Notice: Trying to access array offset on value of type bool in /home/748059.cloudwaysapps.com/znxvfcncpw/public_html/wp-content/themes/sahaja/pages/internal-page.php on line 19
Causes of Anxiety
What Causes Anxiety?
There is no single cause of anxiety disorders.
Genes, environmental influences, personality, and life experiences all play a role in the development of an anxiety disorder.
Certainly, chronic or long-term exposure to major stressors such as abuse, violence, or poverty increases the risk for anxiety. And certain genetic factors, perhaps activated by stressful life experiences, as well as personality traits (e.g., neuroticism), can predispose some of us to anxiety. For example, people who have low self-esteem, poor coping skills and a tendency toward neurosis or harm avoidance are more prone to anxiety. Conversely, an anxiety disorder that began in childhood could itself damage self-esteem and impair emotional resilience.
Let’s take a look at some patterns commonly shared by people with anxiety disorders…
Anxiety as a Personality Trait
Personality is an important aspect of who we are and how we perceive the world. It results from complex interactions between genes and our environment. Our “personhood” is the aggregate of our personality traits. Personality traits, the building blocks of human personality, have varying degrees of influence on our lives, but our lives tend to organize around a handful of traits.
For people suffering from anxiety disorders, neuroticism or harm avoidance is generally a dominant trait.
Many personality models have developed over the years. Two enduring models are those developed by psychologists Gordon Allport and Hans Eysenck. Gordon Allport proposed that there were only five basic characteristics underlying all the 18,000+ adjectives in the dictionary that we use to describe ourselves and that all our traits and behaviors could be organized into five categories, which became known as the “Big Five” dimensions of human personality (acronym OCEAN):
- Openness to experiences. Creative, intellectual, open-minded (vs. shallow, simple, unimaginative, less intelligent)
- Conscientiousness. Responsible, cautious, organized (vs. irresponsible, careless, frivolous)
- Extroversion. Assertive, outgoing, energetic (vs. quiet, reserved, shy)
- Agreeableness. Sympathetic, kind, affectionate (vs. cold, argumentative, cruel)
- Neuroticism. Anxious, unstable, moody (vs. emotionally stable, calm, content)
Hans Eysenck proposed that human personality traits fall into one of three primary dimensions of personality (known as the PEN model): Psychoticism, Extroversion, Neuroticism:
- Psychoticism. Risk-taking, impulsivity, irresponsibility, manipulativeness, sensation-seeking, tough-mindedness, practicality
- Extroversion. Energy, sociability, expressiveness, assertiveness, ambition, dogmatism, aggressiveness
- Neuroticism. Inferiority, unhappiness, anxiety, depression, dependence, irrationality, tenseness, hypochondria, guilt, regret, low self-esteem, obsessiveness, controlled, lack of emotional confidence
Traits like emotional stability and conscientiousness are thought to be directly related to physical and emotional well-being and longevity; in other words, good mental and physical health is linked to changes in these traits over time.
Sometimes there’s a fine line between trait behaviors and the way we process and interpret events is what tips the balance between emotionally healthy and unhealthy.
For example, while the traits of neuroticism and conscientiousness may seem very different, they actually share a common anxious concern for the outcome of a situation — both personality types exhibit a high level of attention to emotional details and some degree of anxiety about negative consequences. But the difference is that those with a high level of neuroticism seem to be attracted to negative emotions while highly conscientiousness people generally avoid it (McCrae, 2003). It’s possible — and normal — to feel anxious concern without experiencing extreme negative emotions, such as fear and dread.
Some of us are more likely than others to be exposed to stressful life experiences, including traumas like car accidents, or being the victim of a crime. Some of this variation is actually traceable to genetics — heritability. Heritability is the amount of the variation within a population that can be explained by genetic differences between individuals. Many studies have shown that around one-fourth of the variation in our life experiences — from having controlling parents to relationship problems — can actually be traced to genetic origins. Three global personality traits — extroversion, neuroticism and openness to experience — have been found to help account for the heritability of life events (Saudino, et al, 1997; Magnus, 1993).
People who are extroverted and open to new experiences are more likely to experience positive and manageable life events; whereas, people with neurotic traits are more likely to experience negative life events.
