metabolism and perception. If scientists can pinpoint which of the changes in these processes induce aging, rather than result from it, it may be possible to intervene and extend the human life span.

So far, research has suggested that severely limiting calorie intake can have a beneficial effect, as can manipulating certain genes in laboratory animals. But recently in Nature, Bruce Yankner, a professor of genetics and neurology at Harvard Medical School, and his colleagues reported on a previously overlooked controller of life span: the activity level of neurons in the brain. In a series of experiments on roundworms, mice and human brain tissue, they found that a protein called REST, which controls the expression of many genes related to neural firing, also controls life span. They also showed that boosting the levels of the equivalent of REST in worms lengthens their lives by making their neurons fire more quietly and with more control. How exactly overexcitation of neurons might shorten life span remains to be seen, but the effect is real and its discovery suggests new avenues for understanding the aging process.

In the early days of the molecular study of aging, many people were skeptical that it was even worth looking into. Cynthia Kenyon, a pioneering researcher in this area at the University of California, San Francisco, has described attitudes in the late 1980s: The ageing field at the time was considered a backwater by many molecular biologists, and the students were not interested, or were even repelled by the idea. Many of my faculty colleagues felt the same way. One told me that I would fall off the edge of the Earth if I studied ageing.

That was because many scientists thought that aging (more specifically, growing old) must be a fairly boring, passive process at the molecular level nothing more than the natural result of things wearing out. Evolutionary biologists argued that aging could not be regulated by any complex or evolved mechanism because it occurs after the age of reproduction, when natural selection no longer has a chance to act. However, Kenyon and a handful of colleagues thought that if the processes involved in aging were connected to processes that acted earlier in an organisms lifetime, the real story might be more interesting than people realized. Through careful, often poorly funded work on Caenorhabditis elegans, the laboratory roundworm, they laid the groundwork for what is now a bustling field.

A key early finding was that the inactivation of a gene called daf-2 was fundamental to extending the life span of the worms. daf-2 mutants were the most amazing things I had ever seen. They were active and healthy and they lived more than twice as long as normal, Kenyon wrote in a reflection on these experiments. It seemed magical but also a little creepy: they should have been dead, but there they were, moving around.

This gene and a second one called daf-16 are both involved in producing these effects in worms. And as scientists came to understand the genes activities, it became increasingly clear that aging is not separate from the processes that control an organisms development before the age of sexual maturity; it makes use of the same biochemical machinery. These genes are important in early life, helping the worms to resist stressful conditions during their youth. As the worms age, modulation of daf-2 and daf-16 then influences their health and longevity.

These startling results helped draw attention to the field, and over the next two decades many other discoveries illuminated a mysterious network of signal transduction pathways where one protein binds another protein, which activates another, which switches off another and so on that, if disturbed, can fundamentally alter life span. By 1997, researchers had discovered that in worms daf-2 is part of a family of receptors that send signals triggered by insulin, the hormone that controls blood sugar, and the structurally similar hormone IGF-1, insulin-like growth factor 1; daf-16 was farther down that same chain. Tracing the equivalent pathway in mammals, scientists found that it led to a protein called FoxO, which binds to the DNA in the nucleus, turning a shadowy army of genes on and off.

That it all comes down to the regulation of genes is perhaps not surprising, but it suggests that the processes that control aging and life span are vastly complex, acting on many systems at once in ways that may be hard to pick apart. But sometimes, its possible to shine a little light on whats happening, as in the Yankner groups new paper.

Figuring out which genes are turned on and off in aging brains has long been one of Yankners interests. About 15 years ago, in a paper published in Nature, he and his colleagues looked at gene expression data from donated human brains to see how it changes over a lifetime. Some years later, they realized that many of the changes theyd seen were caused by a protein called REST. REST, which turns genes off, was mainly known for its role in the development of the fetal brain: It represses neuronal genes until the young brain is ready for them to be expressed.

But thats not the only time its active. We discovered in 2014 that [the REST gene] is actually reactivated in the aging brain, Yankner said.

To understand how the REST protein does its job, imagine that the network of neurons in the brain is engaged in something like the party game Telephone. Each neuron is covered with proteins and molecular channels that enable it to fire and pass messages. When one neuron fires, it releases a flood of neurotransmitters that excite or inhibit the firing of the next neuron down the line. REST inhibits the production of some of the proteins and channels involved in this process, reining in the excitation.

In their new study, Yankner and his colleagues report that the brains of long-lived humans have unusually low levels of proteins involved in excitation, at least in comparison with the brains of people who died much younger. This finding suggests that the exceptionally old people probably had less neural firing. To investigate this association in more detail, Yankners team turned to C. elegans. They compared neural activity in the splendidly long-lived daf-2 mutants with that of normal worms and saw that firing levels in the daf-2 animals were indeed very different.

They were almost silent. They had very low neural activity compared to normal worms, Yankner said, noting that neural activity usually increases with age in worms. This was very interesting, and sort of parallels the gene expression pattern we saw in the extremely old humans.

When the researchers gave normal roundworms drugs that suppressed excitation, it extended their life spans. Genetic manipulation that suppressed inhibition the process that keeps neurons from firing did the reverse. Several other experiments using different methods confirmed their results. The firing itself was somehow controlling life span and in this case, less firing meant more longevity.

Because REST was plentiful in the brains of long-lived people, the researchers wondered if lab animals without REST would have more neural firing and shorter lives. Sure enough, they found that the brains of elderly mice in which the Rest gene had been knocked out were a mess of overexcited neurons, with a tendency toward bursts of activity resembling seizures. Worms with boosted levels of their version of REST (proteins named SPR-3 and SPR-4) had more controlled neural activity and lived longer. But daf-2 mutant worms deprived of REST were stripped of their longevity.

It suggests that there is a conserved mechanism from worms to [humans], Yankner said. You have this master transcription factor that keeps the brain at what we call a homeostatic or equilibrium level it doesnt let it get too excitable and that prolongs life span. When that gets out of whack, its deleterious physiologically.

Whats more, Yankner and his colleagues found that in worms the life extension effect depended on a very familiar bit of DNA: daf-16. This meant that RESTs trail had led the researchers back to that highly important aging pathway, as well as the insulin/IGF-1 system. That really puts the REST transcription factor somehow squarely into this insulin signaling cascade, said Thomas Flatt, an evolutionary biologist at the University of Fribourg who studies aging and the immune system. REST appears to be yet another way of feeding the basic molecular activities of the body into the metabolic pathway.

Neural activity has been implicated in life span before, notes Joy Alcedo, a molecular geneticist at Wayne State University who studies the connections between sensory neurons, aging and developmental processes. Previous studies have found that manipulating the activity of even single neurons in C. elegans can extend or shorten life span. Its not yet clear why, but one possibility is that the way the worms respond biochemically to their environment may somehow trip a switch in their hormonal signaling that affects how long they live.

The new study, however, suggests something broader: that overactivity in general is unhealthy. Neuronal overactivity may not feel like anything in particular from the viewpoint of the worm, mouse or human, unless it gets bad enough to provoke seizures. But perhaps over time it may damage neurons.

The new work also ties into the idea that aging may fundamentally involve a loss of biological stability, Flatt said. A lot of things in aging and life span somehow have to do with homeostasis. Things are being maintained in a proper balance, if you will. Theres a growing consensus in aging research that what we perceive as the body slowing down may in fact be a failure to preserve various equilibria. Flatt has found that aging flies show higher levels of immune-related molecules, and that this rise contributes to their deaths. Keeping the levels in check, closer to what they might have been when the flies were younger, extends their lives.

The results may help explain the observation that some drugs used for epilepsy extend life span in lab animals, said Nektarios Tavernarakis, a molecular biologist at the University of Crete who wrote a commentary that accompanied Yankners recent paper. If overexcitation shortens life span, then medicines that systematically reduce excitation could have the opposite effect. This new study provides a mechanism, he said.

In 2014, Yankners laboratory also reported that patients with neurodegenerative diseases like Alzheimers have lower levels of REST. The early stages of Alzheimers, Yankner notes, involve an increase in neural firing in the hippocampus, a part of the brain that deals with memory. He and his colleagues wonder whether the lack of REST contributes to the development of these diseases; they are now searching for potential drugs that boost REST levels to test in lab organisms and eventually patients.

In the meantime, however, its not clear that people can do anything to put the new findings about REST to work in extending their longevity. According to Yankner, REST levels in the brain havent been tied to any particular moods or states of intellectual activity. It would be a misconception, he explained by email, to correlate amount of thinking with life span. And while he notes that there is evidence that meditation and yoga can have a variety of beneficial effects for mental and physical health, no studies show that they have any bearing on REST levels.

Why exactly do overexcited neurons lead to death? Thats still a mystery. The answer probably lies somewhere downstream of the DAF-16 protein and FoxO, in the genes they turn on and off. They may be increasing the organisms ability to deal with stress, reworking its energy production to be more efficient, shifting its metabolism into another gear, or performing any number of other changes that together add up a sturdier and longer-lived organism. It is intriguing that something as transient as the activity state of a neural circuit could have such a major physiological influence on something as protean as life span, Yankner said.

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How do consumer DNA tests from the US and China stack up? – Abacus

November 30th, 2019 6:46 pm

Spitting intotheplastic test tube, I felt nervous. I was offering up a piece of myself for decoding, and while this timethere was no silver-haired sage, it reminded me of a visit to a fortune teller when I was 21.

Then, I offeredthepalm of my hand in a bid to divine what fate had planned for me. Now, it wasDNA, with my saliva destined for a laboratory in southwest China, totheheadquarters ofChengdu 23Mofang Biotechnology Co., a startup thats seeking to tap a boom in consumer genetics intheworlds most populous nation.

