The Right Brain at the Right Place at the Right Time

Our prehistoric ancestors are the ones who did the heavy mental lifting for which we owe our expanded frontal cortexes. So who has the right brain for today?

 

The Right Brain at the Right Place at the Right Time

What's the Big Idea?


This is a tale of two brains. One is Einstein's brain. The other is the Paleolithic brain. In the past few weeks we have learned significant insights about both, and how each one was uniquely qualified for the mental challenges of its time. 

Let's start with Einstein. While his brain was the same size of a normal human, as some newly published photographs of his brain reveal, those images also show unusual convolutions and folds. The lead researcher of the Einstein brain study, anthropologist Dean Falk, thinks this complex brain architecture may be the result of Einstein using "his motor cortex in extraordinary ways." In other words, by doing the 'muscular thinking' of complex physics, Einstein "programmed his own brain," causing it to expand.

It helped that Einstein had good material to work with. The field of physics was ripe for new insights, Falk observes, meaning that Einstein happened to have "the right brain in the right place at the right time." Well said. 

Now let's contrast the story of Einstein's brain with a seemingly depressing assessment of our contemporary brains by Stanford biologist Gerald Crabtree. In his recent article Our Fragile Intellect, Crabtree argues that human intellectual fitness has been on a slow but steady decay for 3,000 years, due to our relatively easy lifestyle that has freed us from a state of survival by thinking. In other words, civilization has allowed us to be quite dumb and survive just fine. As a result, civilization has left us vulnerable to thousands of naturally occurring mutations.

Crabtree's analysis points to "about 5000 new mutations in the past 3000 years (~120 generations)," a fraction of which "will produce a change within a gene or its regulatory regions that will be harmful." So how do contemporary humans stack up against the people of antiquity. Crabtree argues:

I would wager that if an average citizen from Athens of 1000 BC were to suddenly appear among us, he or she would be among the brightest and most intellectually alive of our colleagues and companies, with a good memory, a broad range of ideas, and a clear-sighted view of important issues.

What's the Significance?

So what should we make of this? For one thing, we ought to give our ancestors the respect they deserve. After all, our prehistoric ancestors are the ones who did the heavy mental lifting for which we owe our expanded frontal cortexes. 

Oxford geneticist Bryan Sykes ecchoed this sentiment in a recent interview with Big Think:

I’m very proud of all of my ancestors that have got their DNA through to me, and I think everybody should be, particularly in America.  Because all of you have ancestors that took a lot of trouble to get here, whether it was across the frozen wastes of Siberia or more recently on ships from Europe or, unfortunately, ships from Africa against your ancestors’ will.  But everybody’s undergone an important and difficult journey to get here.

If we truly want to pay a debt of gratitude to our ancestors we need to not only reassess them, but also ourselves. The 21st century brain has its own set of challenges to figure out. While our ancestors needed to outsmart the competition that was stronger and faster, we need to catch up to our own runaway growth and devise plans for a sustainable future.  

So to brings things back around to Einstein, Crabtree asks, "How did we get from accurately throwing a spear to the theory of relativity?" Crabtree points to a paradox in the field of Artificial Intelligence:

AI promised household robots that would wash dishes, mow the lawn, and bring us freshly cooked croissants and coffee in the morning. Needless to say we do not have these robots now and none of the readers of this piece will probably ever see them, despite the immense financial impetus to build them. This is because common tasks are actually conceptually complex. However, AI is very good at things we superficially consider intellectual, such as playing chess, winning Jeopardy, flying a jet plane, or driving a car.

To understand this paradox, consider the game Foldit, in which players predict protein structures. Humans beat supercomputers at this game in much the same way that we can wash the dishes and put them away better than a robot. We win because Foldit uses spatial reasoning skills that were perfected and selected for in our hunter-gatherer ancestors.

Many kinds of modern refined intellectual activity (by which our children are judged) may not necessarily require more innovation, synthesis, or creativity than more ancient forms: inventing the bow-and-arrow, which seems to have occurred only once about 40 000 years ago, was probably as complex an intellectual task as inventing language. Selection could easily have operated on common (but computationally complex) tasks such as building a shelter, and then 
computationally simple tasks, such as playing chess, became possible as a collateral effect. Loss of any one of 2000-5000 genes prevents us from effectively doing everyday tasks, and selection for the ability to perform them would optimize the function of the entire group of genes. 

So who has the right brain for today? There isn't one. The good news is that we have intellectual diversity. We don't all need to be exceptionally skilled hunter-gatherers, and that is a good thing. We get Mozart. We get Einstein. We get all of the creators of an intellectually robust society that, as Crabtree admits, accelerates knowledge accumulation:

One does not need to imagine a day when we could no longer comprehend the problem, or counteract the slow decay in the genes underlying our intellectual fitness, or have visions of the world population docilely watching reruns on televisions they can no longer build. It is exceedingly unlikely that a few hundred years will make any difference for the rate of change that might be occurring. Remarkably, it seems that although our genomes are fragile, our society is robust almost entirely by virtue of education, which allows strengths to be rapidly distributed to all members. The sciences have come so far in the past 100 years that we can safely predict that the accelerating rate of knowledge accumulation within our intellectually robust society will lead to the solution of this potentially very difficult problem by socially and 
morally acceptable means.

Image courtesy of Shutterstock
Follow Daniel Honan on Twitter @Daniel Honan

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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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