A child’s personality can indicate future risk for developing an anxiety disorder. For example, extremely shy children and those who are targeted by bullies are at higher risk for developing anxiety disorders later in life. Children who can’t tolerate uncertainty tend to become “worriers,” which is a major predictor of generalized anxiety later in life.
State anxiety and trait anxiety are interrelated but different. During state anxiety, we experience an unpleasant emotional response while cognitively appraising (anticipating) and coping with threatening or dangerous situations. Trait anxiety, on the other hand, is a consistent, relatively stable tendency to respond with an increase in state anxiety when anticipating a range of situations (Spielberger, 1999). It’s a general predisposition to experience transient states of anxiety, but it is at least temporarily stable.
Some psychologists view the difference between trait and state anxiety as being similar to the difference between potential energy and kinetic energy (Tovilović, et al, 2009). High trait-anxiety individuals may experience more frequent and more intensive anxiety than low trait-anxiety individuals, but they’re not anxious all the time — they’re just potentially anxious all the time. On the other hand, people who don’t have a high tendency towards anxious responding can still experience short-lived states of state anxiety. For example, all of us, including low trait-anxiety individuals, will experience state anxiety if a situation is perceived as sufficiently threatening.
Does trait anxiety doom us to constant anxiety? No. The effects of traits on our behavior are always mediated by our current state. In the end, states have a more direct influence over our internal mental processing and resulting behavior than do traits.
Thus, any strategy or treatment (e.g., meditation) that significantly influences our state, ultimately helps control or moderate our traits.
The Neurocircuitry of Fear
How does the brain creates fear and anxiety? The neurocircuitry of fear revolves largely around the amygdala, the hippocampus and noradrenergic (noradrenaline) activity.
The amygdala and the hippocampus are a pair of small brain structures in the limbic (emotional) system that work in tandem to generate emotions, attach emotions to memories, and store and index those memories. The almond-shaped amygdala is the brain’s emotion factory, Alert Central, the “gut feeling” center. It alerts you to threats in your environment, directs your evaluation of those events, tells us what we should worry about, and signals the hippocampus to store and map your feelings to memories of the events. The amygdala’s next-door neighbor, the seahorse-shaped hippocampus, encodes events (including threatening ones) into memories and indexes them, much like a directory on a hard drive.
Some neuroscientists believe that emotional memories may actually be stored in the central amygdala, playing a role in anxiety disorders that involve being haunted by trauma memories (e.g., PTSD) or phobias, such as a fear of snakes, spiders, or flying. Others believe that the amygdala doesn’t have its own discrete storage system for emotionally-charged memories; rather it may somehow mark or underline memories created by other brain systems as Emotionally Significant (McGaugh, J., 2001)
The “worrier” trait sometimes found even in children might be a genetic trait, or it could result from a hypersensitive amygdala. People with high levels of trait neuroticism have been found to have hyperactive amygdalas (Perlman, 2009). Richard J. Davidson and colleagues, for example, who frequently study the mental health benefits of mindfulness meditation, also found that high levels of amygdala activation are associated with increased anxiety symptoms and negative affect (Davidson, et al, 2002).
Trait neuroticism has also been linked to increased gray matter concentration in the right amygdala (Omura, 2005). Trait neuroticism may determine not only how we interpret what we see, but which information we pay attention to, what stands out, or whether an environmental stimulus even seems emotionally significant to us in the first place. Neuroticism has been associated with triggering amygdala hyperreactivity in response to fearful facial expressions (Hariri, 2002). Other studies have shown that people with a higher level of trait neuroticism pay more attention to features of the fearful face (the eyes) and are much more likely to interpret emotional images as signaling an immediate threat, compared to those low in trait neuroticism (Perlman, et al, 2009).
To learn how meditation can help relieve state anxiety and improve anxious traits, see How Sahaja Meditation Helps Relieve Anxiety.