Rising awareness of genetically-linked diseases like Alzheimers and a natural human curiosity for insight intothefuture is fueling a global market for direct-to-consumerDNAtesting thats predicted totripleoverthenext six years. In China, wherethegovernment has embraced genetics as part of its push to become a scientific superpower,theindustry is expected to see US$405 million in sales by 2022, according to Beijing research firm EO Intelligence, an eight-fold increase from 2018. Some 4 million people will send away test tubes of spit in China this year, and I had just become one ofthem.

Not only was I entering a world where lack of regulation has spawned an entire industry devoted to identifyingthefuture talents of newborn babiesthroughtheir genes, I was handing over my genetic code to a country wherethegovernment has been accused of usingDNAtesting to profile minority groups a concern that hit home whentheresults showed I was a member of one.

I wanted to see whethertheburgeoning industry delivered on its claims in China, where scientists have gained international attention and criticism for pushingtheboundaries of genetics. And as a child of Vietnamese immigrants totheUS, Ive long been curious about my ancestry and genetic makeup.

To get an idea of how this phenomenon is playing out intheworlds two biggest consumer markets, I comparedtheDNAtesting experience of 23Mofang withthefirm CEO Zhou Kun says it was inspired by:23andMe Inc., one ofthebest known consumer genetics outfits intheUS.

PushingtheEnvelope

Thedifferences betweenthetwo companies are stark.

23andMe was co-founded byAnne Wojcicki, a Wall Street biotech analyst once married toGoogleco-founderSergey Brin.TheMountain View, California-based firm has more than 10 million customers and has collected 1 billion genetic data points, according to itswebsite. Brin and Google were early investors.

By contrast, 23Mofang is run out oftheChinese city of Chengdu, and Zhou, 36, is a computer science graduate who createdthecompany after becoming convinced Chinas next boom would be inthelife sciences sector. 23Mofang expects to have 700,000 customers bytheend of this year, a number he projects will at least double in 2020.

Thedivergence betweenthetwo countries andtheir regulation oftheindustry is just as palpable. Chinas race to dominate genetics has seen it push ethical envelopes, with scientistHe Jiankuisparking a global outcry last year by claiming to have editedthegenes of twin baby girls.Theexperiment, which He said madethem immune to HIV, put a spotlight on Chinas laissez-faire approach to regulating genetic science andthebusinesses that have sprung up around it.

When my reports came back, 23Mofangs analysis was much more ambitious than its American peer. Its results gauged how long I will live, diagnosed a high propensity for saggy skin (recommending I use products including Olay and Estee Lauder creams) and gave me an optimist not prone to mood swings a higher-than-average risk of developing bipolar disorder. 23andMe doesnt assess mental illness, which Gil McVean, a geneticist at Oxford University, says is highly influenced by both environmental and genetic factors.

Thefortune teller who pored over my palm told me I would live to be a very old woman. 23Mofang initially said I had a better-than-average chance of living to 95, before revisingtheresults to say 58% of clients hadthesame results as I did, making me not that special, and perhaps not that long-living.

When I ranthefinding pastEric Topol, a geneticist who foundedtheScripps Research Translational Institute in La Jolla, California, he laughed. Ninety-five years old?Theres no way to put a number on longevity, he said. Its a gimmick. Its so ridiculous.

Zhou saidtheaccuracy ofthelongevity analysis, based on a 2014 genetics paper, is not too bad, thoughthecompany plans to updatetheanalysis with research thats being undertaken on Chinese elderly.

But when it comes to disease,theresults of both companies showed howthescience of genetics, particularly attheconsumer level, is still a moving target.

Its All AbouttheData

After claiming I had a 48% greater risk thanthegeneral population of developing type 2 diabetes, both 23Mofang and 23andMethen revisedtheresults.

First, 23andMe cuttherisk figure from its analysis, posted in an online portal I accessed with a password.Theoverview analysis that I have an increased likelihood of developingthedisease never changed. But a few months later,thefigure was back, with a slightly different explanation: Based on data from 23andMe research participants, people of European descent with genetics like yourshave an estimated 48% chance of developing type 2 diabetes at some point between your current age and 80.

Shirley Wu, 23andMes director of health product, saidthecompany occasionally updates its analysis. My risk figure might have changed if I indicated my ethnicity and age, she said. I hadnt given any biographical details or filled out any surveys on 23andMes site.

Your risk estimates will likely change over time as science gets better and as we have more data, Wu said. We are layering in different non-genetic risk factors, and that potentially updates our estimates.

Algorithms and data underpintheanalysis of both companies, asthey do for other genetic testing firms, so it apparently isnt unusual forDNAanalysis to shift as more research and data into diseases becomeavailable. Still, I was confused.

I reached out to Topol, who said that 23andMes diabetes finding likely didnt apply to me sincethevast majority of people studied forthedisease are of European descent. Wu saidthe American company does have a predominantly European database but has increased efforts to gather data for other ethnicities as well.

23Mofang, meanwhile, also revised my diabetes risk to 26%. My genes hadnt changed, so why hadtheresults? CEO Zhou saidthecompany is constantly updating its research and datasets, and that may changetheanalysis. As time goes by,there will be fewer corrections and greater accuracy, he said.

For now, theres a possibility you can later get a result thats opposite oftheinitial analysis, said Zhou.

Additionally,theaccuracy of genetic analysis varies hugelydepending onthetraits and conditions tested because some are less genetically linkedthan others.

Zhou isnt deterred by criticism. He said 23Mofang employs big data and artificial intelligence to findthecorrelations to diseases without relying on scientists to figure it out.

While its impossible to get things 100% right,thecompanys accuracy will get better with more data, he said.

Ancestry Mystery

You might assume thatthetwo companies would offer similar analysis of my ancestry, which Ive long thought to be three-fourths Vietnamese and one-fourth Chinese (my paternal grandfather migrated from China as a young man). Born in Vietnam and raised intheUS, I now live in Hong Kong, a special administrative region of China.

23andMes analysis mirrored what I knew, but my ancestry according to 23Mofang? 63% Han Chinese, 22% Dai an ethnic group in southwestern China and 3% Uyghur. (It didnt pick up my Vietnam ancestry becausetheanalysis only compares my genetics to those of other Chinese, according tothecompany.)

That led me tothebig question in this grand experiment: How safe is my data afterthesetests?

Human Rights Watch said in 2017 that Chinese authorities collectedDNAsamples from millions of people in Xinjiang,thepredominately Muslim region thats home totheUyghur ethnic group. Chinas use of mass detention and surveillance intheregion has drawn international condemnation. What if Beijing compelled companies to relinquishdata on all clients with Uyghur ancestry? Couldthedetails of my Uyghur heritage fall into government hands and put me at risk of discrimination or extra scrutiny on visits to China?

23Mofangs response tothese questions didnt give me much solace. Regulations enacted in July gavethegovernment access to data held by genetics companies for national security, public health and social interest reasons.Thecompany respectsthelaw, said Zhou. Ifthelaw permitsthegovernments access tothedata, we will give it, he said.

Theauthorities havent made any requests for customer data yet, Zhou pointed out. Chinas State Council, which issuedtheregulations, andtheMinistry of Science & Technology didnt respond to requests for comment.

Over intheUS, 23andMe said it never shares customer data with law enforcement unlesstheres a legally valid requestsuch as a search warrant or written court order.Thecompany said its had seven government requests for data on 10 individual accounts since 2015 and has not turned over any individual customer data. It uses all legal measures to challenge such requests to protect customers privacy, said spokeswoman Christine Pai.

No Protection

New York Universitybioethics professorArt Caplansays privacy protections on genetic information are poor in most countries, including in the USand China.

I dont think anyone can say theyre going to protect you, he said. In China, its even easier for the government. The government retains the right to look.

23andMe appeals to potential customers with the lure of being able to make more informed decisions about your health, but after taking tests on both sides of the Pacific and realizing how malleable the data can be, as well as the myriad factors that determine diseases and conditions, I am left more skeptical than enlightened.

I gave away something more valuable than a vial of spit the keys to my identity. It could become a powerful tool in understanding disease and developing new medicines, but in the end its entrepreneurs like Zhou who will ultimately decide what to do with my genetic data. He plans to eventually look for commercial uses, like working with pharmaceutical companies to develop medicines for specific diseases.

We want to leverage the big database we are putting together on Chinese people, Zhou said. But first, we need to figure out how to do it ethically.

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The biological defects that come with age and how to prevent them – Ladders

November 30th, 2019 6:46 pm

I mightve died fearing the ageing process about as much as everyone else. Unfortunately, about two drags into my fourth cigarette a friend of mine relayed an anecdote about his dying grandfatherunprompted.

So its his ninety-eighth birthday and were watching him try to blow out candles on a cake he probably cant eat anywayfor like an hour.Eventually, I get bored and blow it out for him before asking what he wished for. To which he says: I accidentally peeped the expiration date on the carton of milk in the fridge and it dawned on me that I didnt know which one of us had more time left.

In an instant, I quit smoking and took up gerascophobia. In defense of the soon-to-be-dead-party-pooper, the older we get the louder minute hands become. We try to dull the racket by route of cosmetics, pop culture, copulation and fairy-tales; all to distract ourselves from the inevitable frog march into nothingness. If were honest, every year after 50 extends a catalog of things we cant do anymore. The list begins innocuously enough with things like fit into my favorite pair of whatevers or comprehend the cultural significance of this or that, but then the whole thing ends tragically nuanced.

Were all familiar with the odd way time seems to speed up every year after 21? It makes sense that time adopts the illusion of expedience as we run out of milestones but the reasoning behind this phenomenon is actually even less abstract than that. According to a new paper published in the scientific journalEuropean Review, as wrinkles begin to appear, and our postures sag, our neurons grow larger, increasing the amount of time it takes us to process an image.

