How 'America's Got Talent' Contestant Kodi Lee Shattered Stereotypes About Disability

Lee was able to communicate that 
disability is a part of humanity – not 
separate from it.
America's Got Talent/YouTube

Stan Link, Vanderbilt University

If you haven’t seen Kodi Lee’s May 28 performance on “America’s Got Talent,” it’s worth a watch.

The 22-year-old Lee is blind and has autism. His rendition of Leon Russell’s “A Song for You” brought the crowd to its feet – and thrilled viewers at home.
“Loved this moment so much! Stood up and cheered in my living room!” Oprah tweeted.

Much of the media coverage portrayed Lee as someone who, in developing his musical ability to such a high level, overcame all odds – a common though sometimes troublesome trope used to describe people with disabilities who achieve any measure of success.

Lee is certainly an exciting talent. But as someone who teaches a course on the intersection of disability and music, I was moved by other aspects of Lee’s performance as well.


Lee stunned the judges during his May 28 performance on ‘America’s Got Talent.’

One challenge for people with disabilities can be that others tend to conflate their disability with their personality and identity. Their disability becomes the defining aspect of who they are, which can prevent people from realizing that those with disabilities can have rich interior lives.
So listening to Lee sing about love – mature, adult love – I heard a 22-year-old man whose voice and delivery brimmed with emotion and rang with authenticity.

“I’ve been so many places in my life and time,” he begins. “We’re alone now and I’m singing this song to you,” he croons, evoking deep intimacy and connection.

Infantilizing and de-sexualizing people with disabilities is still commonplace – as though physical or intellectual disability should necessarily exclude the ability to feel desire and the longing to be desired.

Lee shatters these notions. To sing these lines believably means to have lived them or to have imagined their truth.

Perhaps the most joyful aspect of Kodi Lee’s performance, however, is rooted in the dimension of time.

Philosopher and disability theorist Licia Carlson has written that “the experience of disability may be defined in negative terms when people fail to live according to what is considered to be normal time.”
In other words, because many tasks can take longer for someone with a disability, keeping pace can feel like a constant struggle.

This is where music can be such a beautifully transporting experience. It has its own time that’s not tied to that of the real world. With its tempo, rhythm and dramatic pacing, music creates its own temporal universe.
While listening to Lee perform, everyone in the audience was listening along at his speed, which, as the performer, he controlled.

It was a rare opportunity for disabled and non-disabled to be fully present together, under the same umbrella of time and space.
Finally, I think it’s important to return to the title of the show: “America’s Got Talent.”

After the Industrial Revolution, the ability to contribute labor and earn a paycheck became defining features of what it meant to be American.
If being a “true” American traditionally implied independence and autonomy, this one element of national identity alone could be enough to stigmatize people with disabilities.

Kodi Lee belted out an overwhelming assurance – as if it should have ever been needed – that a blind man with autism is also included in the definition of America.


Stan Link, Associate Professor of the Composition, Philosophy and Analysis of Music, Vanderbilt University


This article is republished from The Conversation under a Creative Commons license. Read the original article.

New Category: Game of Thrones


There's a new category on Magatopia for you to enjoy.

Magatopia.com - Game of Thrones

Following is a list of all the online Game of Thrones magazines and blogs linked to on the new page. Magatopia delivers live headline feeds from the following sources:


  • Watchers on the Wall

    Winter is Coming

    The Sun - Game of Thrones

    Hypable

    TheWrap

    Making Game of Thrones

    FanSided – Game of Thrones

    Global News | Game of Thrones

    The Conversation

    George R.R. Martin

    Westeros.org

    Den of Geek!

    Digital Spy

    ScreenRant

    WIRED
Link: Magatopia.com - Game of Thrones


Magatopia.com is the internet's directory to thousands of free online magazines. All of the magazines Magatopia links to have news, articles or columns that you can read online for free.

6 Ways to Protect Your Mental Health From Social Media's Dangers

Photo by Sebastiaan ter Burg
CC BY 3.0
Is social media helping you feel good?

Written by Jelena Kecmanovic, Georgetown University
Original story first published at The Conversation

More than one-third of American adults view social media as harmful to their mental health, according to a new survey from the American Psychiatric Association. Just 5% view social media as being positive for their mental health, the survey found. Another 45% say it has both positive and negative effects.

Two-thirds of the survey’s respondents believe that social media usage is related to social isolation and loneliness. There is a strong body of research linking social media use with depression. Other studies have linked it to envy, lower self-esteem and social anxiety.

As a psychologist who has studied the perils of online interactions and has observed the effects of social media (mis)use on my clients’ lives, I have six suggestions of ways people can reduce the harm social media can do to their mental health.

