New research targets sufferers of social anxiety disorder
A thorough understanding of personality traits could lead to targeted therapies.
- Sufferers of social anxiety have markedly different personality traits than others.
- By understanding these traits, researchers at Uppsala believe targeted therapies could evolve.
- Social anxiety affects 15 million American adults every year.
In his essay, "The problem of anxiety," Sigmund Freud wrote that anxiety is the "fundamental phenomenon and the central problem of neurosis." You will not find a final word on the subject in Freud's writing, however. His theories on anxiety evolved throughout his life. By the end of his illustrious and contentious career, he admitted that he would likely never completely define what anxiety entails.
That doesn't mean his contributions were for naught. No one contributed as much to our understanding of the unconscious drives that fuel our reality. Freud's ideas about sexuality are regularly debated—even he moved away from his earlier work—yet he knew what others, such as Kierkegaard and Rank, recognized: Anxiety is our natural state. To be conscious is to have anxiety. It's the cost of being able to foresee the future. How you deal with that anxiety in large part defines your personality.
Freud terms objective anxiety "anxious readiness." This function arms an individual so that they will not be surprised by sudden threats. Being overly prepared, however, leads to problems: your actions are paralyzed. This is the "freeze" function of our nervous system. This is also the basis of social anxiety: an inability to be in public, or, when you must go out, the sheer terror of being among others.
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New research from Uppsala University, published in the journal PLOS ONE, investigates the ramifications of social anxiety. The conclusion that lead author Tomas Furmark comes to: sufferers of social anxiety disorders exhibit different personality traits than others.
Personality is defined by the Big Five traits: openness to experience, conscientiousness, extroversion, agreeableness, and neuroticism. Each of these traits operate along a spectrum. Are you curious or cautious? Are you compassionate toward your partner or are you emotionally detached? Do you step into the center of a party or are you the perpetual wallflower that leaves out the back door?
Context matters. You might be extroverted in an environment in which you're comfortable, exuding a ton of confidence. Walk next door and suddenly you're reserved and nervous. Anxiety is tethered to environment and your personality isn't fixed. You can change your place on any of the spectrums, which is the goal of therapy.
For sufferers of social anxiety—15 million American adults every year—lateral movement is difficult. Just as depressed people often cannot envision the future, the socially anxious find it challenging to be in public. There's context here as well. The supermarket might be easy but that cocktail party is never going to happen. At the extreme end, social anxiety means only leaving your home for specific, targeted purposes, and even those trips make you anxious.
The team at Uppsala asked 265 volunteers with social anxiety to fill out comprehensive personality surveys. They identified three groups based on cluster analysis: prototypical social anxiety disorder (33 percent), whose members appear highly anxious and introverted; introvert-conscientious social anxiety disorder (29 percent), whose members are introverted but also have high levels of conscientiousness; and unstable-open social anxiety disorder (38 percent), with individuals scoring high on openness.
While the causes of each disorder differ, Fumark and his team identified specific personality traits that appear to be universal: high neuroticism and introversion, emotional instability, and a tendency to turn inward.
The researchers believe that defining these traits helps to expand our understanding of social anxiety disorders, which helps therapists target each subtype. As the team concludes,
"SAD personality subtypes may have different etiologies and it seems plausible that individuals exhibiting vastly different personality characteristics require different treatment strategies."
For example, cognitive behavioral therapy could be utilized with social approach focus to treat SAD sufferers with depression or low energy. Targeted approaches might work better for patients with certain types of traits as compared to others with different traits. As always, the team recommends further research, but this seems to be an important step in understanding the many shades of social anxiety.
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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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