Chronic anxiety, especially if accompanied by repeated stressors or traumatic events, can produce marked changes in these brain structures that are heavily involved in regulating our emotional stability. For example, studies have found that some people who were victims of child abuse or who served in military combat have smaller hippocampi (Bremner, 1995; Stein, 1997). And extended release of stress hormones, such as glucocorticoids, actually cause nerve cells in the hippocampus to atrophy. During a traumatic event, for example, a person’s stress response weakens hippocampal functioning so that the memory never forms, even though the amygdala still managed to capture the essence of the traumatic event. The result is an incomplete emotional memory — a “flashbulb memory” — which may help explain why the explicit details of a traumatic memory may disappear from consciousness, while persisting in our gut reactions, general anxiety response, or even phobias. The good news is that nerve cell atrophy in the hippocampus is reversible, if the stress ends.
Through its connections to the hypothalamus, the amygdala gears your body for action by stimulating stress hormones that produce the physiological responses associated with the fear emotions and prep you to fight or flee. Anxiety can be caused and/or worsened by fluctuations in the levels of brain chemicals (neurotransmitters and neurohormones) such as, serotonin, dopamine, norepinephrine, epinephrine, GABA (Gamma-aminobutyric acid), and the stress hormone cortisol. (Serotonin, GABA and dopamine are neurotransmitters. Norepinephrine and epinephrine are both stress hormones and neurotransmitters.)
Norepinephrine (noradrenaline) is sometimes referred to as “the neurotransmitter of fear,” and as such, plays a central role in anxiety.
Norepinephrine is involved in tripping the fight-or-flight mechanism discussed in Overview and Characteristics of Anxiety Disorders. Surging norepinephrine causes the heart rate to increase, stored glucose (simple sugar) to be released, and increases blood flow to the muscles – all conditions that prepare us to respond to imminent danger. Norepinephrine plays a major role in helping us escape danger, but also in creating or exacerbating anxiety.
These physiological responses (increased heart rate, etc.) increase activity in brain areas that secrete norepinephrine. Increased norepinephrine ultimately increases stimulation of the hypothalamus, which, in turn, increases the stress-related production of stress hormones like cortisol and ACTH (adrenocorticotropic hormone). When the sympathetic nervous system is revved up, the hypothalamus stimulates the adrenal medulla to increase adrenaline (epinephine) output, which increases anxiety symptoms and prevents the hypothalamus from creating a balanced, peaceful state of mind.
In other words, norepinephrine and epinephrine both stimulate the sympathetic nervous system and their secretion is, in turn, stimulated by sympathetic nervous system responses. It can be a vicious cycle that helps perpetuate the anxiety response and may help explain why anxiety seems to literally feed on itself.
Prolonged oversecretion of norepinephrine can cause physiological symptoms that sometimes accompany anxiety disorders, such as muscle tension, which can, in turn, lead to chronic pain syndromes (e.g., back pain) and effects similar to those of the stress hormone cortisol. Increased heart rate can cause high blood pressure and the stored glucose (simple sugar) that’s released can lead to diabetes. Over the long-term, prolonged high levels of cortisol in the bloodstream damages the body all the way down to the cellular level and accelerates aging. Long-term effects can include: decreased bone density, elevated blood pressure, suppressed thyroid function, blood sugar imbalances, decrease in muscle tissue, decreased immunity and increased inflammatory response.
GABA is a ubiquitous neurotransmitter that’s involved in most of the inhibitory chemical actions all over the brain. GABA’s role is to keep other neurotransmitters such as serotonin, epinephrine, norepinephrine and dopamine in check. In fact, the anxiolytic class of benzodiazepine medications work by targeting GABA-A receptors, potentiating transmission of GABA throughout the brain and decreasing the turnover of these key neurotransmitters in limbic areas such as the amygdala.
Working in tandem with serotonin, GABA acts as the inhibitory neurotransmitter to quiet the stress response when a person thinks about stressful events.
Imprinting of emotionally traumatic memories is thought to be mediated, in part, by norepinephrine’s action in the amygdala. The development of conditioned fear, however, is mediated by dopamine-1 receptors in the amygdala, which forge declarative memory associations in conjunction with the hippocampus (Ninan, 1999).
Negative affect symptoms, such as fear, anxiety and irritability, are thought to result from serotonin dysregulation (Nutt, D., et al, 2006) and are particularly prominent in people with both anxiety and depression.