People are often amazed at how much they remember from days that seemed to last forever in their youth, explained the new studys author Adrian Bejan, the J.A. Jones Professor of Mechanical Engineering at Duke University in a pressrelease.Its not that their experiences were much deeper or more meaningful, its just that they were being processed in rapid-fire.

Interestingly enough, almost all of the psychological conditions that narrate our morph into maggot food are effected by well-documented physiological precursors.

Little mutations join forces to pen an aggressive eviction notice apostrophized by medical abnormalities that condemn life on planet earth to be less and less pleasant.This is especially relevant right now because Americas global age is increasing at an exponential rate.

When a society attains economic and agricultural excellence the death rate decreases alongside birthrate, which leads to a larger and older population.James Fries, professor of medicine at Stanford University, indexed the sociological fine-print that punctures this developmental achievement back in 1998. What Fries calls the compression of morbidity dictates that denizens of a thriving nation enjoy healthy lives for most of it until a series of health setbacks plague them all at once toward the final stretch. This is often in the form of chronic illness that appears in tandem with natural biological regressions. As far as the perversion of our mind clocks are concerned, organic changes in saccades frequency, body size, and pathway degradation have been studied to be the primary culprits. This is what physics more discreetly refers to asthe constructional law of low architecture. Elderly people simply receive fewer images in the same amount of time as younger people, drastically decelerating their integration of information. The mechanisms that animate this process are fairly identical to a cameras shutter speed.

The human mind senses time changing when the perceived images change, Bejan adds. The present is different from the past because the mental viewing has changed, not because somebodys clock rings. Daysseemed to last longerin your youth because the young mind receives more images during one day than the same mind in old age.

Overall somatic decline is ensured by similar physiological defects. New data published by researchers at Yale University revealed that our ability to obtain energy by burning belly fat also reduces as we grow older. This impairment is a direct cost of medical and agricultural preferments that have allowed us to defy our intended life expectancy.

Several mechanisms in the body are not selected for longevity,explained the papers lead researcher, Vishwa Deep Dixit. Normally the B cells produce antibodies and defend against infection. But with aging, the increased adipose B cells become dysfunctional, contributing to metabolic disease. This predisposes an animal to diabetes and metabolic dysfunction like inability toburn fat.

Thankfully, successful aging is no longer a consideration beholden to science fiction. Genetics may draft the treatment, but our lifestyle choices govern how gracefully we interpret the consequential beats. Presbycusis for instance (gradual degeneration of the cochlea consequenced by bilateral symmetrical aging) is by all accounts unavoidable. It is the leading cause of hearing loss and affects just about one and two individuals over the age of 75. However, there are cumulative environmental predictors that can worsen the condition and even accelerate its development. Prolonged exposure to headphone frequencies causes the hair cells in the cochlea to bend beyond the point of repair. Uniformly, we all have a reserve capacity of cells, each of which dies without fanfare throughout a given day.

Of course, as we age, this process, which is calledapoptosis, picks up momentum. What you might not know though is our state of mind mandates how quickly and violently this program transpires.

Having a good attitude is very important. We know that stress plays a key role in how we will age. We have these hormones, these stress hormones, that actually play a role in how our cells will die. When we become under stress we have an accelerated loss of cells. So this over a lifetime plays a major role in how functional we will be, explainedSteven Gambert, MD.

Even more consistently than this is the role our diet plays in the pace of our weathering. Diets like the Mediterranean, a regimen rich in vegetables and olive oil, low in meat ingestion, and moderate in alcohol consumption, slackens the agents of aging by checking their pawns, namely chronic maladies associated with old age. A recent study conducted on 23,349 men and women confirmed what previous literature had intimated in years prior. Medical journalist, Caroline Wilbert reports:

During the study period, there were 652 deaths among 12,694 participants who had lower Mediterranean diet scores of 0-4 and 423 deaths among the 10,655 participants who had higher scores of at least 5. In general, those with higher scores were more likely to still be alive at the end of the study.

Similarly, earlier this year a team of European researchers disclosed that routine coffee consumption contributes to DNA integrity and overall longevity. This is earned by the antioxidants residing in dark roasted beans, a compound that helps cells repair themselves more effectively in the wake of the damage done by free radicals. Free radicals, birthed by sunlight, oxygen, and pollution, deteriorate the collagen fibers in the skin. The microbial properties in coffee help staff off these very same germs. Its caffeine acid boosts collagen levels which in turn brakes the aging process.

When it comes to confronting the aspects of aging that we cannot outwit, its important to distinguish a superficial fear of growing old, alternatively phrased as literal molecule deterioration, from a philosophical fear of death; the metaphysical cessation of being. Though Im not deaf to the terror of either, the attenuating of the former cant really refute the latter in and of itself. In other words, extending life for its own sake wont do you any good without some kind of moral equipment to boot. However you go about securing this is valid enough so long as it doesnt infringe on the fundamental rights of others. Rabelais lived for ambiguity, Plath was vitalized by the unreal and dangerous, Van Gogh was energized by lifes series of small things, Hitchens lived for irony (and died for it too), and Camus made a point not to think about any of it too intensely.

Chronological age is the most literal translation of our time here, our biological age is the most honest projection of how much of it weve got left, and our reservoir of purpose judges how successfully we spent it. Ultimately, appealing to your temple and the candles that emblazon it, is a good way to neuter the urge to cry over expired milk, whether the curtain falls when youre 25 or 98.

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Comparing Perceptions of Psoriatic Arthritis Disease Activity – Physician’s Weekly

November 30th, 2019 6:45 pm

While guidelines for psoriatic arthritis recommend a treatment target of remission or low disease activity, consensus is lacking on how to define either. Disease activity is most often measured by DAPSA (Disease Activity index for Psoriatic Arthritis) scorebased mainly on jointsor VLDA/MDA (very low disease activity/minimal disease activity) criteriabased on assessment of joints, skin, and entheses. Previous research indicates that remission/low disease activity rates are higher with the use of DAPSA than with VLDA/MDA, according to Laure Gossec, MD, PhD, but what measurements with either test mean to patients is not well known.

For a study published in Annals of the Rheumatic Diseases, Dr. Gossec and colleagues surveyed patients with psoriatic arthritis of more than 2 years and compared their perceptions of remissions with those of their physicians and VLDA, LDA, and DAPSA scores.

In these patients not selected for good disease control and with usually long disease duration, remission or low disease activity were attained by more than 50% of patients, says Dr. Gossec. Patient-perceived remission/low disease activity was frequent (65.4%). Patient-perceived remission was as frequent as remission based on DAPSA, whereas good status according to VLDA/MDA was reached less frequently. DAPSA-based status appeared to correctly reflect patient-perceived low disease activity, which is an argument to use this score to assess psoriatic arthritis.

As the first to compare treatment targets using composite scores and patient questions on assessment of status, the cross-sectional study used a patient questionnaire developed for this study with patient research partners, but not externally validated. Dr. Gossec also notes that whether the findings would be replicated in patients over time is unknown. She adds, though, that physicians now have more information on patient perceptions of remission, and comparison with composite scores to follow-up patients; DAPSA appeared to agree more with patients assessments, though both scores have strengths and weaknesses.

Comparing patient-perceived and physician-perceived remission and low disease activity in psoriatic arthritis: an analysis of 410 patients from 14 countrieshttps://ard.bmj.com/content/78/2/201

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Expert Insights on Rheumatoid Arthritis From the ACR/ARP 2019 Annual Meeting – Rheumatology Advisor

November 30th, 2019 6:45 pm

The 2019 annual meeting of the American College of Rheumatology (ACR) had an abundance of sessions dedicated to the management of rheumatoid arthritis (RA).

Novel TreatmentModalities

A large focus of the novel RA treatment sessions were the Janus kinase (JAK) inhibitors. Multiple abstracts regarding upadacitinib, an oral JAK-1 selective inhibitor, were presented. Josef Smolen, MD, of the University of Vienna in Austria, discussed 48-week results of the SELECT-MONOTHERAPY trial (A Study Comparing Upadacitinib [ABT-494] Monotherapy to Methotrexate [MTX] Monotherapy in Adults With Rheumatoid Arthritis [RA] Who Have an Inadequate Response to MTX; ClinicalTrials.gov Identifier: NCT02706951). For patients continuing upadacitinib 15 mg/d, ACR20, ACR50, and ACR70 response was 87%, 70%, and 46%, respectively; ACR20, ACR50, and ACR70 response for upadacitinib 30 mg/d was 87%, 72%, and 54%, respectively. The most frequent treatment-emergent adverse events were infection, particularly herpes zoster, and elevations in creatine phosphokinase and alanine aminotransferase levels.

Efficacy and safety data on filgotinib, another JAK-1 selective inhibitor, were presented by Bernard Combe, MD, of Montpellier University in France. The FINCH1 (Filgotinib in Combination With Methotrexate in Adults With Moderately to Severely Active Rheumatoid Arthritis Who Have an Inadequate Response to Methotrexate; ClinicalTrials.gov Identifier: NCT02889796) study was a phase 3 randomized controlled trial comparing filgotinib 100 mg/d and 200 mg/d with the active comparator, adalimumab 40 mg every 2 weeks, or placebo in addition to a stable dose of methotrexate. The efficacy of filgotinib 200 mg/d was found to be noninferior to adalimumab, achieving a Disease Activity Score in 28 joints/C-reactive protein (DAS28-CRP) score of 3.2 in 60% of participants at week 24.

