What Hope Actually Meant to Martin Luther King Jr.

Once upon a time, hope meant confronting suffering, not avoiding it. Have overly sugary connotations about hope diminished its true grit?

Andre C. Willis: So what I can share with you today is not an answer to the question of “What is hope?” but I can share with you about how a tradition that I’m involved in studying and that I’m linked to has a take on what ways of hoping may be better or more useful than others.
So my understanding of this tradition that I have studied and engaged with for a few years now is the African American Protestant tradition of hoping, that’s crafted over centuries of despair and dehumanization. And I think it has something to teach our nation.

Our nation that has in some ways undermined this very tradition of hoping. And the nation in some ways has trivialized hope itself, made hope into something that’s largely a market-driven quest for getting our aspirations, for reaching our goals, for achieving our aims.

I think one of the things that not unpacking this distinction between Obama’s hopes and King’s hopes—based on the painting which I’m going to describe now—is it leaves us more vulnerable to romantic conceptions of hope. We tend to fall into this way of thinking about hope that’s more reflective almost of what Shelley called in 'Prometheus Unbound', 1822, he said he wants “to hope till hope creates from its own wreck the thing it contemplates.” It’s a beautiful line, right, and I’m susceptible and seduced by that kind of hope.

But when I think about King and Obama and this painting I tend to get more clear about what is deep hope, right. So I want to highlight quickly the distinctions between both King and Obama and then I’ll be done, because I think this will help us understand both what I’m trying to get at and where we are now. So first, King’s hope, his description of hope is always disappointed and never realized, while Obama’s hope guides us past disappointment and is realizable. So here we have a clear difference between the Protestant embrace of a tragic sense of life and the kind of democratic politics of hope that aims to resist the politics of cynicism. And that’s fine. So the important thing to remember though is that the difference in the Protestant embrace of tragedy attenuates our inclinations for happy ending. It works against that romantic conception that I argue, I pointed out Shelley was referencing in the 1822 'Prometheus Unbound' quote, right. Its romantic sense: to hope until hope reaches what it contemplates.

Second, King’s hope is a discipline of the present moment. It’s a social practice done in community with the aim of reminding us that our lives are always incomplete and unfinished. Our deep hopes will not come to fruition, is King’s point. In this way we might say that King’s hope is a way of relationship. It is a relating to suffering. It tells us to just keep going.
Obama’s hope on the other hand is the aspiration for the future. It’s a rational belief about the probability of attainment. Attaining one’s ambitions.

We might say that Obama’s hope attends to the pressures of achievement by affirming aspirations for the future. So I quickly want to caution you from taking what I’m saying as a way of thinking about Martin’s account as just another form of tragic hope, dark hope, melancholic hope, “I hope against hope”, hope of the hopeless, right. Because I think that I take King’s hope to simply be a reminder of the idea of the tragic in our life, the notion that our mortal days will not be fulfilled. So it’s dark in that sense, but I don’t want to pitch it as a dark hope, right. I want to pitch it as a deep hope. And when people go with melancholic hope or blues hope, I think they often end up romanticizing a kind of hope that seduces us into thinking there may be a hope without suffering. That is, the idea of a “dark” hope relies on the idea of a “light” hope, and that has all kinds of problems, right, analogically.

But just the fact that both things sort of seem like they have to exist together is misleading and it skirts the fundamental insight of Martin, which is to remind us of a certain kind of suffering.
Now for King, a man who we often associate with things like the 'I Have A Dream' speech, right, the song 'We Shall Overcome'. He’s telling us in ’59, ’63 and later on in ’68 he gives a sermon called 'Unfulfilled Dreams' where he continues this theme that all our hopes are blasted and our dreams are shattered.

In other words the person we think of as the amazing hoper and dreamer is really trying to tell us something much different. He’s trying to tell us our hopes are perfidious. As George Buttrick notes, “We die with half our music in us.”