Researchers have also identified a small brain protein, Neuropeptide S, that can switch off the negative feelings associated with trauma memories. Neuropeptide S extinguishes trauma responses by acting on a tiny group of neurons in the amygdala, which stores trauma memories. Activating these receptors in mice has been found to make traumatic responses disappear faster, which is good news for people who are haunted by persistent fears, such as those commonly associated with Posttraumatic Stress Disorder.
Enzymes may play a role.
Much of the genetic research related to mental health focuses on linking psychological disorders to gene variants that control neurotransmitters. But in 2005, scientists at the Salk Institute studying the link between stress and 17 “anxiety genes,” uncovered the role of enzymes in causing anxiety disorders. They found increased activity or overexpression of two enzymes in anxious mice that are shared by humans — glyoxalase 1 and glutathione reductase — that are involved in oxidative stress metabolism. Oxidative stress involves the release of free radicals that cause cell degeneration.
They found that increased activity of these two enzymes turns normally relaxed mice into “Nervous Nellies” and makes already-jittery mice even more anxious. As with some humans suffering from an anxiety disorder, the sights and sounds of unfamiliar environments triggered panic in mice with anxious dispositions, causing them to freeze, a typical fight-or-flight response. Unlike their calmer counterparts, the naturally nervous mice would not explore and were wary of open spaces, much like human agoraphobics. Surprisingly, these enzymes, rather than neurohormones such as norepinephrine, were causing the high anxiety levels in almost half of the anxious mice.
Traumatic Events and Conditioned Fear
Clinical anxiety can be triggered by one or more severe psychosocial stressors.
Psychosocial stressors are stress-triggering events that can impact our social and psychological behavior, such as loss, relationship problems and any other stressor or life change that we find challenging to cope with.
Traumatic events can trigger anxiety disorders, especially in individuals who are more susceptible to experiencing anxiety due to psychological, genetic, or biochemical factors. Posttraumatic Stress Disorder and Acute Stress Disorder are the obvious examples of how this mechanism may manifest. But specific traumatic events in childhood, particularly those that threaten family integrity, such as spousal or child abuse, can also lead to other anxiety and emotional disorders. Some types of specific phobias, for instance of spiders or snakes, may be triggered and perpetuated after a single traumatic exposure.
Freezing is a common initial fight-or-flight response. We don’t necessarily fight or flee immediately, even if instinct tells us we should. We may simply freeze, just like lab rats. You can place a rat in a cage, play a sound, and simultaneously deliver a shock to the rat. The rat displays a fear reaction: it freezes in place. After a few rounds of sound + shock, the rat starts to fear the sound, even when it’s not accompanied by the shock. This fear response is called a conditioned response. Innately, the rat had an unconditioned innate fear of shocks, but it can be conditioned to be afraid of sounds, too, once it learns to associate the sound with the shock. And it learns to be afraid very quickly. So do humans.
Conditioned fear may increase our survival odds, but it can also cause us to needlessly associate harmless stimuli with danger and respond anxiously; for example, a combat veteran may duck and take cover when he hears a car backfiring in the distance because the sound triggers flashbacks of enemy gunfire or explosions.
Fear distorts our perception of reality and plays tricks on memory. The fear systems in the brain have their own perceptual channels and their own dedicated circuitry for storing traumatic memories. We have systems devoted to explicit or declarative memories (e.g., events) and systems devoted to procedural memories (e.g., learned processes), like how to play a piano or ride a bicycle. And then there are our emotional memories. A particular stressor or stimulus can even trigger multiple memories. For example, if you spot a snake in the grass, fear conditioning might kick in and trigger almost simultaneously both a declarative memory or memories (images of past snakes you’ve seen, where you were when you saw them) and an emotional memory (e.g., a fear memory of almost being bitten).
The declarative memory of past snake encounters is encoded and managed by the hippocampus, which, you’ll recall, indexes memories. The emotional memory of a threat from an actual coiled rattlesnake, on the other hand, is mediated by the amygdala itself. A trace of that memory was stored by the amygdala for speedy retrieval, as well as for the long term in the hippocampus.
Memories forged under strong emotions are difficult to erase, which is one reason why anxiety can be so persistent. It’s as if the brain is preprogrammed to prevent the overriding of fear responses. We have many neural pathways running from the primitive amygdala to the more evolved and more rational neocortex, but far fewer running from the neocortex to the amygdala, which might have allowed the neocortex to tell the amygdala: “Calm down, relax. You’re not in danger.” Over time, the brain of the anxious person is conditioned — literally programmed — to allow the fear response system to take control at the slightest sign of threat, which prevents conscious awareness — and rational judgment — from ruling.