Updates onPharmacotherapy Safety Data

Several important abstracts regarding pharmacologic safety data in RA were presented at the meeting. Daniel H. Solomon, MD, of Brigham and Womens Hospital in Boston, Massachusetts, presented safety data on methotrexate based on his prespecified secondary analyses of CIRT (Cardiovascular Inflammation Reduction Trial Inflammation Imaging Study; ClinicalTrials.gov Identifier: NCT02576067), which was a randomized controlled trial that included adults with cardiovascular disease and diabetes or metabolic syndrome. Participants were randomly selected to receive low-dose methotrexate (<20 mg/wk) or placebo and were followed for a mean of 27 months. Relative rates of gastrointestinal, infectious, pulmonary, and hematologic adverse events were increased in patients receiving methotrexate compared with participants who were receiving placebo. Notably, there were no differences in the relative rates of malignant, mucocutaneous, neuropsychiatric, musculoskeletal, or renal adverse events.

In addition to upadacitinib as previously mentioned, safetyprofiles of other JAK inhibitors were also presented. Tofacitinib has beenassociated with blood clots in patients who have additional risk factors forthromboembolism. High-dose tofacitinib 10 mg twice daily should not be used inthe treatment of RA. Risk factors for thromboembolism include previouscardiovascular events, cancer, clotting disorders, use of hormonalcontraceptives, and pending major surgery or prolonged immobilization. Datafrom phase 3b/4 trials evaluating tofacitinib 11 mg/d with methotrexate werepresented by Stanley B. Cohen, MD, of the Metroplex Clinical Research Center inDallas, Texas. Importantly, no new safety risks were observed, which wassimilar to that seen with the tofacitinib immediate-release 5 mg twice dailydosage.

A very important and potentially practice-changing updatewas presented by Michael George, MD, of the University of Pennsylvania inPhiladelphia. Dr George analyzed the risk for serious infection associated withlong-term use of glucocorticoids for the treatment of RA. Medicare claims dataon more than 170,000 individuals were used for the analysis. Among older patientswith RA on stable treatment with conventional synthetic and biologic disease-modifyingantirheumatic drugs (DMARDs), prednisone at dosages <5 mg/d weresignificantly associated with increased risk for serious infections. Seriousinfections included urinary infections, pneumonia, bacteremia, and skin or softtissue infections. This study has important management implications forrheumatologists as long-term use of glucocorticoids should be minimized.

Updates onEpidemiology Research in RA

In terms of epidemiology and RA disease trajectory, datafrom the Risk RA Prospective Study were presented by Aase Hensvold of theKarolinska Institute in Stockholm, Sweden. This study followed patients whowere referred to the rheumatology clinic from the primary care setting becauseof positive anti-cyclic citrullinated antibodies but who lacked arthritis uponexamination. A detailed ultrasound evaluation was performed at baseline andfollow-up. Slightly less than half of the enrolled individuals with anti-cycliccitrullinated antibodies developed ultrasound-detectable arthritis at a medianfollow-up time of 11 months. However, participants who had tenosynovitisdetected by ultrasound at baseline were more likely to progress to RA at follow-up.The study highlights the utility of a baseline ultrasound evaluation for thepurpose of prognostication in patients with early or preclinical RA.

Data presented by Elena Myasoedova, MD, PhD, of the MayoClinic College of Medicine and Science in Rochester, Minnesota, explored thechanging epidemiology of RA from a population-based incidence cohort. She foundthat although the incidence of RA has been constant over the past approximately24 years, there has been a decrease in the number of patients with RA withpositive rheumatoid factor and an increase in patients with seronegativedisease. When comparing patients who met the 2010 European League AgainstRheumatism (EULAR)/ACR criteria with those who met the 1987 ACR criteria only,patients in the former group had higher joint counts and were more likely to beever smokers. However, overall the prevalence of smoking declined during the 30-yearstudy period.

Several sessions at the ACR annual meeting featuredcomorbidities in RA. Joshua F. Baker, MD, of the University of Pennsylvania,performed a cross-sectional analysis of diabetes and RA using the VeteransAffairs RA registry. Type 2 diabetes mellitus was present in 26% of patients atenrollment. Multivariable analysis noted that high baseline disease activitywas associated with a greater risk of incident diabetes; prednisone use wascontrolled for in analysis. Interestingly, tumor necrosis factor inhibitor usewas associated with a significantly lower risk for diabetes. This study impliesthat better disease control may lower the risk for subsequent metaboliccomplications such as type 2 diabetes mellitus in patients with RA.

Cardiovascular risk was discussed by Jon T. Giles, MD, ofColumbia University in New York City. Dr Giles presented information about indicatorsof actionable levels of atherosclerosis in patients with RA who traditionallyare labeled as having low or intermediate cardiovascular risk that is based onstandard risk algorithms. Dr Giles found that actionable levels of coronaryartery calcium determined by traditional risk factors such as older age, eversmoking, antihypertensive use, and aspirin use may not necessarily be adequatefor individuals with RA. Particularly, RA disease activity should be anadditional component of the risk algorithm. Using his modified risk algorithm, DrGiles found that a large proportion of patients with RA who were traditionallycategorized as having lower cardiovascular risk may benefit from additionalscreening and prevention strategies. Similarly, Bryant England, MD, of theUniversity of Nebraska, presented data on multimorbidity in RA from acommercial claims database. Compared with baseline enrollment and one-yearfollow-up, the percentage of patients with multimorbidity considerablyincreased for patients with RA compared with those without RA. Therefore, screeningfor and management of chronic conditions in patients with RA is necessary atthe initial visit to prevent the progression of multimorbidity.

The epidemiology of inflammatory arthritis related to immunecheckpoint inhibitors (ICI) that are used in the treatment of cancer waspresented by Tawnie Braaten, MD, of Johns Hopkins School of Medicine in Baltimore,Maryland. Patients with ICI-induced inflammatory arthritis were found to have ratesof seropositivity and persistent disease activity at 3 and 6 months aftercessation of ICIs. Longer duration of ICI use and combination ICIs wereassociated with persistent inflammatory arthritis. Three-quarters of patientsunderwent immunosuppression, which did not appear to affect tumor response.This study is important because the use of ICIs continues to grow in cancertherapy, and patients with resultant inflammatory arthritis will increasinglybe referred to rheumatology practices.

Practice-Changing Updates

Several abstracts related to tapering both conventionalsynthetic and biologic DMARDs were presented at the meeting. In a late-breakingabstract presented by Siri Lillegraven, PhD, of Diakonhjemmet Hospital in Oslo,Norway, patients with RA who were in sustained remission during treatment with conventionalsynthetic DMARDs and who continued therapy tended to have flares less often andwith less radiographic joint progression than patients whose therapy wastapered. The risk of adverse events related to continued therapy on biologicDMARDs and JAK inhibitors was further explored in a meta-analysis presented by DorotheVinson, of Assistance Publique Hospital of Marseille in France. She reportedthat tapering biologic DMARDs and JAK inhibitors did not lead to a decreasedrisk for serious infections, serious adverse events, or malignancy compared withcontinuing treatment.

While the efficacy and safety of pharmacotherapies tend toshape our practice as rheumatologists, Alexis Ogdie-Beatty, MD, of the PerelmanSchool Medicine at the University of Pennsylvania, along with Ben Nowell, PhD,of the Global Healthy Living Foundation in New York City, highlighted thegrowing use of smartphone applications in clinical and research practice. Theirinteresting session titled, Doctor, Should I Get this App? explored therapidly expanding collection of smartphone apps geared toward behavior changes suchas lifestyle improvement with a focus on weight loss, stress, and sleep. Withfurther review by the rheumatology community, these apps may be recommended to patientswith RA to improve certain issues affecting quality of life that may not beamenable to pharmacologic therapies.

Conclusion

There were many interesting and ground-breaking abstractsrelated to RA at this years ACR annual meeting. Data on the safety andefficacy of JAK inhibitors were widely discussed and will continue to be animportant topic of continued research. The decision to taper vs continue conventionalsynthetic and biologic DMARDs in light of important safety data will needfurther investigation. Perhaps with increasing use of mobile technology,monitoring patients between appointments will allow for accelerated research onthe treatment of RA.

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Expert Insights on Rheumatoid Arthritis From the ACR/ARP 2019 Annual Meeting - Rheumatology Advisor

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Genetics and Weather in NL Producing Highest Incidence of Arthritis in Canada – VOCM

November 30th, 2019 6:45 pm

Genetics and weather are coming against Newfoundlanders and Labradorians who have the highest incidence of arthritis in Canada.

One in four Newfoundlanders and Labradorians suffer from one form of arthritis or another.

That from the Arthritis Societys Jennifer Henning. She says arthritis is an inflammation of the joint, but there are some 100 different types of the disease which is split into two major categories, inflammatory and degenerative.

Rheumatoid arthritis is an autoimmune attack on the joints by the bodys own immune system. It can happen at any time, and affect the entire body.

Osteoarthritis is the most common form and comes as the result of wear and tear, injury or the general aging process. It involves a degeneration of the cartilage between the bones of the joint.

Both types of arthritis result in significant pain and loss of mobility.

Henning says unfortunately, weather doesnt help.

She says in laymans terms, the body is tighter because its cold, and when its wet the tissues swell, causing a greater amount of pain and inflammation.

She says genetics also play a strong role especially in the inflammatory type of arthritis.

Rheumatoid arthritis is more common in women and is often triggered by a traumatic event like childbirth, injury or illness.

