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Why factory farms are a "perfect storm" for disease pandemics
We've known this virus was coming. We just didn't do anything about it.
- As far back as 2007, researchers warned about a novel coronavirus emerging from SARS.
- Long before that, experts knew that factory farms create the conditions for pandemics.
- Pandemics will be part of our lives as long as we continue our current methods of meat production.
In 2007, a team of researchers at The University of Hong Kong published a review warning of potential dangers of SARS-related coronaviruses emerging in the near future. Four years after the SARS outbreak of 2003 the team poured over a sampling of over 4,000 publications that had reported on the crisis. They wanted to understand the conditions that might lead to another outbreak. This paragraph is worth pointing out:
"Coronaviruses are well known to undergo genetic recombination, which may lead to new genotypes and outbreaks. The presence of a large reservoir of SARS-CoV-like viruses in horseshoe bats, together with the culture of eating exotic mammals in southern China, is a time bomb. The possibility of the re-emergence of SARS and other novel viruses from animals or laboratories and therefore the need for preparedness should not be ignored."
A common sentiment when disaster strikes: we had no idea it was coming. Often, we have plenty of warning. We just don't pay attention.
While the spotlighted origin of COVID-19 has been on a live animal market in Wuhan, perhaps we should be paying attention to a much larger issue, one that has been staring us in the face for decades: factory farms.
Honing in on China defeats the larger point. The influenza pandemic of 1918-19, which has gotten so much press of late, originated in Kansas, yet we don't hear other nations demanding retribution; the same goes for 2009's Swine Flu outbreak (thanks North Carolina!). Pandemics are linked not by geography, but by a singular human desire: our love for cheap meat.
The word "virus" comes from the Latin for "toxin," coined by Dutch botanist Martinus Beijernick while studying tobacco plants. He observed an agent even smaller than bacteria decimating the species. Blow up a virus to the size of a tennis ball and a human would have to be 500 miles tall. (A bacterium would be a beach ball.) Decades later, British biologist Peter Medawar called a virus "a piece of bad news wrapped up in a protein." They long predate and will long outlast us.
A virus isn't even alive. It is inert until it enters an animal, such as us. Viruses also aren't particularly picky: if they can affect a species, they will. If that means passing over into other species, great—survival of the fittest and all that. Humans have always been prey to viruses but pandemics are relatively new. They only began when the conditions were right, when tribes began merging into cities and animal domestication commenced. Crowded fields of animals commingling with large human populations is the original recipe for disaster.
Small farms are bad enough, but factory farms, in the words of Michael Greger, author of Bird Flu: A Virus of Our Own Hatching, are a "perfect storm environment." He continues:
"If you actually want to create global pandemics, then build factory farms."
Greger was cited by Paul Shapiro, author of Clean Meat, who we spoke with in 2017. Speculating on a future in which laboratory-grown meat is generated from pluripotent cells from animals, he said,
"We don't know what some unintended consequences might be but it's hard to imagine that there will be anything like the tremendous downsides to continuing to raise and slaughter tens of billions of animals for food globally."
Systems work until they don't. Right now, the very factory farms in question are experiencing an existential crisis. Thanks to COVID-19 their demand has increased, creating even more stressful working conditions than normal. Tragically, some manufacturers aren't offering sick pay, and as you might have guessed, employees are showing up to work ill. From New York City to Mississippi to South Dakota, workers are testing positive for the novel coronavirus. What happens to our meat supply when these farms can no longer supply the meat we demand? How do we battle an addiction when the dealers are sick?
Systems work until they don't, then they collapse. Not with a whimper but a bang.
Cows in a milking parlour on a large farm. The cows are milked by milking machine twice a day on April 24, 2019 in Verkhniy Ikorets, Russia.
Photo by Ute Grabowsky/Photothek via Getty Images
A few years ago, public health expert Larry Brilliant stopped by the Big Think office to discuss the most pressing issues facing humanity if a pandemic were to occur. He offered two: the diseases that ravage our biology, and more importantly, our preparation to combat those diseases. Brilliant was especially concerned in regards to the second.
"We have a White House which would almost reflexly discard anything that has the word 'public' in it, and one of those words is 'public health.' And they have not shown a keen interest in pandemics. The whole idea of 'America First,' which might be good for many things, is singularly not good for a global pandemic."
Brilliant says we've had 30 to 40 diseases, almost all of which are viruses, that jump from animals to humans at a rate of roughly one a year. The number is increasing—not catastrophically, he says, at least not yet. The reason for concern? Humans and animals living in such close proximity due to clear-cutting of forests and factory farms. This proximity is creating a "natural virus experiment."
How to stop this experiment? We have to curb our enthusiasm for meat. Eating less of it, sure, and being more discerning about where you source meat. Words like "natural" don't mean anything on a package; even "free range" is suspect. Knowing your farmer is important. Or, as Shapiro advocates, the emerging market of "clean meat," which is actual meat cultured in laboratories. A consumer-priced burger isn't there yet, but we're getting closer.