So you might ask then, "What is the purpose of this sort of hope and why would I want to subscribe to it?” And that’s just it. This hope is not up for subscription. It’s a way of relating to suffering and facing the ultimate fact that we shall likely not achieve all of the promises of life. But this is just what life is, in this strand of Protestantism. It is not life’s failing.
King tells us that the tentacles of evil are always present, taking meaning out of life but we must go on. We must have the will to refuse. We must have what Tillich called “the courage to be.” This, I think, is the link between Martin King and the Watts painting. Both are fundamentally trying to affirm a relationship between suffering to continuing, right. And Martin is dealing with the death of dreams. Watts, I think, is dealing with the death of his, reportedly his stepdaughter. Remember Du Bois lost little Burghardt in 1899. Burghardt was 18 months old. Du Bois wrote that he was feeling a hope, “A hope not hopeful but un-hopeless.” The message is once again that our hopes are shattered. This shattering provides a path to suffering that allows deeper meaning. This is what deep hope is about.

So when students ask me “Why do I hope?” I turn to Martin. And these questions, of course, have recently increased. Not because people are necessarily more depressed but because I think they don’t understand the deep hope that Martin was trying to call us to.

So let me just end by saying this. Obama’s not the only—it’s not Obama’s fault that we’re not attentive to the deep hopes that Martin was trying to call us to based on his interpretation of the painting. Global marketers have made hope into a rational calculation for personal gain.
Many academics have subjected hopes to standards of analytic precision and conceptual clarity which has kind of degraded it. It’s been certainly diminished by Christian leaders who reduced hope to a form of compliance. This has led to a loss in our appetite for hope, deep hope. That is, we want the romantic hope but not the deep kind that’s in touch with suffering. This is the kind of tradition that I’ve been studying. The tradition that Martin and Jeremiah Wright, Fred Sampson link to the painting of George Frederic Watts in 1886. And thus I leave you with an invitation to the painting as well as one to deep hope. Thank you very kindly.

Here's an exercise: If there's someone near you right now, ask them to define hope. Quickly. What did they say: was it motivational? Did it deal with future ambition, expectation, and desire? Historically, hope has not always had such sugary connotations, and at one point—not so long ago, actually—it was more about confronting suffering in the present than mentally projecting yourself forward to a time where you have overcome your suffering. Drawing from an 1886 painting by George Frederic Watts called 'Hope', which inspired Martin Luther King Jr.'s 1959 sermon 'Shattered Dreams', Andre C. Willis presents a view of deep hope, a method of facing adversity that is woven together from the African American Protestant tradition.


This video was filmed at the Los Angeles Hope Festival, a collaboration between Big Think and Hope & Optimism, a three-year initiative which supported interdisciplinary academic research into significant questions that remain under-explored.

CRISPR therapy cures first genetic disorder inside the body

It marks a breakthrough in using gene editing to treat diseases.

Credit: National Cancer Institute via Unsplash
Technology & Innovation

This article was originally published by our sister site, Freethink.

For the first time, researchers appear to have effectively treated a genetic disorder by directly injecting a CRISPR therapy into patients' bloodstreams — overcoming one of the biggest hurdles to curing diseases with the gene editing technology.

The therapy appears to be astonishingly effective, editing nearly every cell in the liver to stop a disease-causing mutation.

The challenge: CRISPR gives us the ability to correct genetic mutations, and given that such mutations are responsible for more than 6,000 human diseases, the tech has the potential to dramatically improve human health.

One way to use CRISPR to treat diseases is to remove affected cells from a patient, edit out the mutation in the lab, and place the cells back in the body to replicate — that's how one team functionally cured people with the blood disorder sickle cell anemia, editing and then infusing bone marrow cells.

Bone marrow is a special case, though, and many mutations cause disease in organs that are harder to fix.

Another option is to insert the CRISPR system itself into the body so that it can make edits directly in the affected organs (that's only been attempted once, in an ongoing study in which people had a CRISPR therapy injected into their eyes to treat a rare vision disorder).

Injecting a CRISPR therapy right into the bloodstream has been a problem, though, because the therapy has to find the right cells to edit. An inherited mutation will be in the DNA of every cell of your body, but if it only causes disease in the liver, you don't want your therapy being used up in the pancreas or kidneys.