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Genetics and Weather in NL Producing Highest Incidence of Arthritis in Canada - VOCM

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Rheumatoid Arthritis Will Change Your Life. It Doesn’t Have to Ruin It. – HealthCentral.com

November 30th, 2019 6:45 pm

When I was a little girl, I had high-flying dreams and they had very little to do with my juvenile arthritis, a childhood illness similar to rheumatoid arthritis (RA). First, I wanted to be a ballerina and practiced dance moves on my parents' Persian rug. Then I watched Jacques Cousteau and his crew of marine biologists diving in waters all over the world and scuttled the dancing dream in favor of serving on his ship, the Calypso, and spending much of my life under water. But at age 16, I went home after a two-year hospital stay in a power wheelchair, trailing recommendations from my then-medical team to lower my expectations of life to those resembling a turnip's. Because of the disease, y'know.

It would be easy to dismiss this as a function of attitudes in a land and time far away from now. But these perceptions persist, if not in others, then certainly in ourselves. Its a strange thing, this shift in assumption and expectation. The minute you get a diagnosis of chronic illness, its as if the rug is pulled out from under you. Your future, which had just shone with possibility, now seems dull, hopeless, and framed in less-than.

Do you really have to give it all up and accept a life of sitting on the sidelines? No. Not by a long shot. The key is to adapt and change your approach. But more on that in a bit. First, lets take a look at the obstacles.

I've lived with RA for more than half a century and have learned that the only predictable thing about this condition is that you never know what it'll do next. Sometimes, you're lucky and find a medication that works, suppressing the symptoms so you can get back to your life. At other times, its all you can do to get dressed in the morning. And, of course, all the stages in between.

Fifty years ago, an American psychologist by the name of Martin Seligman did a study that led to a classic theory of depression. He divided dogs into two groups. Both would receive shocks, but one group of dogs would be able to escape, the other not. The dogs that had no control over the situation curled up in a ball, whimpering. Seligman developed a theory called learned helplessness, stating that when people have no agency (that is, no control), they are more likely to develop depression.

When you have no ability to predict how your RA will feel in the morningand therefore what you will be able to doyou can feel helpless. If youre feeling that kind of helplessness for weeks or months, it spreads into other areas of your life, making you feel depressed. It may even be accompanied by its bratty cousin, "Feel Like Giving Up." And that's OK. Because RA affects every part of your life and it's hard to re-learn how to be you. There's nothing wrong with having a moment (or 10) of intense frustration. But what's really important is to make sure it doesn't stick around.

So much of living with RA is about kicking that cousin out of your psyche. Again, your doctor can help, as can therapy, family and friends, and a community of others like you. Having support will help you fight back and find other ways of taking up the reins of your life.

The great thing about life is that there is no one way to do anything. Whether it's opening a jar, having a family, or building your own business, there are ways around that big boulder called RA in the middle of your path. These tips can help:

Talk to your doctor. Your rheumatologist is one of the most important members on your team. If your RA is getting in the way of you creating a life, call them. You might need to adjust your treatment so you can start the journey back to living first, with RA just muttering in the background. Many people also include diet, exercise, supplements, and alternative treatments in how they approach living with RA.

Give yourself extra time to achieve your goals. Maybe your RA diagnosis won't require a complete change in direction for your life. You might be able to stay on your current career path or even keep training for that big race you've been wanting to tackle, but it's probably going to take a little extra time to get there. Getting the right treatment working for you can take time, and flares don't respect your "to-do" list.

Don't expect to follow "normal" timelines when it comes to working toward big goalsRA is bound to get in the way. When it comes to dreams, pursuing them is what matters, not how you go about it. You are free to create your own path, one that respects and accommodates your RA. For instance, I used to work as a policy analyst, frequently working from home four days a week on research and writing tasks. This enabled me to work much more effectively, with fewer sick days.

When RA brings physical limitations, use your mental muscle instead. I will forever be grateful to my parents for the way they dealt with the lost teenager who came home from the hospital. They told me that although my body might not work very well, there was nothing wrong with my mind and they expected me to use it. This meant working hard in school so I could get to college. By then, I had realized the importance of focusing on what I was able to do (and not just because I couldn't swim, so working with Cousteau was a wash).

Finding alternate routes to getting where I wanted to go eventually became a bit of a hobby and by now, I can almost always find a way around an obstacle. Remember that although your condition might get in the way of you becoming a trapeze artist, you can absolutely find another way to be in the circus.

Go easy on yourself, but not too easy. Frustration about struggling with RA might get misdirected toward yourself. Try not to be angry at yourself or your body. It'll get you nowhere, except derailed, and it isnt something you would tolerate for anyone else. Be kind and understanding to yourself.

Human beings have a gift of adaptation, being able to live in almost any climate, under any conditions, and changing their approach to survive. Use that gift to create your life. Yes, with RA, but a life in which you tear down limits of low expectations.

Following your dreams is a process, sometimes a long one, with side tracks and pauses, and often infuriatingly so. But persevering, accommodating your own needs to move slower, to take pauses, but then reassessing and getting back to your path is possible. The only way to live with RA is to become as stubborn as a goat and refuse to stay down. You learn to withstand long periods of having to put your dream (and your life) on hold while you deal with your condition and its nonsense. During those times of flares and pain, you hone a single-minded focus by getting through each day. When it is over, when you are better and get your life back, you use that focus to pick up your dream and work on it some more.

After many years of attending university, with many challenges, I graduated with my masters degree in social work. After immigrating to Canada from Denmark, and with the offer of a government job in human rights, I thought of those doctors who'd had zero expectations of the girl with a chronic illness and disability. In that moment, I wanted very much to write them a letter, telling them how their assumptions of my inability had had the exact opposite effect: They had only spurred me on.

In my family, that's called the "Show the Bastards" gene. I'll bet you have one, too.

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Arthritis treatment safe for cats with kidney disease [Ask the Vet’s Pets] – Reading Eagle

November 30th, 2019 6:45 pm

", "", "" ] }, { "position": "bottom", "content": [ "Follow us ", "", "" ] } ] }, { offCanvas: { pageSelector: "#mm-off-canvas-content" } }); var mmenuapi = $("#mm-menu").data( "mmenu" ); $("#menuFlyOutLogInPopUp").click(function() { mmenuapi.close(); displayLogInPopUp();});checkStatus(); /*var loginDivTemp = document.getElementById("loginDiv"); var subscribeDivTemp = document.getElementById("subscribeDiv"); var loginDivClone = loginDivTemp.cloneNode(true); var subscribeDivClone = subscribeDivTemp.cloneNode(true); var loginPlaceholder = document.getElementById("loginDivPlaceholder"); var subscribePlaceholder = document.getElementById("subscribeDivPlaceholder"); loginPlaceholder.appendChild(loginDivClone); subscribePlaceholder.appendChild(subscribeDivClone); $("#fade").click(function () { closeSplashAndSetCookie(); });*/ }); function displayLogInPopUp() { document.getElementById('fade').style.display='block'; document.getElementById('logInPopUpForm').style.display='block'; } function getParameterByName(name) { var match = RegExp('[?&]' + name + '=([^&]*)').exec(window.location.search); return match && decodeURIComponent(match[1].replace(/+/g, ' ')); } //what-input.js !function (e, t) { "object" == typeof exports && "object" == typeof module ? module.exports = t() : "function" == typeof define && define.amd ? define("whatInput", [], t) : "object" == typeof exports ? exports.whatInput = t() : e.whatInput = t() }(this, function () { return function (e) { function t(o) { if (n[o]) return n[o].exports; var i = n[o] = { exports: {}, id: o, loaded: !1 }; return e[o].call(i.exports, i, i.exports, t), i.loaded = !0, i.exports } var n = {}; return t.m = e, t.c = n, t.p = "", t(0) }([function (e, t) { e.exports = function () { var e = document.documentElement, t = "initial", n = null, o = ["input", "select", "textarea"], i = [16, 17, 18, 91, 93], r = { keyup: "keyboard", mousedown: "mouse", mousemove: "mouse", MSPointerDown: "pointer", MSPointerMove: "pointer", pointerdown: "pointer", pointermove: "pointer", touchstart: "touch" }, u = [], d = !1, a = { 2: "touch", 3: "touch", 4: "mouse" }, s = null, p = function () { window.PointerEvent ? (e.addEventListener("pointerdown", c), e.addEventListener("pointermove", m)) : window.MSPointerEvent ? (e.addEventListener("MSPointerDown", c), e.addEventListener("MSPointerMove", m)) : (e.addEventListener("mousedown", c), e.addEventListener("mousemove", m), "ontouchstart" in window && e.addEventListener("touchstart", v)); var t = !1; try { var n = Object.defineProperty({}, "passive", { get: function () { t = !0 } }); window.addEventListener("test", null, n) } catch (e) { } e.addEventListener(l(), m, !!t && { passive: !0 }), e.addEventListener("keydown", c), e.addEventListener("keyup", c) }, c = function (e) { if (!d) { var u = e.which, a = r[e.type]; if ("pointer" === a && (a = w(e)), t !== a || n !== a) { var s = !(!document.activeElement || -1 !== o.indexOf(document.activeElement.nodeName.toLowerCase())); ("touch" === a || "mouse" === a && -1 === i.indexOf(u) || "keyboard" === a && s) && (t = n = a, f()) } } }, f = function () { e.setAttribute("data-whatinput", t), e.setAttribute("data-whatintent", t), -1 === u.indexOf(t) && (u.push(t), e.className += " whatinput-types-" + t) }, m = function (t) { if (!d) { var o = r[t.type]; "pointer" === o && (o = w(t)), n !== o && (n = o, e.setAttribute("data-whatintent", n)) } }, v = function (e) { window.clearTimeout(s), c(e), d = !0, s = window.setTimeout(function () { d = !1 }, 200) }, w = function (e) { return "number" == typeof e.pointerType ? a[e.pointerType] : "pen" === e.pointerType ? "touch" : e.pointerType }, l = function () { return "onwheel" in document.createElement("div") ? "wheel" : void 0 !== document.onmousewheel ? "mousewheel" : "DOMMouseScroll" }; return "addEventListener" in window && Array.prototype.indexOf && (r[l()] = "mouse", p(), f()), { ask: function (e) { return "loose" === e ? n : t }, types: function () { return u } } }() }]) }); //headerweatericon.js if (window.matchMedia("(min-width: 39.9375em)").matches) { var weatherScript = document.createElement("script"); weatherScript.src = "/js/min/weatherbug.min.js"; document.head.appendChild(weatherScript); } $(document).foundation(); function getCookie(cname) { var name = cname + "="; var decodedCookie = decodeURIComponent(document.cookie); var ca = decodedCookie.split(';'); for(var i = 0; i

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Ask the doctors: Arthritis pain may be relieved by prolotherapy – The Spokesman-Review

November 30th, 2019 6:45 pm

Dear Doctor: Im a 66-year-old man whose right knee really hurts from arthritis. My sister keeps talking about something called prolotherapy. What is it, and can it help?

