Overview & Characterisitcs | Guided Meditation | Sahaja Online Overview & Characterisitcs | Guided Meditation | Sahaja Online

Anxiety

Overview & Characterisitcs

Overview and Characteristics

We all experienced anxiety from time to time — tension, uneasiness, apprehension, uncertainty and fear that results from anticipating a stressful event or situation. And a certain level of situational anxiety is normal — even adaptive. For example, if you’re about to be tested in some important way, anxiety and fear of failure spurs you on to prepare well. But in people with anxiety disorders, this fear is excessive and often irrational.

Unlike the relatively mild, brief and acute anxiety that might be triggered by a stressful situation, anxiety disorders last at least six months and symptoms tend to worsen if they’re not treated. Anxiety in its extreme forms can be terrifying, paralyzing, and debilitating. Fear and uncertainty can rule the lives of people suffering from anxiety disorders. Chronic anxiety can interfere with job and family responsibilities on a daily basis and wreak havoc on careers and relationships. Chronic anxiety prevents us from living fulfilled lives because it keeps us so busy worrying about the future that we can’t simply enjoy the present. Our attention is focused on some distant horizon that we may or may not ever reach.

Collectively, anxiety disorders, which affect about 18.1 percent (40 million) of U.S. adults in any given year, are the most prevalent class of mental health disorder. They are, for example, more prevalent than mood disorders (such as major depression, dysthymia or bipolar disorders), which occur in 9.5 percent of the general population (Kessler, 2005).

The two primary characteristics of anxiety disorders are:

  1. the presence of anxiety
  2. the avoidance behaviors designed to ward off the anxiety

 

While each anxiety disorder has distinctive symptoms, the symptoms of each always involve excessive, irrational fear and anxiety, apprehensiveness and dread. Anxious people develop avoidance behaviors to protect themselves from experiencing the anxiety, such as persistent, recurring thoughts, rituals, or phobic behaviors. Those who suffer from anxiety often describe feeling as if they’re prisoners in their own bodies. When a situation provokes anxiety, their bodies may react in disturbing ways… heart palpitations, dizziness, trembling. They may be consumed by their thoughts, filled with dread and a sense of impending doom, victims of a fight-or-flight response run wild.

Fight or Flight?

We all have an innate fight-or-flight mechanism that’s designed to protect us from imminent danger by preparing us to either fight or flee. Our fight-or-flight response is our sympathetic nervous system kicking into gear in response to a perceived threat. Within nanoseconds of perceiving a threat, your amygdala sounds a general alarm and your entire body is suddenly on high alert, ready to either fight or flee. The endocrine system promptly floods the body with stress hormones, such as cortisol, adrenaline (epinephrine), noradrenaline (norepinephrine). When we’re operating under the influence of an excess of these chemicals, we become anxious, panicky, fearful and possibly even aggressive. Your breathing quickens, your heart races and your blood pressure skyrockets, infusing your body with oxygen while your liver releases glucose for quick fuel. Nonessential physiological processes switch off. Digestion stops, your skin chills, and your blood is diverted to muscles in preparation for a burst of emergency action.

This is the route that anxious anticipation follows in the brain. It’s what neuroscientist Joseph LeDoux referred to as “the low road” (LeDoux, J., 1996). LeDoux discovered that the experience of fear follows two distinctly different pathways in the brain: one conscious and rational (“the high road”), the other primitive and unconscious  (“the low road”). The low road is a shortcut through the wilderness of brain circuitry that allows the brain to start responding to a threat within thousandths of a second. The high road is simultaneously encoding much more detailed and specific information, but those extra steps takes seconds longer, which, in the event of real danger, could spell the difference between life and death.

To illustrate, let’s say that you detect a form slithering through the grass that you decide is a snake (or even think you might have seen a snake, which, for all intents and purposes is the same thing to the amygdala). Your sensory organs (e.g., eyes and ears) transmit sensory data to the thalamus, where the information is then transmitted throughout the brain along two pathways. One stream of data takes the high road; it heads to the visual cortex, where it will be integrated with other sensory data and any rich, elaborate memories and associations your brain has for snake. The other data stream takes the low road — heads straight to the amygdala in down and dirty form, without any rich, elaborate sensory data. The amygdala, which directs signal traffic in the brain, blasts an alarm to the brain stem, alerting the body to a potential threat. In a fraction of a second, before you even have time to formulate the word Snake!, your body freezes in its tracks; your heart is pumping harder and the rest of your fight-or-flight response kicks in. Your amygdala screams: Run! Meanwhile, it takes several seconds for “the high road” to process all the data, form a conclusion and choose the appropriate response.

The brain instinctively knows how to execute the fight-flight response — no training required. In fact, it’s so good at it that it can actually be difficult to stop it from happening. Unless you pause, think, and willfully choose to let the smarter, rational, cortical parts of your brain override the panicky amygdala, you’ll do exactly what the amygdala tells you: You’ll run.