A new CRISPR therapy: Now, researchers from Intellia Therapeutics and Regeneron Pharmaceuticals have demonstrated for the first time that a CRISPR therapy delivered into the bloodstream can travel to desired tissues to make edits.

We can overcome one of the biggest challenges with applying CRISPR clinically.

—JENNIFER DOUDNA

"This is a major milestone for patients," Jennifer Doudna, co-developer of CRISPR, who wasn't involved in the trial, told NPR.

"While these are early data, they show us that we can overcome one of the biggest challenges with applying CRISPR clinically so far, which is being able to deliver it systemically and get it to the right place," she continued.

What they did: During a phase 1 clinical trial, Intellia researchers injected a CRISPR therapy dubbed NTLA-2001 into the bloodstreams of six people with a rare, potentially fatal genetic disorder called transthyretin amyloidosis.

The livers of people with transthyretin amyloidosis produce a destructive protein, and the CRISPR therapy was designed to target the gene that makes the protein and halt its production. After just one injection of NTLA-2001, the three patients given a higher dose saw their levels of the protein drop by 80% to 96%.

A better option: The CRISPR therapy produced only mild adverse effects and did lower the protein levels, but we don't know yet if the effect will be permanent. It'll also be a few months before we know if the therapy can alleviate the symptoms of transthyretin amyloidosis.

This is a wonderful day for the future of gene-editing as a medicine.

—FYODOR URNOV

If everything goes as hoped, though, NTLA-2001 could one day offer a better treatment option for transthyretin amyloidosis than a currently approved medication, patisiran, which only reduces toxic protein levels by 81% and must be injected regularly.

Looking ahead: Even more exciting than NTLA-2001's potential impact on transthyretin amyloidosis, though, is the knowledge that we may be able to use CRISPR injections to treat other genetic disorders that are difficult to target directly, such as heart or brain diseases.

"This is a wonderful day for the future of gene-editing as a medicine," Fyodor Urnov, a UC Berkeley professor of genetics, who wasn't involved in the trial, told NPR. "We as a species are watching this remarkable new show called: our gene-edited future."

UFOs: US intelligence report finds no aliens but plenty of unidentified flying objects

A new government report describes 144 sightings of unidentified aerial phenomena.

Photo by Albert Antony on Unsplash
Surprising Science

On June 25, 2021, the Office of the Director of National Intelligence released a much-anticipated report on UFOs to Congress.

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Android has won the phone world war

A global survey shows the majority of countries favor Android over iPhone.

Credit: Electronics Hub
Strange Maps
  • When Android was launched soon after Apple's own iPhone, Steve Jobs threatened to "destroy" it.
  • Ever since, and across the world, the rivalry between both systems has animated users.
  • Now the results are in: worldwide, consumers clearly prefer one side — and it's not Steve Jobs'.
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COVID and "gain of function" research: should we create monsters to prevent them?

Gain-of-function mutation research may help predict the next pandemic — or, critics argue, cause one.

Credit: Guillermo Legaria via Getty Images
Coronavirus

This article was originally published on our sister site, Freethink.

"I was intrigued," says Ron Fouchier, in his rich, Dutch-accented English, "in how little things could kill large animals and humans."

It's late evening in Rotterdam as darkness slowly drapes our Skype conversation.

This fascination led the silver-haired virologist to venture into controversial gain-of-function mutation research — work by scientists that adds abilities to pathogens, including experiments that focus on SARS and MERS, the coronavirus cousins of the COVID-19 agent.

If we are to avoid another influenza pandemic, we will need to understand the kinds of flu viruses that could cause it. Gain-of-function mutation research can help us with that, says Fouchier, by telling us what kind of mutations might allow a virus to jump across species or evolve into more virulent strains. It could help us prepare and, in doing so, save lives.

Many of his scientific peers, however, disagree; they say his experiments are not worth the risks they pose to society.