Dear Reader: Prolotherapy is an injection-based approach to treating pain in the soft tissues of the joint. Specifically, a small amount of a liquid irritant is introduced at the site where a tendon or ligament attaches to the bone. The idea is that the irritant will set off a localized inflammation reaction, which will then trigger the release of growth factors that promote the healing of soft tissues.

The roots of prolotherapy date back to the ancient Greeks, who believed that deliberately causing inflammation in a certain area of the body could stimulate the tissues to repair themselves. In the 1930s and 1940s, several physicians expanded on the concept. They experimented with various solutions and developed techniques sometimes referred to as needle surgery to target connective tissue in the joints.

Today, prolotherapy injections typically consist of sugar- or salt-based solutions to which a local anesthetic, such as lidocaine, is added. Patients seek the treatment to help with joint pain and stiffness resulting from injury, overuse or inflammatory conditions such as arthritis and degenerative disc disease. Areas of the body targeted by the practice include the knees, back, hips, ankles, shoulders and hands.

Treatment protocols usually consist of a series of three to eight injections given over weeks or months, depending on the specific case. The injections can be moderately painful, and patients often use Tylenol or stronger medications to manage localized aches and tenderness. Patients are advised to limit activity for several days after each injection, and they may be asked to supplement the therapy with specific exercises that focus on range of motion.

Since creating inflammation is the point of prolotherapy, the use of NSAIDs, or non-steroidal anti-inflammatories, to address the resulting pain and discomfort is not recommended. Possible side effects of the procedure include bleeding, bruising or swelling at the injection site. These can last for a week or more. Allergic reactions to the injected solution, infection and nerve damage are possible, but rare.

Does prolotherapy work? In some case studies, patients report improvement in pain and strength in the affected areas. But studies of the treatment have yielded mixed results. Some have argued that the studies showing benefit have been too small and not scientifically rigorous. The one area of agreement appears to be the need for large and scientifically rigorous studies.

Although prolotherapy is gaining in popularity, the National Institutes of Health identify it as a complementary and alternative medical treatment. And since its considered an experimental therapy, many insurance companies wont cover it. Costs can range from $400 to $1,000 per treatment, depending on the provider.

As with all alternative therapies, we think its wise for you to check with your doctor to see whether prolotherapy may be helpful for you.

Send your questions to askthedoctors@mednet.ucla.edu.

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Ask the doctors: Arthritis pain may be relieved by prolotherapy - The Spokesman-Review

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Revealed: NHS plans to ration 34 everyday tests and treatments – The Guardian

November 30th, 2019 6:45 pm

Millions of patients in England will be stopped from having an X-ray on their sore back, hernia repair surgery or scan of their knee to detect arthritis under controversial plans from NHS and doctors to ration unnecessary treatment.

The Guardian has seen a list of 34 diagnostic tests and treatments that in future patients will only be able to get in exceptional circumstances as part of a drive to save money and relieve the pressure on the NHS.

The sweeping changes they are set to propose include many forms of surgery, as well as ways of detecting illness including CT and MRI scans, and blood tests, for cancer, arthritis, back problems, kidney stones, sinus infections and depression. Three of the procedures have since been dropped from the list.

If implemented, the clampdown would involve an unprecedentedly radical restriction on patients right to access and doctors ability to recommend procedures, some of which have been used routinely for decades.

It would also see patients told to use physiotherapy or painkillers to dull the pain of an arthritic knee rather than undergo an exploratory operation called an arthroscopy. Kidney stones would no longer be removed in an operating theatre and instead would be treated with sound wave therapy to reduce the pain.

Similarly, in future adenoids would not be removed because evidence now shows that it is not necessary, doesnt work well and can cause problems like bleeding and infection, according to the rationale set out in the document for curtailing that procedure.

Disclosure of the list prompted fears that the move amounts to a major escalation of NHS rationing.

An NHS spokesperson said the document was out of date and had not been approved or implemented. They added there was strong support from senior doctors in the Academy of Medical Royal Colleges for action to eliminate wasteful interventions that dont benefit patients.

The Patients Association warned that if implemented the changes would force patients to either endure the pain of their condition or pay for private care to tackle it.

Putting barriers in the way of people expecting to have so many previously commonplace tests and treatments would lead to harm and distress, said Rachel Power, the associations chief executive.

Patients have seen the range of treatments offered by the NHS cut back over recent years, and the NHS has been upfront about this being to save cash. Often there are good reasons for not using these low value treatments as a first choice, but they are appropriate for some patients.

We are unhappy at any new barriers being erected between patients and the treatments they need.

This is of a piece with the restrictions on prescribing over the counter medicines [which NHS England brought in last year], and patients have told us of the harm and distress this broad programme of restrictions has caused them, she added.

As a result of this rationing, we know that patients who can afford to pay privately are doing so, while those who cant are going without and suffering. This is exactly what having an NHS is supposed to prevent.

The 50-page document is the result of months of detailed and until now secret discussions between four key medical and NHS bodies involved in the NHSs evidence-based interventions programme, which aims to identify procedures that do not work.

They are NHS England; the Academy of Medical Royal Colleges (AOMRC), which represents the UKs 220,000 doctors professionally; NHS Clinical Commissioners, which speaks for GP-led clinical commissioning groups; and the National Institute for Health and Care Excellence (Nice), which advises the government and NHS which treatments are effective and represent value for money.

They believe many of the interventions should be scrapped, or at most used very sparingly, because they could make patients anxious or even put them in danger. For example, they are suggesting that the prostate-specific antigen test, which is used to detect prostate cancer the commonest form of cancer in men is used much less often.

The document says: Blood tests to check your prostate are not needed except for very specific cases. Blood tests can lead to further investigation that may also be unnecessary and can cause anxiety.

The four medical bodies planned to put the proposals out to public consultation this month but had to delay because of general election purdah rules.

Hospitals would be told not to operate on patients to try to slow the progress of osteoporosis (brittle bone disease), or if they have sinusitis, or to remove a disc from the spine of someone suffering from crippling pain.

Dr Richard Vautrey, chair of the British Medical Associations GPs committee, said any changes should be based on the best available evidence and not cost-cutting.

In the current climate, NHS resources must be used wisely but any restriction on treatments must be based on up to date clinical evidence and not solely on cost.

Doctors must always be able to provide the best care possible and use their clinical expertise to refer patients for the most appropriate treatments when that is needed.

Prof Carrie MacEwan, chair of the AOMRC, defended the planned restrictions. Medicine continually evolves and its right that we dont carry out tests, treatments or procedures when the evidence tells us they are inappropriate or ineffective and which, in some cases, can do more harm than good.

The list is drawn up by medical experts and senior specialist clinicians who have reviewed the latest evidence from around the world and its absolutely right we act on that evidence in the best interests of patients and so that we can focus our resources on things that we know do work, she added.

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Oregon State University Has Provided a New Treatment for Athritis – Science Times

November 30th, 2019 6:44 pm

(Photo : pixabay)

Theresearchprovided by the Oregon State University provided the first complete cellular-level look at what goes on in joints that are affected by osteoarthritis, which is considered as a costly and debilitating condition that affects almost one-quarter of adults in America.

The study was published inNature Biomedical Engineering, and it gave an insight into how factors like drugs, diet, and exercise can affect the joint's cells, which is important because cells do the work of maintaining, developing and repairing the tissue.

Arthritis treatment

Theresearchdone by the OSU College of Engineering's Brian Bay and the scientists from the Royal Veterinary College in London and University College London created a sophisticated scanning technique to view joints of mice that have arthritis and joints of healthy mice.

Brian Bay said that the techniques for quantifying changes in arthritic joints had been constrained by a lot of factors. Restrictions on the length of scanning time and the sample size are two of them, and the level of radiation used in some of the techniques ultimately damages or destroys the samples that are being scanned. The nanoscale resolution of intact, loaded joints had been considered unattainable.

Brain Bay and scientists from 3Dmagination Ltd, the University of Manchester, Edinburgh Napier University, the Diamond Light Source, and the Research Complex at Harwell created a way to conduct nanoscale by capturing the images of bones and whole joints under precisely controlled loads.

The scientists enhanced the resolution without compromising the study's field of view, decrease the total radiation exposure to preserve the tissue mechanics, and to prevent movement during the scanning.

Brian Bay stated that with a low-dose of pink-beam synchrotron X-ray tomography and mechanical loading with nanometric precision, scientists could measure the structural organization simultaneously and functional response of the tissues. That means that scientists can look at the joints of the patient from the tissue layers down to the cellular level with a large field of view and high resolution without having to cut out the samples.