1. Limit when and where you use social media

Using social media can interrupt and interfere with in-person communications. You’ll connect better with people in your life if you have certain times each day when your social media notifications are off – or your phone is even in airplane mode. Commit to not checking social media during meals with family and friends, and when playing with children or talking with a partner. Make sure social media doesn’t interfere with work, distracting you from demanding projects and conversations with colleagues. In particular, don’t keep your phone or computer in the bedroom – it disrupts your sleep.

2. Have ‘detox’ periods

Schedule regular multi-day breaks from social media. Several studies have shown that even a five-day or week-long break from Facebook can lead to lower stress and higher life satisfaction. You can also cut back without going cold turkey: Using Facebook, Instagram and Snapchat just 10 minutes a day for three weeks resulted in lower loneliness and depression. It may be difficult at first, but seek help from family and friends by publicly declaring you are on a break. And delete the apps for your favorite social media services.

3. Pay attention to what you do and how you feel

Experiment with using your favorite online platforms at different times of day and for varying lengths of time, to see how you feel during and after each session. You may find that a few short spurts help you feel better than spending 45 minutes exhaustively scrolling through a site’s feed. And if you find that going down a Facebook rabbit hole at midnight routinely leaves you depleted and feeling bad about yourself, eliminate Facebook after 10 p.m. Also note that people who use social media passively, just browsing and consuming others’ posts, feel worse than people who participate actively, posting their own material and engaging with others online. Whenever possible, focus your online interactions on people you also know offline.

4. Approach social media mindfully; ask ‘why?’

If you look at Twitter first thing in the morning, think about whether it’s to get informed about breaking news you’ll have to deal with – or if it’s a mindless habit that serves as an escape from facing the day ahead. Do you notice that you get a craving to look at Instagram whenever you’re confronted with a difficult task at work? Be brave and brutally honest with yourself. Each time you reach for your phone (or computer) to check social media, answer the hard question: Why am I doing this now? Decide whether that’s what you want your life to be about.

5. Prune

Over time, you have likely accumulated many online friends and contacts, as well as people and organizations you follow. Some content is still interesting to you, but much of it might be boring, annoying, infuriating or worse. Now is the time to unfollow, mute or hide contacts; the vast majority won’t notice. And your life will be better for it. A recent study found that information about the lives of Facebook friends affects people more negatively than other content on Facebook. People whose social media included inspirational stories experienced gratitude, vitality and awe. Pruning some “friends” and adding a few motivational or funny sites is likely to decrease the negative effects of social media.

6. Stop social media from replacing real life

Using Facebook to keep abreast of your cousin’s life as a new mother is fine, as long as you don’t neglect to visit as months pass by. Tweeting with a colleague can be engaging and fun, but make sure those interactions don’t become a substitute for talking face to face. When used thoughtfully and deliberately, social media can be a useful addition to your social life, but only a flesh-and-blood person sitting across from you can fulfill the basic human need for connection and belonging.The Conversation
Jelena Kecmanovic, Adjunct Professor of Psychology, Georgetown University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Kami Rita Sherpa Breaks Record as He Climbs Mount Everest for the 24th Time


Image courtesy of Seven Summit Treks Pvt. Ltd. Used with permission.
Broke his own record for most summits on Mount Everest

Written by Sanjib Chaudhary
Original story first published at Global Voices

Climbing Mount Everest is on every adrenaline junkie’s wishlist, but Everest summiteer Kami Rita Sherpa has checked this off his list a record amount of times. Defying all odds, he climbed the world’s highest peak twice in a week this year – earlier on 15 May and again on 21 May 2019 – making his number of Everest ascents 24.
Seven Summit Treks, the company he works with, announced on Facebook:
21 May 2019 !
24th Ascents of Mt Everest 8848m by Kami Rita Sherpa, HUGE CONGRATULATIONS TO OUR SENIOR GUIDE.
This morning 6:30 AM Kami Rita climbed the Mt Everest for 24 times (2nd Ascents of this season) and broke his own record of 23rd Ascents! […]
According to the Tashi Lakpa Sherpa, MD at Seven Summit Treks, this morning at 6:30 AM Kami Rita climbed the highest peak via South Side with A TEAM OF INDIAN POLICE. “Guiding a team of Indian Police Mt Everest Expedition 2019 this morning Kami Rita Sherpa climbed Mt Everest for 24 times; he made the entire country proud, this is a golden mark in the history of mountaineering🇳🇵 ” Sherpa added.
Kami Rita belongs to the Sherpa ethnic group native to the most mountainous regions of Nepal and the Himalayas. Many Sherpas are good mountaineers and experts in their local area and they have long been serving as professional guides to foreign mountaineers who want to brave the extreme altitudes.

