Dealing with loneliness during the pandemic
Sheltering at home is anti-instinctual behavior. Yet doing so saves lives.
- Mental health disorders are on the rise during the COVID-19 pandemic.
- Lack of social contact is anti-instinctual behavior for humans, yet it is needed during this particular crisis.
- How we cope with social distancing and sheltering at home will in large part dictate how long this crisis lasts.
There have been many comparisons between the COVID-19 pandemic and previous historical incidents. Obviously, the last great flu pandemic of 1918-19 has been receiving a lot of attention. There's also quantitative comparisons. Pundits compare this pandemic death toll to wars and terrorist attacks. This week, America surpassed the death toll in Vietnam. In previous weeks, rates were compares to the War in Afghanistan and 9/11.
Comparing a virus to a war isn't fair, though the headlines can be forgiven. We're trying to wrap our heads around the enormity of tragedy. One feature of consciousness is qualia, instances of subjective experience. In order to understand something—say, a glass of wine—we relate to it by stating "this is like this." This Bordeaux smells like peppercorn and chocolate. Comparison gives us a point of reference in an effort to understand concepts. We do it with everything.
While death tolls are one thing, conditions on the ground are entirely different. Consider 9/11. During the months following that day, New Yorkers were more likely to say hello to random passerby on the street. There was an uptick in kindness and charity. People were present for one another on an unprecedented scale. There was a real feeling of "we're in this together."
Feeling like you're a part of something requires presence, which is exactly what's lacking as we shelter at home. Even on 9/11, as I walked from downtown Manhattan to my girlfriend's apartment in the Upper East Side—I lived in Jersey City and had no way of returning home—I would stop to talk to people on the street. We were able to look one another in the eyes. Life was briefly upended, sure, but we could still physically be there for one another. We could even touch each other.
Why loneliness is a danger to individuals and societies | Andrew Horn
Lack of contact is driving loneliness during this pandemic. Health care workers are experiencing an increase in mental health conditions. Being on the front lines is emotionally taxing. But those forced to shelter at home, especially when living alone, are also facing increased anxiety and depression.
An avoidance of social contact is an evolutionary mismatch, argue three researchers in a recent essay published in the journal, Current Biology. Evolutionary biology dictates that we come together during times of crisis. We're social animals. The inability to make contact is frustrating and leads to trauma as self-isolation persists.
The authors (Guillaume Dezecache, Chris Frith, and Ophelia Deroy) write that the media is driving narratives counter to natural behavior. During tragedies, we tend to want to help others more than take care of ourselves. Empathy is our biological inheritance. The media, they write, has adopted a Hobbesian view of the world: every man for himself.
The focus on irrational hoarding of supplies is one example. While running from a fire is a natural reaction to danger, they note that our intuitive responses are cooperation, not selfishness. News outlets perpetuate problems by homing in on aberrant behavior. In fact, they drive the problem. We believe supplies are running short, creating this Hobbesian mentality: I must hoard as well.
This mindset seems worse in cities. As they write,
"In all likelihood, the mismatch between our misperception of the severity of the threat and its consequences is likely to become even more destructive in dense urban areas in which social isolation is a costly good."
A man rests on an empty Staten Island Ferry on March 24, 2020 in New York City.
Photo by Spencer Platt/Getty Images
Then there's the flip side: refusing to social distance or shelter at home. Because the threat is invisible we tend to downplay the risks. This is in stark contrast to 9/11, in which more fearful minds associated any Muslim with terrorism. Fortunately, this trend was relatively rare in New York City, though anti-Islam sentiments exploded across the nation, usually in regions with less diverse cultures.
Sine we cannot see this virus, and therefore don't necessarily understand how it's transmitted or concern ourselves much if we're not in a high-risk group, we don't take precautions. The short-term benefit of contact might, however, fuel the long-term detriment of increased hospitalization and death.
Nonchalance isn't the only reason for such behavior. It might be something much more ingrained in us.
"It is because our infection-avoidance mechanisms are overwhelmed by a much stronger drive to affiliate and seek close contact."
As the authors conclude, the more we can stave off loneliness for the greater good of society—at-risk populations, such as the elderly and immunodeficient; health care workers; supply chains providing hospitals with necessary resources; workers contracted to produce those supplies—dictates how we emerge on the other side of this pandemic.
Sadly, there is no easy response. Collectively we're facing a range of terrible outcomes. The best we can do is strive for the least tragic result. We passed 60,000 deaths in America today. How high that number climbs is in large part in our hands, yet keeping it low requires anti-instinctual behavior. That conundrum is shaping what our society will look like in the future.
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New research establishes an unexpected connection.
- A study provides further confirmation that a prolonged lack of sleep can result in early mortality.
- Surprisingly, the direct cause seems to be a buildup of Reactive Oxygen Species in the gut produced by sleeplessness.
- When the buildup is neutralized, a normal lifespan is restored.
We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?
A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.
The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.
An unexpected culprit
The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.
What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.
"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.
"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)
Image source: Tomasz Klejdysz/Shutterstock/Big Think
The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.
You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.
For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.
Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.
The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.
However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."
The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.
As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.
The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."
The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.
"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.
Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."
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