He also stated that the two features of the study make it helpful in advancing the study of osteoarthritis. By using intact joints and bones, all of the functional aspects of the complex tissue that is layering are preserved. The small size of the mouse bones leads to imaging that is seen on the scale of the cells that maintain, develop, and repair the tissues.

The effect of osteoarthritis on health

Osteoarthritis is the degeneration of joints, and according to the Centers for Disease Control and Prevention, it affects more than50 million American adults. Around 18% of men and 25% of women suffer from osteoarthritis.

As the senior population in America increases, the prevalence of arthritis will likely rise in the coming years. The CDC estimates that by 2040 there will be 78 million arthritis patients, more than one-quarter of the projected total adult population, two-thirds of those with arthritis are expected to be women. By 2040, 34 million adults in America will have limits in the activities that they do because of arthritis.

Brian Bay said that osteoarthritis will affect most of the adults during their lifetime to the point where a hip joint or a knee joint needs replacement with a difficult and costly surgery after years of pain and disability. This new treatment that OSU has to develop can prevent any severe arthritis from forming that could save millions of adults from having to go through the difficulties of arthritis.

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Oregon State University Has Provided a New Treatment for Athritis - Science Times

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Sustained Remission in RA Fails with Programmed Infliximab Treatment – Rheumatology Network

November 30th, 2019 6:44 pm

A new discontinuation strategy for infliximab in patients with rheumatoid arthritis, in which the biologic dose was determined by the serum level of tumor necrosis factor (TNF)-, was unsuccessful for sustained biologic-free remission, say researchers recently writing in Annals of the Rheumatic Diseases.

It is well known that proinflammatory cytokines such as TNF- play central roles in the occurrence and progression of rheumatoid arthritis. As the therapeutic effects of infliximab, an inhibitor of TNF-, plus methotrexate have been demonstrated in several clinical studies, the goal of rheumatoid arthritis treatment has expanded from the achievement of clinical remission to sustained remission without biological disease-modifying antirheumatic drugs (bDMARDs), out of concern for adverse events or treatment cost. Several studies have suggested that few patients with established rheumatoid arthritis can discontinue bDMARDs without losing remission, while those in sustained deep remission are more likely to be able to discontinue bDMARDs. Moreover, a significant interaction has been demonstrated between the infliximab dose and TNF- level in the clinical response, suggesting that serum levels of TNF- could be a key indicator for optimal dosing of infliximab to achieve a clinical remission and a sustained discontinuation of infliximab for the treatment of rheumatoid arthritis. However, this hypothesis has not been confirmed in a randomized controlled trial.

The aim of this study is to determine whether the programmed infliximab treatment strategy (for which the dose of infliximab was adjusted based on the baseline serum TNF-) is beneficial to induction of clinical remission after 54 weeks and sustained discontinuation of infliximab for oneyear, wrote the authors of the study, led by Yoshiya Tanaka, M.D., Ph.D., of the University of Occupational and Environmental Health in Kitakyushu, Japan.

This multicenter trial, dubbed RRRR, included 337 patients with infliximab-nave rheumatoid arthritis with inadequate response to methotrexate. Participants were randomized to receive either the programmed treatment of 3mg/kg infliximab until week six and after 14 weeks the dose of infliximab was adjusted based on the baseline levels of serum TNF- until week 54, or standard treatment with 3mg/kg of infliximab. Patients who achieved a simplified disease activity index (SDAI) 3.3 at week 54 discontinued infliximab. The primary endpoint was the proportion of patients who sustained discontinuation of infliximab at week 106.

At week 54, 39.4 percent of the programmed group and 32.3 percent the standard group attained remission (SDAI 3.3). At week 106, the one-year sustained discontinuation rate was 23.5 percent and 21.6 percent, respectively, representing a nonsignificant 2.2 percent difference (95%CI 6.6 percentto 11.0 percent; p=0.631).

In both arms, baseline SDAI <26 was a statistically significant predictor of sustained discontinuation at one year (OR=2.97 in the programmed arm and 2.83 in the standard arm), the authors wrote. This exploratory analysis implies that the success of sustained discontinuation of infliximab depends on disease activity at baseline, and that sufficient disease control by adequate dose ofmethotrexate is required before infliximab is administered.

There was no statistically significant difference in the proportion of deep remission (DAS28 <2.2), at the last administration of infliximab between the groups, which could result in failure of sustained discontinuation of infliximab. Still, the incidence rates of infections and other safety signals were comparable between the groups, suggesting that dose escalation was tolerated in the study.

Thus, the fine tuning of infliximab-dose based on serum levels of TNF represents a key factor for achievement of remission defined by SDAI and DAS28-ESR, but may not be related to deep remission.

If serum levels of rheumatoid factor are less than 45, serum levels of TNF- are higher than 1.65, or disease activity is controlled with less than 10mg/kg of methotrexate, standard treatment may be intense enough to achieve successful discontinuation of infliximab, the authors wrote.

In order to facilitate decision-making bypatients and rheumatologists, the authors suggested that more effort is needed to determine the patient profile most likely to benefit from discontinuation of bDMARDs.

"Taken together, the findings of the RRRR study (Remission induction by Raising the dose of Remicade in RA) reveal that the programmed treatment strategy using different doses of infliximab based on the baseline levels of serum TNF- did not increase the sustained remission rate 1year after withdrawal of infliximab treatment at week 106. However, in order to facilitate decision-making by patients and rheumatologists, more efforts are needed to determine the patient profile most likely to benefit from discontinuation of biological DMARDs," the authors wrote.

REFERENCE

Yoshiya Tanaka, Koji Oba, Takao Koike, et al. Sustained discontinuation of infliximab with a raising-dose strategy after obtaining remission in patients with rheumatoid arthritis: the RRRR study, a randomised controlled trial. Annals of the Rheumatic Diseases. October 19, 2019. doi: 10.1136/annrheumdis-2019-216169

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Humans and autoimmune diseases continue to evolve together – Medical News Today

November 30th, 2019 6:44 pm

The ability to fight disease is a driving force in human survival. Inflammation has emerged as a key weapon in this process. As pathogens change and evolve, the immune system adapts to keep up.

However, to what extent might such evolutionary adaptations also give rise to autoimmune conditions such as lupus and Crohn's disease?

This was a central question in a recent Trends in Immunology review by two scientists from Radboud University, in Nijmegen, Netherlands.

To address the issue, first author Jorge Domnguez-Andrs, a postdoctoral researcher in molecular life science, and senior author Prof. Mihai G. Netea, chair of experimental internal medicine, examined studies in the fields of virology, genetics, microbiology, and immunology.

They focused on people of African or Eurasian descent and how their ancestral origins may have influenced their risk of autoimmune diseases.

Of particular interest was how common pathogens in different communities related to changes in people's DNA, particularly when this involved inflammation.

The team found that the genetic changes made it harder for pathogen infections to take hold.

Over time, however, it seems that inflammation-related diseases, such as inflammatory bowel disease, Crohn's disease, and lupus, have emerged alongside improvements in immune defenses.

The findings also suggest that the human immune system continues to evolve and adapt to changes in environment and lifestyle.

"There seems to be a balance," says Domnguez-Andrs.

"Humans evolve to build defenses against diseases," he continues, "but we are not able to stop disease from happening, so the benefit we obtain on one hand also makes us more sensitive to new diseases on the other hand."

He observes that autoimmune diseases in today's humans tend to emerge later in life. These would not have caused health problems for our ancestors because their lives were much shorter.

"Now that we live so much longer," he explains, "we can see the consequences of infections that happened to our ancestors."

One of the examples that Domnguez-Andrs and Netea cover in detail in their review is malaria.

"Among various infectious diseases," they write, "malaria has exerted the highest evolutionary pressure on the communities across the African continent."

Malaria is a mosquito-borne disease that makes people very ill with flu-like symptoms, such as chills and a high fever.

While there has been much progress in the fight to control and eliminate the potentially fatal disease, it continues to threaten nearly half of the world's population, according to the World Health Organization (WHO).

The cause of malaria is parasites belonging to the species Plasmodium. These parasites spread to humans through the bites of infected female Anopheles mosquitoes.

Domnguez-Andrs and Netea note that Plasmodium has been infecting people in Africa for millions of years. During that period, the immune systems of those human populations have evolved stronger resistance to infection by increasing inflammation.

However, the downside of increasing inflammation to withstand infectious disease is that it favors health problems that tend to occur later in life.

Modern humans of African descent are more prone to developing such conditions, which include atherosclerosis and other cardiovascular diseases.

Another example of how ancestral changes in DNA leave imprints in the immune systems of modern humans is the interbreeding of early Eurasians with Neanderthals.

Modern humans whose genomes harbor remnants of Neanderthal DNA have immune systems that are better able to withstand staph infections and HIV-1. However, they are also more prone to asthma, hay fever, and other allergies.

Improvements in technology are making it more possible to find the downsides that can accompany disease-fighting adaptations.

Next generation sequencing, for example, is allowing scientists to delve more deeply into what happens at the DNA level between pathogens and the organisms that they infect.

Not only is new technology getting better at revealing genetic changes that occurred in our ancestors, but it is also showing that the human immune system continues to evolve and adapt.

In Africa, there are still tribes that hunt for food as their ancestors did. Thanks to new tools, scientists can see how the gut bacteria of these tribes are more diverse than those of, for example, contemporary African American people, who buy food in stores.

Other changes that have had an effect on DNA are the improvements in hygiene that have occurred in recent centuries. These have reduced exposure to pathogens and the diversity of gut bacteria.