Genetic Links and Family Dynamics
Anxiety disorders do tend to run in families, but characteristics caused by nature and nurture can sometimes look a lot alike.
Genetic factors can certainly play a role in causing anxiety, but family dynamics and psychological influences are often at work, as well.
For example, parents often project their own fears onto their children. While these children may have inherited some neurotic traits, they can also “learn” fears, obsessions and phobias just by observing a parent’s phobic, obsessive or fearful reactions to events repeatedly over time, which can condition them to respond to stressful stimuli like their parents do.
There’s no single “fear” gene that causes anxiety to spiral out of control. Like other complex psychological traits, fear and anxiety are influenced by the interaction of many genes. Following are some genes that have been implicated in anxiety disorders:
- The short variant of the serotonin transporter allele (5-HTTLPR) of the famous “depression gene,” 5-HT T, has also been linked to state anxiety and the personality trait of neuroticism. It has even been jokingly referred to as “the Woody Allen gene” for its links to evoke hand-wringing anxiety, instability, moodiness and negative thinking. 5-HTTLPR is associated with lower serotonergic production and reuptake (Lesch et al, 1996; Sen et al, 2004; Garpenstrand et al, 2001; Hariri, 2002). It’s worth pointing out, however, that the long variant of this same gene has been linked to high emotional resilience.
- People with variants of the gene RGS2 are believed to be at higher risk for anxiety disorders. Nine different variations of RGS2 have been associated with shy, inhibited behavior in children, introverted personalities in adults, and increased activity in areas of the brain such as the amygdala and the insula, which process fear and anxiety (Smoller, 2009).
- Variants in the ALAD gene increase risk for Social Phobia (Smoller, 2008)
- Variants in the DYNLL2 gene increase risk for Generalized Anxiety Disorder (Smoller, 2008)
- Variants in the PSAP gene increase risk for Panic Disorder (Smoller, 2008)
- A variant of the CNTNAP2 gene has been associated with social anxiety-related traits, such as impaired social interaction and communication skills (features also associated with autism spectrum disorders and a condition called selective mutism, which may manifest as an early-onset variant of social anxiety disorder)(Stein, 2011).
- Variants in the COMT gene, which regulates dopamine signaling, may play a role in causing anxiety and negative emotions (Hovatta, 2008). COMT (catabolic enzyme named catechol-O-methyltransferase) encodes an enzyme that breaks down dopamine, weakening its signal. COMT’s two alleles are Val158 and Met158. People carrying two copies of the Met158 allele may find it harder to regulate emotional arousal, a sensitivity which may, in combination with other hereditary and environmental factors, make them more prone to anxiety disorders. The Met158 allele is thought to elevate levels of circulating dopamine in the brain’s limbic system, which supports memory, emotional arousal and attention. More dopamine in the prefrontal cortex could result in an “inflexible attentional focus” on unpleasant stimuli — Met158 carriers may find that they have a hard time tearing themselves away from arousing stimuli, even though it’s bad.
Interestingly, the Met158 allele of the COMT gene is a relatively recent mutation, existing only in humans. Is the human species, as a whole, becoming more anxious, or at least at greater risk for anxiety? Maybe. But consider the prevalence of the COMT gene’s two alleles, Val158 and the emotional-arousal allele, Met158. Around half the population carries one copy of each allele; the other half is roughly divided between carrying two copies of Val158 and two copies of Met158. This perfectly illustrates the reality that a single gene variation typically only explains a small portion of — or one dimension of — anxious behavior. Otherwise, half the population would have an anxiety disorder! Genes are not destiny.
One thing’s for sure: emotional resilience, the ability to cope with stressful life events more effectively, helps neutralize the risk of developing anxiety disorders, regardless of any genetic predispositions we may have.
Bremner JD, Randall P, Scott TM, et al. MRIbased measurement of hippocampal volume in combat related posttraumatic stress disorder. American Journal of Psychiatry. 1995;152:973–981.