Kami Rita hails from Thame village in Nepal’s Solukhumbu District, known for its famous climbers. Thame has produced famous climbers including Apa Sherpa (aka Super Sherpa) who held the previous record of most Mount Everest summits and Ang Rita Sherpa who has climbed Everest 10 times without supplemental oxygen that has earned him the sobriquet ‘The Snow Leopard’.

Kami Rita climbed Everest on 13 May 1994 for the first time and has also climbed K2 and Lhotse one time each, Manaslu twice and Cho Oyu eight times, totalling 36 ascents of peaks over 8,000m according to Seven Summit Treks.

After climbing Everest so many times, Kami Rita has seen the visible effects of climate change on Everest. Speaking to BBC Nepali earlier this year, Kami Rita said:
पहिले १२/१३ वटा भर्याङ चढ्नुपर्थ्यो भने अहिले तीन-चारवटाले पुग्छ। […]
पहिले क्याम्प टूमै कति धेरै हिउँ हुन्थ्यो। अहिले हिमनदी मात्र छ। […] बाल्कोनीभन्दा माथि कम्मरसम्म हिउँ हुन्थ्यो अहिले ढुङ्गामात्र देखिन्छ।
Earlier we had to climb 12-13 ladders [at Kumbu Icefall] but we can do with 3-4 these days. […]
In earlier days Camp 2 used to see a lot of snow. Now there’s only a glacier. […] Above Balcony there used to be snow up to hips, now you see only rocks.
Around 300 climbers have died on Everest and only a few dead bodies have been brought down. Now, the melting of ice in Everest is exposing the dead bodies buried in the snow.

A recent report by the International Centre for Integrated Mountain Development states that the Himalayas will lose more than one-third of their ice by the end of the century. In addition, many climbers leave tents, climbing equipment, gas canisters and human poop, making Everest a literal dumping site. However, climbing Everest is a big business with hundreds of aspirants seeking the help of Sherpa guides to reach the summit.

Like every other year, new records have already been made with South Africa’s Saray N’ Kusi Khumalo becoming the first black African woman to successfully climb Everest. And some climbers have died and have gone missing on Mount Everest this year too. But the craze of climbing Everest, it seems, will never subside.

 Originally published, here, by Sanjib Chaudhary under the terms of a Creative Commons Attribution 3.0 Unported (CC BY 3.0) license.

The man who is ageing too fast

"El tiempo desde la ventana"
 by Oneras is licensed 
under CC BY-SA 2.0
Nobuaki Nagashima has Werner syndrome, which causes his body to age at super speed. This condition is teaching us more about what controls our genes, and could eventually help us find a way to slow ageing – or stop it altogether.

Written by Erika Hayasaki
Original story first published at Mosaic

Nobuaki Nagashima was in his mid-20s when he began to feel like his body was breaking down. He was based in Hokkaido, the northernmost prefecture of Japan, where for 12 years he had been a member of the military, vigorously practising training drills out in the snow. It happened bit by bit – cataracts at the age of 25, pains in his hips at 28, skin problems on his leg at 30.

At 33, he was diagnosed with Werner syndrome, a disease that causes the body to age too fast. Among other things, it shows as wrinkles, weight loss, greying hair and balding. It’s also known to cause hardening of the arteries, heart failure, diabetes and cancer.

I meet Nagashima under the white light of a Chiba University Hospital room, around 25 miles west of Tokyo. A grey newsboy cap covers his hairless head freckled with liver spots. His eyebrows are thinned to a few wisps. Black-rimmed glasses help with his failing eyesight, his hip joints – replaced with artificial ones after arthritis – ache as he stands to slowly walk across the room. These ailments you might expect to see in an 80-year-old. But Nagashima is just 43.

He tells me that he has been in and out of hospital ever since his diagnosis. That his deteriorating health forced him to leave the military. Nagashima has had five or six surgeries, from his toes to hips to eyes, to treat ageing-related ailments. He’s lost 15 kilograms since he was first diagnosed. He needs a walking stick to do a distance over a few metres, and has a temporary job at the City Hall, going to the office when his body will allow but working from home when it doesn’t.

He remembers driving home after his diagnosis, crying to himself. When he told his parents, his mother apologised for not giving birth to a stronger person. But his father told him that if he could endure this disease, he was indeed strong, and maybe scientists would learn from him, gaining knowledge that could help others.