Now, suppose it turns out that this slithering form you saw wasn’t a snake at all, just a curvy stick. And maybe this was precisely the high road conclusion. This disconnection between the high road and the low road helps explain what often happens to people with anxiety disorders. As LeDoux said, “While, in terms of survival, it may be better to mistake a stick for a snake, people who have pathological fears may be treating sticks as snakes much of the time.”

In other words, while wariness is adaptive and it’s advantageous for us to be more anxious in a dangerous environment, someone in the grip of an anxiety disorder mistakenly perceives far too many sticks to be snakes. Fear too easily becomes the New Normal. Sometimes the fight-or-flight response misfires. Panic attacks, for example, are the perfect illustration of fight-or-flight misfiring.

State vs. Trait?

Anxiety can manifest as a state or a trait. States are temporary, short lived — a response to an imminent situation. States that become chronic can become traits. Traits are more pervasive, enduring features of personality and character.

Traits are tendencies to behave consistently over time in certain ways.

We have genetic predispositions for some of our personality traits, which may help explain why some are more resistant to change. Individual differences in personality influence how we process the world around us. Neuroticism or harm avoidance, for example, which is a core characteristic of anxiety disorders, is an actual personality trait in some people who have anxiety disorders; for others, neuroticism is more of a transient state that was triggered by a stressful situation.

Trait neuroticism can include such traits as:  anxiety, depression or moodiness, emotional instabilty, dependence, irrationality, tenseness, hypochondria, guilt, regret, low self-esteem, obsessiveness, inferiority, unhappiness, controlled, lack of emotional confidence. For an in-depth look neuroticism and harm avoidance as a personality trait, see What Causes Anxiety.

To learn how meditation can help relieve state anxiety and improve anxious traits, see: How Sahaja Meditation Helps Relieve Anxiety.

Age, Gender and Cultural Factors

The individual experience of anxiety is always personal and contextual, shaped by biology, age, cultural and sociological expectations.

Gender

In general, women are susceptible to anxiety disorder than men. With the exceptions of Obsessive-Compulsive Disorder (OCD) and Social Anxiety Disorder, women have roughly twice the risk for most anxiety disorders, compared to men.

A number of factors may increase the reported risk in women, including cultural pressures to meet everyone else’s needs except their own, and a stronger tendency to report anxiety to doctors.

Men and women often respond to stress differently, thus they may exhibit different symptoms. A stress response that may manifest as fight-or-flight in men may manifest as “tend-and-befriend” in women. Evolutionarily, males may have confronted stressors either by overcoming or fleeing them, whereas women may have responded by nurturing offspring and affiliating with social groups.

Male and female brains may actually be wired differently with respect to how each experiences stress. fMRI studies of people under stress found that men show increased activity in the right prefrontal cortex (areas involved in analysis and decision-making), whereas women show increased activity in the emotional limbic system (Wang, 2001). Women were processing stressful decisions emotionally; men slipped into unemotional, problem-solving mode. While these changes may be partly the product of socialization, the neurological changes have been found to last longer in women, which may help explain why the rate of depression and anxiety disorders is twice as high in women.

Age

In general, specific phobias, OCD, GAD and separation anxiety tend to emerge early in childhood, while social phobia and panic disorder are often diagnosed during the teen years. Acute Stress Disorder and PTSD are more prevalent in adults, but can occur at any age. Between 3 to 5 percent of children and adolescents have some form of anxiety disorder, which puts them at higher risk of developing additional anxiety disorders, depression, and substance abuse as adults.

Sociocultural Factors

There is some evidence that anxiety levels in children and college students has significantly increased over the past two decades, compared to younger people in the 1950s. Anxiety has been associated with a lack of social connections and a sense of a more threatening environment. Populations that are economically deprived or socially alienated have higher levels of anxiety disorders.

Comorbidity with Other Disorders

Anxiety disorders can sometimes co-occur with medical conditions such as asthma, cardiovascular disease, irritable bowel syndrome (IBS, chronic pain, and cancer (Roy-Burne, 2008). While there may not be a direct causal link to these disorders, anxiety can certainly make them worse. Chronic stress, in addition to creating a pervasive anxious state, does long-term physiological damage. Stress hormones, in excess, damage our bodies all the way down to the cellular level, compromising our immune systems.