A virus and a firestorm

The Dutch virologist, based at Erasmus Medical Center in Rotterdam, caused a firestorm of controversy about a decade ago, when he and Yoshihiro Kawaoka at the University of Wisconsin-Madison announced that they had successfully mutated H5N1, a strain of bird flu, to pass through the air between ferrets, in two separate experiments. Ferrets are considered the best flu models because their respiratory systems react to the flu much like humans.

The mutations that gave the virus its ability to be airborne transmissible are gain-of-function (GOF) mutations. GOF research is when scientists purposefully cause mutations that give viruses new abilities in an attempt to better understand the pathogen. In Fouchier's experiments, they wanted to see if it could be made airborne transmissible so that they could catch potentially dangerous strains early and develop new treatments and vaccines ahead of time.

The problem is: their mutated H5N1 could also cause a pandemic if it ever left the lab. In Science magazine, Fouchier himself called it "probably one of the most dangerous viruses you can make."

Just three special traits

Recreated 1918 influenza virionsCredit: Cynthia Goldsmith / CDC / Dr. Terrence Tumpey / Public domain via Wikipedia

For H5N1, Fouchier identified five mutations that could cause three special traits needed to trigger an avian flu to become airborne in mammals. Those traits are (1) the ability to attach to cells of the throat and nose, (2) the ability to survive the colder temperatures found in those places, and (3) the ability to survive in adverse environments.

A minimum of three mutations may be all that's needed for a virus in the wild to make the leap through the air in mammals. If it does, it could spread. Fast.

Fouchier calculates the odds of this happening to be fairly low, for any given virus. Each mutation has the potential to cripple the virus on its own. They need to be perfectly aligned for the flu to jump. But these mutations can — and do — happen.

"In 2013, a new virus popped up in China," says Fouchier. "H7N9."

H7N9 is another kind of avian flu, like H5N1. The CDC considers it the most likely flu strain to cause a pandemic. In the human outbreaks that occurred between 2013 and 2015, it killed a staggering 39% of known cases; if H7N9 were to have all five of the gain-of-function mutations Fouchier had identified in his work with H5N1, it could make COVID-19 look like a kitten in comparison.

H7N9 had three of those mutations in 2013.

Gain-of-function mutation: creating our fears to (possibly) prevent them

Flu viruses are basically eight pieces of RNA wrapped up in a ball. To create the gain-of-function mutations, the research used a DNA template for each piece, called a plasmid. Making a single mutation in the plasmid is easy, Fouchier says, and it's commonly done in genetics labs.

If you insert all eight plasmids into a mammalian cell, they hijack the cell's machinery to create flu virus RNA.

"Now you can start to assemble a new virus particle in that cell," Fouchier says.

One infected cell is enough to grow many new virus particles — from one to a thousand to a million; viruses are replication machines. And because they mutate so readily during their replication, the new viruses have to be checked to make sure it only has the mutations the lab caused.

The virus then goes into the ferrets, passing through them to generate new viruses until, on the 10th generation, it infected ferrets through the air. By analyzing the virus's genes in each generation, they can figure out what exact five mutations lead to H5N1 bird flu being airborne between ferrets.

And, potentially, people.

"This work should never have been done"

The potential for the modified H5N1 strain to cause a human pandemic if it ever slipped out of containment has sparked sharp criticism and no shortage of controversy. Rutgers molecular biologist Richard Ebright summed up the far end of the opposition when he told Science that the research "should never have been done."

"When I first heard about the experiments that make highly pathogenic avian influenza transmissible," says Philip Dormitzer, vice president and chief scientific officer of viral vaccines at Pfizer, "I was interested in the science but concerned about the risks of both the viruses themselves and of the consequences of the reaction to the experiments."

In 2014, in response to researchers' fears and some lab incidents, the federal government imposed a moratorium on all GOF research, freezing the work.

Some scientists believe gain-of-function mutation experiments could be extremely valuable in understanding the potential risks we face from wild influenza strains, but only if they are done right. Dormitzer says that a careful and thoughtful examination of the issue could lead to processes that make gain-of-function mutation research with viruses safer.

But in the meantime, the moratorium stifled some research into influenzas — and coronaviruses.