We can also add vegetarian and flexitarian arguments here. Yet I'm wary of recent vegan arguments that humans were not designed to eat meat. You can't rewrite history—humans are humans thanks in part to our consumption of meat, as thinkers such as Daniel Lieberman and Richard Wrangham have pointed out. We can—and should—argue about the future, but let us at least understand where we come from.
One thing is certain: stopping this virus experiment will require seriously rethinking the system that's creating it. At least the next time someone asks, "how could this have happened?," tell them we already know the answer. We've known it for generations. What we do about it moving forward is the story we've yet to write.
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Geologists discover a rhythm to major geologic events.
- It appears that Earth has a geologic "pulse," with clusters of major events occurring every 27.5 million years.
- Working with the most accurate dating methods available, the authors of the study constructed a new history of the last 260 million years.
- Exactly why these cycles occur remains unknown, but there are some interesting theories.
Our hearts beat at a resting rate of 60 to 100 beats per minute. Lots of other things pulse, too. The colors we see and the pitches we hear, for example, are due to the different wave frequencies ("pulses") of light and sound waves.
Now, a study in the journal Geoscience Frontiers finds that Earth itself has a pulse, with one "beat" every 27.5 million years. That's the rate at which major geological events have been occurring as far back as geologists can tell.
A planetary calendar has 10 dates in red
Credit: Jagoush / Adobe Stock
According to lead author and geologist Michael Rampino of New York University's Department of Biology, "Many geologists believe that geological events are random over time. But our study provides statistical evidence for a common cycle, suggesting that these geologic events are correlated and not random."
The new study is not the first time that there's been a suggestion of a planetary geologic cycle, but it's only with recent refinements in radioisotopic dating techniques that there's evidence supporting the theory. The authors of the study collected the latest, best dating for 89 known geologic events over the last 260 million years:
- 29 sea level fluctuations
- 12 marine extinctions
- 9 land-based extinctions
- 10 periods of low ocean oxygenation
- 13 gigantic flood basalt volcanic eruptions
- 8 changes in the rate of seafloor spread
- 8 times there were global pulsations in interplate magmatism
The dates provided the scientists a new timetable of Earth's geologic history.
Tick, tick, boom
Credit: New York University
Putting all the events together, the scientists performed a series of statistical analyses that revealed that events tend to cluster around 10 different dates, with peak activity occurring every 27.5 million years. Between the ten busy periods, the number of events dropped sharply, approaching zero.
Perhaps the most fascinating question that remains unanswered for now is exactly why this is happening. The authors of the study suggest two possibilities:
"The correlations and cyclicity seen in the geologic episodes may be entirely a function of global internal Earth dynamics affecting global tectonics and climate, but similar cycles in the Earth's orbit in the Solar System and in the Galaxy might be pacing these events. Whatever the origins of these cyclical episodes, their occurrences support the case for a largely periodic, coordinated, and intermittently catastrophic geologic record, which is quite different from the views held by most geologists."
Assuming the researchers' calculations are at least roughly correct — the authors note that different statistical formulas may result in further refinement of their conclusions — there's no need to worry that we're about to be thumped by another planetary heartbeat. The last occurred some seven million years ago, meaning the next won't happen for about another 20 million years.
Brain cells snap strands of DNA in many more places and cell types than researchers previously thought.
The urgency to remember a dangerous experience requires the brain to make a series of potentially dangerous moves: Neurons and other brain cells snap open their DNA in numerous locations — more than previously realized, according to a new study — to provide quick access to genetic instructions for the mechanisms of memory storage.
The extent of these DNA double-strand breaks (DSBs) in multiple key brain regions is surprising and concerning, says study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute for Learning and Memory, because while the breaks are routinely repaired, that process may become more flawed and fragile with age. Tsai's lab has shown that lingering DSBs are associated with neurodegeneration and cognitive decline and that repair mechanisms can falter.
"We wanted to understand exactly how widespread and extensive this natural activity is in the brain upon memory formation because that can give us insight into how genomic instability could undermine brain health down the road," says Tsai, who is also a professor in the Department of Brain and Cognitive Sciences and a leader of MIT's Aging Brain Initiative. "Clearly, memory formation is an urgent priority for healthy brain function, but these new results showing that several types of brain cells break their DNA in so many places to quickly express genes is still striking."
In 2015, Tsai's lab provided the first demonstration that neuronal activity caused DSBs and that they induced rapid gene expression. But those findings, mostly made in lab preparations of neurons, did not capture the full extent of the activity in the context of memory formation in a behaving animal, and did not investigate what happened in cells other than neurons.
In the new study published July 1 in PLOS ONE, lead author and former graduate student Ryan Stott and co-author and former research technician Oleg Kritsky sought to investigate the full landscape of DSB activity in learning and memory. To do so, they gave mice little electrical zaps to the feet when they entered a box, to condition a fear memory of that context. They then used several methods to assess DSBs and gene expression in the brains of the mice over the next half-hour, particularly among a variety of cell types in the prefrontal cortex and hippocampus, two regions essential for the formation and storage of conditioned fear memories. They also made measurements in the brains of mice that did not experience the foot shock to establish a baseline of activity for comparison.