Apart from the X and Y sex chromosomes, we inherit two copies of every gene in our bodies – one from our mother and one from our father. Werner syndrome is what’s called an autosomal recessive disorder, meaning it only shows when a person inherits a mutated version of a gene called WRN from both parents.

Nagashima’s parents are ageing normally. They each have one functional copy of WRN, so their bodies don’t show any symptoms of the disease. But he was unfortunate to have received two mutated copies of WRN. His grandparents are still alive and as well as one might expect for a couple in their 90s, and the family are unaware of any other Werner cases in their family history.

WRN was discovered only in 1996, and since then there have been few examples of Werner. As of 2008, there were only 1,487 documented cases worldwide, with 1,128 of them in Japan.

Lest this seem like a uniquely Japanese condition, George Martin, co-director of the International Registry of Werner Syndrome at the University of Washington, thinks the number of actual cases globally is around seven times higher than the numbers recorded today. He says most cases around the world will not have come to the attention of any physicians or registries.

The huge imbalance in Japanese cases he puts down to two factors. First, the mountains and islands of the Japanese landscape and the isolating effect that’s had on the population through history – people in more isolated regions in the past were more likely to end up having children with someone more similar to them genetically. A similar effect is seen in the Italian island of Sardinia, which also has a cluster of Werner cases. Second, the startling nature of the condition, and the higher frequency with which it appears in Japan (affecting an estimated one in a million people worldwide but one in 100,000 in Japan), means the Japanese medical system is more aware than most when Werner syndrome appears.

In Chiba University Hospital, they hold records of 269 clinically diagnosed patients in total, 116 of whom are still alive. One of them is Sachi Suga, who can only get around in a wheelchair. Her muscles are so weak she can no longer climb in and out of the bath, which makes it difficult to keep up the Japanese practice of ofuro, the ritual of relaxing each night in a deep tub of steaming hot water. She used to cook breakfast regularly for herself and her husband, but now she cannot stand at a stove for more than a minute or two at a time. She’s resorted to preparing quicker-to-make miso soup the night before, which he eats before leaving for work at 5.30am.
Waif-like in a short black wig, Suga has tiny wrists as delicate as glass, and she speaks to me in a hoarse, throaty whisper. She tells me of the home aid worker who visits three times a week to help wrap her ulcer-covered legs in bandages. She has terrible back and leg pain. “It hurt so much, I wanted my legs to be cut off.” Yet on the positive side, the 64-year-old has long surpassed the average life expectancy of around 55 for people with Werner syndrome.

Only a handful of people with Werner currently attend Chiba. Recently, they started a support group. “Once our conversation started, I forgot about the pain completely,” says Suga. Nagashima says the meetings often end with the same question: “Why do I have this disease?”


If you were to unravel the 23 pairs of chromosomes in one of your cells you would end up with about two metres of DNA. That DNA is folded up into a space about a 10,000th of that distance across – far more compacted than even the tightest origami design. This compacting happens with help from proteins called histones.

DNA, and the histones that package it up, can acquire chemical marks. These don’t change the underlying genes, but they do have the power to silence or to amplify a gene’s activity. Where the marks are put or what form they take seems to be influenced by our experiences and environment – in response to smoking or stress, for instance. Some seem to be down to random chance, or the result of a mutation, as in cancer. Scientists call this landscape of markings the epigenome. We do not know yet exactly why our cells add these epigenetic marks, but some of them seem to be connected to ageing.

Steve Horvath, professor of human genetics and biostatistics at the University of California, Los Angeles, has used one type of these, called methylation marks, to create an “epigenetic clock” that, he says, looks beyond the external signs of ageing like wrinkles or grey hair, to more accurately measure how biologically old you are. The marks can be read from blood, urine, organ or skin tissue samples.

Horvath’s team analysed blood cells from 18 people with Werner syndrome. It was as if the methylation marking was happening on fast-forward: the cells had an epigenetic age notably higher than those from a control group without Werner.


Nagashima’s and Suga’s genetic information is part of a database held by Chiba University. There is also a Japan-wide database of Werner syndrome and the International Registry at the University of Washington. These registries are providing researchers with insights into how our genes work, how they interact with the epigenome, and how that fits with ageing as a whole.

Scientists now understand that WRN is key to how the whole cell, how all our DNA works – in reading, copying, unfolding and repairing. Disruption to WRN leads to widespread instability throughout the genome. “The integrity of the DNA is altered, and you get more mutations… more deletions and aberrations. This is all over the cells,” says George Martin. “Big pieces are cut out and rearranged.” The abnormalities are not just in the DNA but in the epigenetic marks around it too.