"This reduced microbiota diversity in Western societies," the authors observe, "has been associated with a higher incidence of the so-called 'diseases of civilization,' such as cardiovascular diseases, diabetes, obesity, and autoimmune disorders, which are very unusual in hunter-gatherer societies, compared with communities living a Western-type lifestyle."

Domnguez-Andrs and Netea are extending their research to populations whose ancestry is other than African or Eurasian.

"Today, we are suffering or benefiting from defenses built into our DNA by our ancestors' immune systems fighting off infections or growing accustomed to new lifestyles."

Jorge Domnguez-Andrs, Ph.D.

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Humans and autoimmune diseases continue to evolve together - Medical News Today

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Who needs the flu vaccine? | Valley Health – Mat-Su Valley Frontiersman

November 30th, 2019 6:44 pm

The burden of flu on our society is tremendous The Centers for Disease Control and Prevention (CDC) estimates that influenza has resulted in between 9.3 million 49.0 million illnesses, between 140,000 960,000 hospitalizations and between 12,000 79,000 deaths annually since 2010.

The CDC recommends that everyone 6 months of age and older should get an influenza (flu) vaccine every year, with rare exceptions.

The primary reason to not get the flu vaccine is an allergy to one of the components of the vaccine (for example gelatin) or an allergy to eggs (because the virus is raised in eggs). If you have had the rare neurologic condition called Guillian-Barre Syndrome, you also should not get the vaccine.

The standard flu shot is given into the muscle of the arm and this is the form recommended for most persons. There is an intradermal form that is injected into the skin using a much smaller needle. This form can be given to persons age 18 to 64 years.

Persons over age 65 are recommended to get the high dose form of the vaccine Fluzone high dose. This form of the vaccine contains four times as much antigen (the part of the vaccine that causes the body to form antibodies against the flu virus) as the standard vaccine. The higher dose is intended to give older persons better protection by causing a better immune response. Vaccines are also available that contain an adjuvant. An adjuvant is an ingredient that helps to cause a greater immune response. This form of the vaccine is recommended for persons age 65 and older.

A nasal form of the vaccine is also available. This form of the vaccine provides protection against two forms of influenza A and two forms of influenza B. It may be given to persons age 2 through 49 years. This form of the vaccine contains a weakened but living form of the viruses. It is not recommended for pregnant women, persons with weakened immune systems and young children with asthma or who are taking aspirin. Ask your doctor if you can use this form of the vaccine.

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The flu vaccine is especially important for persons at high risk of complications from the flu. High risk groups include: persons over the age of 65 years; persons with diabetes; persons with asthma or chronic lung diseases (chronic obstructive pulmonary disease and cystic fibrosis); persons with chronic kidney or liver disease; persons with weakened immune systems (those with HIV or AIDS). Certain cancers (especially leukemia), persons receiving chemotherapy or radiation therapy for cancer and persons on drugs that weaken the immune system are also at increased risk. Again it is important to ask your healthcare provider about your risk and whether it is safe for you to get the vaccine.

If despite getting the vaccine you get the flu, avoid contact with other persons (as much as possible except to seek medical help) until your fever has been gone for 24 hours.

Dr. Samuel Abbate is a local physician practicing in Wasilla.

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Who needs the flu vaccine? | Valley Health - Mat-Su Valley Frontiersman

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Boston docs: Early treatment helps African babies with HIV – Boston Herald

November 30th, 2019 6:44 pm

Early treatment with antiretroviral therapy, an HIV drug not usually administered right after birth, can help babies born with the virus that infects 300-500 infants in sub-Saharan Africa every day, Boston doctors have determined.

We find that ART initiation within hours after birth is doable and translates into multiple benefits for the infants lower frequencies of reservoir cells and improved immune responses, said corresponding author of the study published in Science Translational Medicine, Dr. Mathias Lichterfeld, associate infectious disease physician at Brigham and Womens Hospital.

Antiretroviral therapy is a combination of at least three drugs that are highly effective at suppressing HIV and stopping its progression.

The therapy is not typically given to babies right after birth, but new research shows the number of infected cells in HIV-positive babies given the treatment within days or hours of birth was extremely small compared to infected infants who started treatment later.

What excites me most about this work is that making a comparatively small change in the timing of treatment may have a large impact on long-term treatment outcomes, said Lichterfeld.

The study was conducted in two major maternity hospitals in the Francistown and Gaborone regions of Botswana, a country with the third-highest HIV-1 prevalence in the world.

HIV progresses much faster in infants than in adults because of their weaker immune systems.

Infants enrolled in the study began treatment right after birth and researchers compared their results to those of infants not in the study who received the drug within a median of four months after birth. The babies were then followed for two years with blood sampling at regular intervals.

The study was small and focused on 10 HIV-positive babies that were enrolled. A total of 40 infants have been recruited into the study and samples from the remaining babies are now being analyzed.

A new clinical trial has also been started with some of the same infants in which a different treatment is being evaluated.

As of June, an estimated 24.5 million people globally were accessing antiretroviral therapy, according to the Joint United Nations Program on HIV/AIDS.

Antiretroviral therapy does not cure HIV, but helps infected patients live longer and healthier lives. It also reduces the risk of HIV transmission by lessening the amount of the virus in the body, which in turn gives the immune system a chance to recover.

Nearly 38 million people across the globe were living with HIV as of last year and about 8 million didnt know they were infected.

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Boston docs: Early treatment helps African babies with HIV - Boston Herald

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HIV, my baby and me: ‘I was 17 years old when I was diagnosed’ – BBC News

November 30th, 2019 6:44 pm

Media playback is unsupported on your device

"People will judge me, but I'd just say walk a mile in my shoes."

Jane, not her real name, was 17 years old when she was diagnosed with HIV.

"I'd only slept with one person when I got HIV, I know people will hear that and think it's a sob story, but it's the truth," she told BBC News NI.

When Jane was diagnosed she was one of the youngest women in Northern Ireland known to have the virus.

HIV is a virus which, over time, damages the human immune system leading to illness and infection.

There are 1,130 people receiving treatment for HIV in Northern Ireland. It is not known how many more people are living with the virus undiagnosed.

The charity Positive Life says there is still a myth that it's a "gay man's disease".

Figures show that in Northern Ireland almost 40% of those living with HIV contracted the virus through heterosexual contact and more than 200 women have been diagnosed HIV-positive.

"When I was first diagnosed, I started to research stuff online and I watched some films where people had HIV and it really scared me," said Jane.

"It showed people getting really sick and their skin started to get really bad and it showed people dying. I thought: 'Is this what is going to happen to me?'"

In 2018, 96,142 people were receiving HIV-related care across the UK.

HIV - Human Immunodeficiency Virus - is a virus which, over time, damages the human immune system.

Media playback is unsupported on your device

The immune system is the body's defence against infectious organisms and infections. Problems with the immune system can lead to illness and infection.

Aids - Acquired Immunodeficiency Syndrome - is the result of damage to the immune system caused by HIV.

Jane's mother admits she initially struggled with her daughter's diagnosis.

"At the start, I had all the stereotypes and stigmas in my head that you could think of.

"I just thought: 'This can't be happening to her.' And how unfair it was to be happening to someone her age, to someone who wasn't promiscuous.

"But I know now it doesn't matter if you're promiscuous or not, it only takes one time, and the rest of your life can be changed forever."

Those living with HIV have the same life expectancy as those without the condition, thanks to antiviral treatments used since 1996.

Following her diagnosis, Jane began medication which suppressed the virus and made HIV levels virtually undetectable in her system.

This meant it couldn't be transmitted - even through sexual activity.

Since then, Jane has given birth to a baby boy.

"During my pregnancy I was on three different types of tablets to make sure that my baby wouldn't get HIV," she said.

"I have a wee boy now, but the medication worked, because he doesn't have HIV.

"HIV isn't going to stop me being there for my son. I still have a roof over my head, I have family support."

There were 4,500 pregnancies to HIV-positive women in the UK and Ireland between 2015 and 2018.

Of those, less than 20 have transmitted the virus to their children, either through pregnancy, birth or breastfeeding.

There are still many misconceptions about HIV, according to the charity Positive Life.

"People will still ask if you can catch HIV off a toilet seat or by using the cutlery of people who are HIV-positive - there is still a lot of negative language around it, " said Positive Life's Jacquie Richardson.

"The three biggest myths we hear are that it's a gay man's disease, that it's contracted as a result of a promiscuous lifestyle and that you'll die if you've a diagnosis.

"We're working very hard to counter those myths."

GETTY

in Northern Ireland

There is still a lot of work to be done to educate the public about women and HIV, said Ms Richardson.

"Many people wouldn't even consider that if a woman is HIV-positive she can now, through early diagnosis and medication, have a baby that doesn't have HIV, and that's a powerful message," she said.

"That's why stories like Jane's are so important in challenging all the myths and misconceptions.

"This is a young woman from Northern Ireland, engaging in her first sexual activity, in a heterosexual relationship and she contracts HIV - all of the stereotypes and assumptions people associate with HIV are turned on its head by this very powerful story."

Jane's mother believes more should be done to educate young people about the risks of contracting HIV.

"HIV is still such a taboo subject," she said. "My daughter's story shows it's possible for a young girl in her prime to get HIV and I believe more could be done around sexual education in schools."

She added: "Because of organisations like Positive Life, we're more informed now. We know her HIV can't be cured, but it can be treated.

"But that also means she is going to be on very strong medication for the rest of her life and that does worry me."

Jane is determined not to be defined by being HIV-positive.

"I can't change the past, but what I would say to anyone, if you're sexually active, whether it's your first time or not, just be safe," she said.

"I have to live with the fact that I'm HIV-positive, but I won't let it ruin my life."

Continued here:
HIV, my baby and me: 'I was 17 years old when I was diagnosed' - BBC News

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