The creation of a fear memory doubled the number of DSBs among neurons in the hippocampus and the prefrontal cortex, affecting more than 300 genes in each region. Among 206 affected genes common to both regions, the researchers then looked at what those genes do. Many were associated with the function of the connections neurons make with each other, called synapses. This makes sense because learning arises when neurons change their connections (a phenomenon called "synaptic plasticity") and memories are formed when groups of neurons connect together into ensembles called engrams.
"Many genes essential for neuronal function and memory formation, and significantly more of them than expected based on previous observations in cultured neurons … are potentially hotspots of DSB formation," the authors wrote in the study.
In another analysis, the researchers confirmed through measurements of RNA that the increase in DSBs indeed correlated closely with increased transcription and expression of affected genes, including ones affecting synapse function, as quickly as 10-30 minutes after the foot shock exposure.
"Overall, we find transcriptional changes are more strongly associated with [DSBs] in the brain than anticipated," they wrote. "Previously we observed 20 gene-associated [DSB] loci following stimulation of cultured neurons, while in the hippocampus and prefrontal cortex we see more than 100-150 gene associated [DSB] loci that are transcriptionally induced."
Snapping with stress
In the analysis of gene expression, the neuroscientists looked at not only neurons but also non-neuronal brain cells, or glia, and found that they also showed changes in expression of hundreds of genes after fear conditioning. Glia called astrocytes are known to be involved in fear learning, for instance, and they showed significant DSB and gene expression changes after fear conditioning.
Among the most important functions of genes associated with fear conditioning-related DSBs in glia was the response to hormones. The researchers therefore looked to see which hormones might be particularly involved and discovered that it was glutocortocoids, which are secreted in response to stress. Sure enough, the study data showed that in glia, many of the DSBs that occurred following fear conditioning occurred at genomic sites related to glutocortocoid receptors. Further tests revealed that directly stimulating those hormone receptors could trigger the same DSBs that fear conditioning did and that blocking the receptors could prevent transcription of key genes after fear conditioning.
Tsai says the finding that glia are so deeply involved in establishing memories from fear conditioning is an important surprise of the new study.
"The ability of glia to mount a robust transcriptional response to glutocorticoids suggest that glia may have a much larger role to play in the response to stress and its impact on the brain during learning than previously appreciated," she and her co-authors wrote.
Damage and danger?
More research will have to be done to prove that the DSBs required for forming and storing fear memories are a threat to later brain health, but the new study only adds to evidence that it may be the case, the authors say.
"Overall we have identified sites of DSBs at genes important for neuronal and glial functions, suggesting that impaired DNA repair of these recurrent DNA breaks which are generated as part of brain activity could result in genomic instability that contribute to aging and disease in the brain," they wrote.
The National Institutes of Health, The Glenn Foundation for Medical Research, and the JPB Foundation provided funding for the research.
Research shows that those who spend more time speaking tend to emerge as the leaders of groups, regardless of their intelligence.
- A new study proposes the "babble hypothesis" of becoming a group leader.
- Researchers show that intelligence is not the most important factor in leadership.
- Those who talk the most tend to emerge as group leaders.
If you want to become a leader, start yammering. It doesn't even necessarily matter what you say. New research shows that groups without a leader can find one if somebody starts talking a lot.
This phenomenon, described by the "babble hypothesis" of leadership, depends neither on group member intelligence nor personality. Leaders emerge based on the quantity of speaking, not quality.
Researcher Neil G. MacLaren, lead author of the study published in The Leadership Quarterly, believes his team's work may improve how groups are organized and how individuals within them are trained and evaluated.
"It turns out that early attempts to assess leadership quality were found to be highly confounded with a simple quantity: the amount of time that group members spoke during a discussion," shared MacLaren, who is a research fellow at Binghamton University.
While we tend to think of leaders as people who share important ideas, leadership may boil down to whoever "babbles" the most. Understanding the connection between how much people speak and how they become perceived as leaders is key to growing our knowledge of group dynamics.
The power of babble
The research involved 256 college students, divided into 33 groups of four to ten people each. They were asked to collaborate on either a military computer simulation game (BCT Commander) or a business-oriented game (CleanStart). The players had ten minutes to plan how they would carry out a task and 60 minutes to accomplish it as a group. One person in the group was randomly designated as the "operator," whose job was to control the user interface of the game.
To determine who became the leader of each group, the researchers asked the participants both before and after the game to nominate one to five people for this distinction. The scientists found that those who talked more were also more likely to be nominated. This remained true after controlling for a number of variables, such as previous knowledge of the game, various personality traits, or intelligence.
How leaders influence people to believe | Michael Dowling | Big Think www.youtube.com
In an interview with PsyPost, MacLaren shared that "the evidence does seem consistent that people who speak more are more likely to be viewed as leaders."
Another find was that gender bias seemed to have a strong effect on who was considered a leader. "In our data, men receive on average an extra vote just for being a man," explained MacLaren. "The effect is more extreme for the individual with the most votes."
The great theoretical physicist Steven Weinberg passed away on July 23. This is our tribute.