Davidson, Richard J.. David A. Lewis, Lauren B. Alloy, David G. Amaral, George Bush, Jonathan D. Cohen, Wayne C. Drevets, Martha J. Farah, Jerome Kagan, Jay L. McClelland, Susan Nolen-Hoeksema, Bradley S. Peterson. Neural and Behavioral Substrates of Mood and Mood Regulation. Biol Psychiatry 2002;52:478–502
Garpenstrand H, Annas P, Ekblom J, Oreland L, Fredrikson M (2001) Human fear conditioning is related to dopeminergic and serotonergic biological markers. Behav Neurosci 115(2): 358–364.
Hariri AR, Mattay VS, Tessitore A, Kolachana B, Fera F, et al. (2002) Serotonin transporter genetic variation and the response of the human amygdale. Science 297: 400–403.
Hettema, JM, Neale, MC, Kendler, KS. A review and meta-analysis of the genetic epidemiology of anxiety disorders. Am J Psychiatry 2001;1581568- 1578.
Hovatta, Iiris. Biological Psychiatry, October 15, 2008.
LeDoux, Joseph. The Emotional Brain: The Mysterious Underpinnings of Emotional Life. New York: Touchstone Books, 1996.
Lesch KP, Bengel D, Heils A, Sabol SZ, Greenberg BD, et al. (1996) Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science 247(5292): 1527–1531.
Kendler, K.S. & Baker, J.H. ‘Genetic influences on measures of the environment: a systematic review.” Psychological Medicine 37:615-626 (2007).
McCrae RR, Costa PTJ (2003) Personality in Adulthood: A Five-Factor Theory Perspective. New York: Guilford.
Ninan, PT. The functional anatomy, neurochemistry, and pharmacol-ogy of anxiety. (1999) J Clin Psychiatry 60:12–17.
Nutt, D., Demyttenaere, K., Janka, Z., Nordfjord, T.A., Bourin, M, luigi, P., Carrasco, J.L., Stahl, S.. Journal of Psychopharmacology. 2006.
Omura K, Constable TR, Canli T (2005) Amygdala gray matter concentration is associated with extraversion and neuroticism. Neuroreport 16(17): 1905–1908.
Pezawas, L, Meyer-Lindenberg, A, Drabant, EM, Verchinski, BA, Munoz, KE, Kolanchana, BS, Egan, MF, Maaatta, VS, Hariri, AR, Weinberger, DR.. 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depression. Nat Neurosci. 2005 Jun;8(6):828-34. Epub 2005 May 8.
Sen S, Burmeister M, Ghosh D (2004) Meta-analysis of the association between a serotonin transporter promoter polymorphism (5-HTTLPR) and anxiety-related personality traits. Am J Med Genet B 127B: 85–89.
Smoller, Jordan. Archives of General Psychiatry. March 2009.
Spielberger, C. D., Sydeman, S. J., Owen, A. E., & Marsh, B. J. (1999). Measuring anxiety and anger with the State-Trait Anxiety Inventory (STAI) and State-Trait Anger Expression Inventory (STAXI). In M. E. Maruish (Ed.), The use of psychological testing for treatment planning and outcomes assessmen(pp. 993-1021). Mahwah, NJ: Lawrence Erlbaum Associates.
Stein MB, Hanna C, Koverola C, et al. Structural brain changes in PTSD: Does trauma alter neu roanatomy? In:Yehuda R, McFarland AC, eds. Psychobiology of posttraumatic stress disorder. Annals of the NewYork Academy of Sciences, 821. NewYork:New York Academy of Sciences, 1997.
Stein MB, Yang BZ, Chavira DA, Hitchcock CA, Sung SC, Shipon-Blum E, Gelernter J.. A common genetic variant in the neurexin superfamily member CNTNAP2 is associated with increased risk for selective mutism and social anxiety-related traits. Biol Psychiatry. 2011 May 1;69(9):825-31. Epub 2010 Dec 30.
Tovilović, Snežana, Novović, Zdenka, Mihić, Ljiljana, Jovanovic, Veljko. The Role of Trait Anxiety In Induction of State Anxiety. PSIHOLOGIJA, 2009, Vol. 42 (4), str. 491-504.
Trono, Didier. Neuron, December 2009.