The National Academy of Science whipped up some new guidelines, and in December of 2017, the call went out: GOF studies could apply to be funded again. A panel formed by Health and Human Services (HHS) would review applications and make the decision of which studies to fund.

As of right now, only Kawaoka and Fouchier's studies have been approved, getting the green light last winter. They are resuming where they left off.

Pandora's locks: how to contain gain-of-function flu

Here's the thing: the work is indeed potentially dangerous. But there are layers upon layers of safety measures at both Fouchier's and Kawaoka's labs.

"You really need to think about it like an onion," says Rebecca Moritz of the University of Wisconsin-Madison. Moritz is the select agent responsible for Kawaoka's lab. Her job is to ensure that all safety standards are met and that protocols are created and drilled; basically, she's there to prevent viruses from escaping. And this virus has some extra-special considerations.

The specific H5N1 strain Kawaoka's lab uses is on a list called the Federal Select Agent Program. Pathogens on this list need to meet special safety considerations. The GOF experiments have even more stringent guidelines because the research is deemed "dual-use research of concern."

There was debate over whether Fouchier and Kawaoka's work should even be published.

"Dual-use research of concern is legitimate research that could potentially be used for nefarious purposes," Moritz says. At one time, there was debate over whether Fouchier and Kawaoka's work should even be published.

While the insights they found would help scientists, they could also be used to create bioweapons. The papers had to pass through a review by the U.S. National Science Board for Biosecurity, but they were eventually published.

Intentional biowarfare and terrorism aside, the gain-of-function mutation flu must be contained even from accidents. At Wisconsin, that begins with the building itself. The labs are specially designed to be able to contain pathogens (BSL-3 agricultural, for you Inside Baseball types).

They are essentially an airtight cement bunker, negatively pressurized so that air will only flow into the lab in case of any breach — keeping the viruses pushed in. And all air in and out of the lap passes through multiple HEPA filters.

Inside the lab, researchers wear special protective equipment, including respirators. Anyone coming or going into the lab must go through an intricate dance involving stripping and putting on various articles of clothing and passing through showers and decontamination.

And the most dangerous parts of the experiment are performed inside primary containment. For example, a biocontainment cabinet, which acts like an extra high-security box, inside the already highly-secure lab (kind of like the radiation glove box Homer Simpson is working in during the opening credits).

"Many people behind the institution are working to make sure this research can be done safely and securely." — REBECCA MORITZ

The Federal Select Agent program can come and inspect you at any time with no warning, Moritz says. At the bare minimum, the whole thing gets shaken down every three years.

There are numerous potential dangers — a vial of virus gets dropped; a needle prick; a ferret bite — but Moritz is confident that the safety measures and guidelines will prevent any catastrophe.

"The institution and many people behind the institution are working to make sure this research can be done safely and securely," Moritz says.

No human harm has come of the work yet, but the potential for it is real.

"Nature will continue to do this"

They were dead on the beaches.

In the spring of 2014, another type of bird flu, H10N7, swept through the harbor seal population of northern Europe. Starting in Sweden, the virus moved south and west, across Denmark, Germany, and the Netherlands. It is estimated that 10% of the entire seal population was killed.

The virus's evolution could be tracked through time and space, Fouchier says, as it progressed down the coast. Natural selection pushed through gain-of-function mutations in the seals, similarly to how H5N1 evolved to better jump between ferrets in his lab — his lab which, at the time, was shuttered.

"We did our work in the lab," Fouchier says, with a high level of safety and security. "But the same thing was happening on the beach here in the Netherlands. And so you can tell me to stop doing this research, but nature will continue to do this day in, day out."

Critics argue that the knowledge gained from the experiments is either non-existent or not worth the risk; Fouchier argues that GOF experiments are the only way to learn crucial information on what makes a flu virus a pandemic candidate.

"If these three traits could be caused by hundreds of combinations of five mutations, then that increases the risk of these things happening in nature immensely," Fouchier says.

"With something as crucial as flu, we need to investigate everything that we can," Fouchier says, hoping to find "a new Achilles' heel of the flu that we can use to stop the impact of it."

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