Comorbidity (co-occurrence) amongst anxiety disorders seems to be the rule rather than the exception. Most people do not experience a single anxiety disorder in isolation. In some cases, disorder A may cause disorder B; in others, both anxiety disorders share common risk factors and  underlying causes. (Goisman, et al, 1995; Robins, 1991; Goldenberg et al, 1996; Neal, Kendler, 1995)

Anxiety is highly comorbid with depression, especially Major Depression. Put another way, having an anxiety disorder is the single biggest risk for developing depression. More than half of the people who receive treatment annually for an anxiety or depressive disorder suffer from a comorbid second depressive or anxiety disorder (Hirschfeld, 2001). Anxiety, comorbid with depression, has been associated with a 2.5-fold increased likelihood of hospitalization. People suffering from concurrent Panic Disorder have a 3.2-fold increased risk (Kessler, 1998). Of all the anxiety disorders, Posttraumatic Stress Disorder (PTSD) has the highest rate of comorbidity with other mental health disorders, compared even to alcohol abuse.

A common comorbidity scenario might be: someone experiences significant life stressors such as relationship conflict, personal loss, or a life threat that triggers clinical anxiety. The presence of anxiety serves as a compounding stressor, leading (especially in patients with a genetic/familial history) to Major Depression, usually within a year or so. This risk is extremely high (more than 20-fold) for people with Panic Disorder and Generalized Anxiety Disorder (GAD). The risk levels off after the first year, but may continue to persist as a 2-fold or greater risk for many years after that (Hirschfeld, 2001).

Recent studies have suggested that anxiety sensitivity — the fear of feeling anxious — can put some people who are already above-average worriers at risk for depression (Viana, 2009). Two of the four dimensions of anxiety sensitivity were found to predict depression symptoms: 1) the fear of losing cognitive control and; 2) the fear of exhibiting publicly observable anxiety symptoms. (The other two dimensions, fear of cardiovascular symptoms and fear of respiratory symptoms, were not found to be significant predictors of depression.)

Anxiety sensitivity is really about a person’s interpretation of their own anxiety symptoms. People who are anxiety-sensitive fear their anxiety because they feel that something catastrophic is going to happen when those anxious sensations arise; for example, they may have a heart attack or exhibit embarrassing symptoms in public. Ultimately, the solution lies in altering their perception of anxious sensations by helping them learn to interpret their experiences in a positive and less fearful way.

References

“NIMH: The numbers count—Mental disorders in America.” National Institute of Health. Available at www.nimh.nih.gov/publicat/numbers.cfm.

Goisman, RM, Goldenberg   I, Vasile   RG, Keller   MB. Comorbidity of anxiety disorders in a multicenter anxiety study. Compr Psychiatry 1995;36303- 311.

Goldenberg, IM, White   K, Yonkers   K, Reich   J, Warshaw   MG, Goisman   RM, Keller   MB. The infrequency of “pure culture” diagnoses among the anxiety disorders. J Clin Psychiatry 1996;57528- 533.

Hettema, JM, Neale,  MC, Kendler, KS. A review and meta-analysis of the genetic epidemiology of anxiety disorders. Am J Psychiatry 2001;1581568- 1578.

Hirschfeld, Robert M. A.. The Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care. Prim Care Companion J Clin Psychiatry. 2001; 3(6): 244–254.

Kendler, K.S. & Baker, J.H. ‘Genetic influences on measures of the environment: a systematic review.” Psychological Medicine 37:615-626 (2007).

Kessler RC, Stang PE, Wittchen HU, et al. Lifetime panic-depression comorbidity in the National Comorbidity Survey. Arch Gen Psychiatry. 1998;55:801–808.

Kessler, Ronald C., PhD, Wai Tat Chiu, AM, Olga Demler, MA, MS, and Ellen E. Walters, M.S.. Prevalence, Severity, and Comorbidity of Twelve-month DSM-IV Disorders in the National Comorbidity Survey Replication (NCS-R). Arch Gen Psychiatry. 2005 June; 62(6): 617–627.

LeDoux, Joseph. The Emotional Brain: The Mysterious Underpinnings of Emotional Life. New York: Touchstone Books, 1996.

Magnus K, Diener E, Fujita F, Pavot W.. Extraversion and neuroticism as predictors of objective life events: a longitudinal analysis. J Pers Soc Psychol. 1993 Nov;65(5):1046-53.

Neale   MC, Kendler   KS. Models of comorbidity for multifactorial disorders. Am J Hum Genet 1995;57935- 953.

Perlman SB, Morris JP, Vander Wyk BC, Green SR, Doyle JL, et al. (2009) Individual Differences in Personality Predict How People Look at Faces. PLoS ONE 4(6): e5952.

Robins,  LN, edRegier   DA.ed Psychiatric Disorders in America.  New York, NY Free Press.  1991.

Saudino KJ, Pedersen NL, Lichtenstein P, McClearn GE, Plomin R. Can personality explain genetic influences on life events? J Pers Soc Psychol. 1997 Jan;72(1):196-206.

Viana, Andres, Rabian, Brian. Journal of Anxiety Disorders, December 2009; 23(8):1126-1131.

Wang, J.J.. SCAN (Social Cognitive and Affective Neuroscience),  2001.