The million-dollar question is whether these marks are imprints of diseases and ageing or whether the marks cause diseases and ageing – and ultimately death. And if the latter, could editing or removing epigenetic marks prevent or reverse any part of ageing or age-related disease?
Before we can even answer that, the fact is, we know relatively little about the processes through which epigenetic marks are actually added and why. Horvath sees methylation marks as like the face of a clock, not necessarily the underlying mechanism that makes it tick. The nuts and bolts may be indicated by clues like the WRN gene, and other researchers have been getting further glimpses beneath the surface.

In 2006 and 2007, Japanese researcher Shinya Yamanaka published two studies which found that putting four specific genes – now called Yamanaka factors – into any adult cell could rewind it to an earlier, embryonic state, a stem cell, from which it could then be turned into any other type of cell. This method, which earned Yamanaka the Nobel Prize, has become a mainspring for stem cell studies. But what made this all the more interesting was that it completely reset the epigenetic age of the cells to a prenatal stage, erasing the epigenetic marks.

Researchers replicated Yamanaka’s experiments in mice with a condition called Hutchinson–Gilford progeria syndrome, which has similar symptoms to Werner but only affects children (Werner is sometimes called adult progeria). Remarkably, the mice rejuvenated briefly, but they died within a couple of days. Totally reprogramming the cells had also led to cancer and loss of the cells’ ability to function.

Then in 2016, scientists at the Salk Institute in California engineered a way to partially rewind the cells of mice with progeria using a lower dose of the Yamanaka factors for a shorter period. The premature ageing slowed down in these mice. They not only looked healthier and livelier than progeria mice who hadn’t had the treatment, but their cells were also found to have fewer epigenetic marks. Moreover, they lived 30 per cent longer than the untreated mice. When the researchers applied this same treatment to normally ageing mice, their pancreases and muscles also rejuvenated.
Separately, the same scientists are also using gene editing technology on mice to add or subtract other epigenetic marks and see what happens. They’re also trying to modify the histone proteins to see if that can alter genes’ activity. Some of these techniques have already shown results in reversing diabetes, kidney disease and muscular dystrophy in mice. The team are now trying similar experiments on rodents to see if they can reduce the symptoms of arthritis and Parkinson’s disease.

The big question remains: is the disappearance of the epigenetic marks related to the reversal of cell development – and possibly the ageing of the cell – or an unrelated side-effect? Scientists are still trying to understand how changes in epigenetic marks relate to ageing, and how Yamanaka factors are able to reverse age-related conditions.

Horvath says that, from an epigenetic point of view, there are clear commonalities in ageing across many regions of the body. Epigenetic ageing in the brain is similar to that of the liver or the kidney, showing similar patterns of methylation marks. When you look at it in terms of these marks, he says, “ageing is actually rather straightforward, because it’s highly reproducible in different organs”.

There’s a feverishness around the idea of resetting or reprogramming the epigenetic clock, Horvath tells me. He sees huge potential in all of it, but says it has the feel of a gold rush. “Everybody has a shovel in their hand.”
Jamie Hackett, a molecular biologist at the European Molecular Biology Laboratory in Rome, says the excitement comes from the suggestion that you can have an influence over your genes. Previously there was a fatalistic sense of being stuck with what you are given, and nothing you can do about it.


Back in the Chiba hospital room, Nagashima removes one of his high-top sneakers, which he has cushioned with insoles to make walking more bearable.

He tells me about his former girlfriend. They had wanted to marry. She was understanding after his diagnosis and even took a genetic test so they could be sure they would not pass the condition on to their kids. But when her parents discovered his condition, they disapproved. The relationship ended.

He has a new girlfriend now. He wants to make her his life partner, he tells me, but to do so he must get up the courage to ask for her parents’ permission.

Nagashima slips down a brown sock, revealing a white bandage wrapped around the sole of his swollen foot and ankles. Beneath, his skin is raw, revealing red ulcers caused by his disease. “Itai,” he says. It hurts. Then he smiles. “Gambatte,” he says – I will endure.

References:
Steve Horvath and colleagues say that the DNAm GrimAge estimator (named after the Grim Reaper) is the best epigenetic predictor of lifespan, time to heart disease, time to cancer and age at menopause.

Horvath and team find that Werner syndrome is associated with increased epigenetic age of blood cells.

Researchers at the Salk Institute show how epigenetic editing can affect the health of mice.

A team at the University of Washington review WRN mutations found around the world.

Erika Hayasaki has written about twin science, which offers a window into current epigenetic research.

 Originally published, here, by Erika Hayasaki under the terms of a Attribution 4.0 International (CC BY 4.0) license.

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