COVID-19 could lead to an epidemic of clinical depression
The health care system isn't ready for that, either.
Isolation, social distancing and extreme changes in daily life are hard now, but the United States also needs to be prepared for what may be an epidemic of clinical depression because of COVID-19.
We are clinical psychological scientists at the University of Washington's Center for the Science of Social Connection. We study human relationships, how to improve them, and how to help people with clinical depression, emphasizing evidence-based approaches for those who lack resources.
We do not wish to be the bearers of bad news. But this crisis, and our response to it, will have psychological consequences. Individuals, families and communities need to do what they can to prepare for a depression epidemic. Policymakers need to consider – and fund – a large-scale response to this coming crisis.
A perfect storm of depression risks
Most of us know the emotional components of depression: sadness, irritability, emptiness and exhaustion. Given certain conditions, these universal experiences take over the body and transform it, sapping motivation and disrupting sleep, appetite and attention. Depression lays waste to our capacity to problem-solve, set and achieve goals and function effectively.
The general public understands depression as a brain disease. Our genes do influence how easily we may fall into clinical depression, but depression is also, for most of us, substantially influenced by environmental stress. The unique environmental stressors of the COVID-19 crisis suggest that an unusually large proportion of the population may develop depression. This pain is likely to be distributed inequitably.
Health care workers, first responders, and others on the front lines are at risk for depression from COVID-19.
Anthony Kwan/Getty Images
Stress and loss
Exacerbating the widespread stress of this crisis, many of us are suffering significant personal losses and grief reactions, which are robust predictors of depression. The ongoing and unpredictable course of these stressors adds an additional layer of risk.
As this crisis unfolds, death tolls will rise. For some, especially those on the front lines, acute experiences of grief, trauma and exhaustion will compound the stress and place them at even greater risk.
Prolonged social isolation - our primary strategy to reduce the spread of the virus - adds another layer of risk. Our bodies are not designed to handle social deprivation for long. Past studies suggest that people forced to "shelter in place" will experience more depression. Those living alone and lacking social opportunities are at risk. Loneliness breeds depression.
Families, who must navigate unusual amounts of time together in confined spaces, may experience more conflict, also increasing risk. China experienced an increase in divorce following their COVID-19 quarantine. Divorce predicts depression, especially for women, largely due to increased economic hardship over time.
The biggest stressor for many is financial. Unemployment and economic losses will be severe. Research on past recessions suggests that rising unemployment and financial insecurity lead to increased rates of depression and suicide. Home foreclosures during the 2008 recession produced a 62% increased risk of depression among those foreclosed.
The mental health burden of economic recession will be distributed inequitably. When the stock market crashed in 2008, the rich experienced large wealth losses but not increased rates of depression. In contrast, those who experience unemployment, debt and financial deprivation during recessions are at significant risk for depression due to increased stress and difficult life circumstances. Minority-owned businesses may be at particular risk for buckling under the strain.
Recovery will be harder
While the COVID-19 crisis increases risk for depression, depression will make recovery from the crisis harder across a spectrum of needs.
Given depression's impact on motivation and problem-solving, when our economy recovers, those who are depressed will have a harder time engaging in new goal pursuits and finding work. When the period of mandated social isolation ends, those who are depressed will have a harder time re-engaging in meaningful social activity and exercising.
When the threat of coronavirus infection recedes, those who are depressed will face increased immunological dysfunction, making it more likely they will suffer other infections. Depression amplifies symptoms of chronic illness. The inequitable distribution of the burden of the crisis will exacerbate existing racial health disparities, including disparities in access to depression treatment.
What to do?
Self-help suggestions are readily available. A good list, more evidence-based than most, is here. It is our experience, however, that such self-help encouragements for depression are not enough, and at times even insulting, for those who are truly struggling.
We need higher-level shifts in policy and how we approach the problem. Economic relief measures from the federal government are crucial responses both to economic recession and psychological depression. We call for a public health campaign to increase awareness of depression and treatment options, and for improvements in mental health sick-leave policies and insurance reimbursement to minimize barriers to treatment access.
How we talk about depression must change. The distress we feel is a normal human response to a severe crisis. Acknowledging and accepting these feelings prevents distress from turning into disorder. Describing depression solely as a brain disease increases helplessness and substance use among those who are depressed and decreases help-seeking. Emphasizing the causal role of our environmental context, in contrast, matches how depressed individuals across different ethnicities view the causes of their suffering, decreases stigma and increases help-seeking.
Finally, we recommend specific treatment options be prioritized. As we have discussed elsewhere, easy-to-train, cross-culturally applicable and effective treatment options exist. We wish for an army of practitioners to be trained and embedded in community and treatment centers across the country, and this army should represent the great diversity of our country.
Depression costs the U.S. economy US$210 billion yearly. That is under normal conditions. An epidemic of depression requires a multi-faceted, multi-level response.
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Researchers in Mexico discover the longest underwater cave system in the world that's full of invaluable artifacts.
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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