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Understanding Asthma

Asthma can become a substantial burden for its sufferers, negatively affecting quality of life again and again over a lifetime. For some, asthma is inconvenient; for others, it can be debilitating, taking a heavy toll on the person’s normal daily activities. In 2008, for example, more than half (59 percent) of children and one-third (33 percent) of adults missed school (4 days on average) or work (5 days on average) because of asthma. And asthma, on average, costs its victims $3,300 in medical expenses each year (Centers for Disease Control and Prevention, 2012).

In the U.S. alone, around 8.2 percent of adults and 9.5 percent of children currently suffer from asthma, but the asthma population continues to grow. In 2001, one in 14 people had asthma, but by 2009, that figure had grown to 1 in 12 (CDC, 2012). This startling jump in asthma rates has led physicians and researchers to realize that asthma is a more complex illness than was commonly believed. We used to blame asthma primarily on pollutants and allergens, but studies now suggest that only 50 to 60 percent of asthma cases have an allergic component (Greenwood, 2011; AAFA, 2012).

What causes asthma?

Asthma is a chronic inflammatory disorder of the airways characterized by symptoms such as wheezing, coughing, shortness of breath, chest tightness and bronchospasms. Many studies have documented that asthma can be caused by a combination of genetic, environmental, and psychoemotional factors, not the least of which is an inability to manage stress (e.g., Martinez, 2007; Sharma et al, 2008).

There is broad consensus among researchers that asthma is not caused by one specific genetic switch; i.e., there is no single “asthma gene.” One gene known as ORMDL3 increases the risk of child onset asthma by 60 to 70 percent (Miriam et al, 2007). Another gene, INPP4A, has been implicated as an asthma candidate (Sharma, 2008). A gene called DENND1B affects cells and other signaling molecules that are involved in the immune system overreaction common to asthma sufferers (Sleiman 2010). Genes can even help determine who responds to asthma medication and who doesn’t. Asthma patients who inherited two copies of the GLCCI1 gene variant have been found to be far less likely to respond to steroid inhalers than people with two copies of the more common version of the gene (Kelan et al, 2011).

But most evidence suggests that most asthma-related gene variants determine risk for the disease in a context-dependent manner — that is, they operate in concert with environmental factors and with certain variants of other genes, possibly during a specific developmental phase of the disease.

For example, a variant of the INPP4A gene known as the +110832A/G (Thr/Ala) variant has been found to influence the INPP4A’s stability and is heavily associated with asthma (Sharma, 2008). In the end, general genetic switches are often the essential determinants for whether we will develop a genetic condition or not. You can think of these “general” genes as analogous to the main power switch for your home, which needs to be flipped to ON in order for you to have electricity available for any one room or appliance.

The prevailing medical wisdom for asthma management seems to be that people with asthma can prevent asthma attacks through education; for example, by learning to use inhaled corticosteroids and other daily long-term control medicines and by avoiding asthma triggers (e.g., tobacco smoke, mold, air pollution, colds and flu). But while education is an important element of asthma management, the other critical part of the equation is attacking the disease process at the roots.

A Key Asthma Culprit: Stress

Stress plays a heavy role in the asthma disease process, often interacting with environmental triggers to exacerbate symptoms. In fact, acute stressful life events have been found to double the risk of having an asthma attack and triple the risk for those under chronic stress (Sandberg et al, 2000).

Through a number of pathways, stress, or rather, the inability to manage it, increases the airway inflammatory response and bronchoconstriction that environmental irritants, allergens and infections trigger in people with asthma (Chen, Miller, 2007). In fact, studies indicated that people with asthma may actually be more sensitive in certain critical ways; that is, stress modifies the inflammatory response in people who have asthma in ways that it doesn’t in people who don’t.

How Stress Modifies Inflammation in People with Asthma

Stress and the asthma immune response.

Exposure to external asthma triggers inflames airways and trips a cellular immune response involving T helper (Th) cells. The Th-1 cells deploy cytokines, chemical messengers that bind to the receptors of infected target cells. The Th-2 cells release cytokines that trigger the humoral or antibody response. The cytokines induce B cells to release IgE antibodies, which bind to allergens residing in the airway and release allergy mediators such as histamines and leukotrienes. Histamines and leukotrienes cause edema, smooth muscle constriction, and mucus, which trigger asthma symptoms such as wheezing, chest tightness, and shortness of breath. This pathway is the early asthma response.

The more prolonged late-phase asthma response occurs when Th-2 cells release the cytokine IL-5, which recruits eosinophils (white blood cells) and leukotrienes into the airways. The eosinophils cause inflammation and obstruction and damage airway cells. The leukotrienes cause edema or swelling caused by watery fluid buildup and further bronchial constriction.

This exaggerated inflammatory response is not just triggered by allergens or environmental pollutants. In people with asthma, stressful life events trigger it, too. But in order for these downstream inflammatory processes in the airways to occur, the stressor must be appraised as threatening and unmanageable. This threat appraisal pattern increases negative emotions (e.g., anger, fear, shame) and decreases positive emotions (e.g., vigor, joy, calmness) and triggers negative thoughts about the self and the future. These emotional and cognitive processes sensitize the Th-2 pathway, which triggers a more pronounced inflammatory response to environmental asthma triggers and ultimately leads to increased frequency, duration, and severity of asthma symptoms  (Miller, Chen, 2007).

When confronted with a stressful life event, we immediately perform a cognitive appraisal to decide whether we can handle the stressor. The degree to which we appraise our coping resources as insufficient to meet the demands of stressors is referred to as perceived stress. High perceived stress is common in people with asthma and has been strongly associated with asthma-related problems, such as reduced adherence to medication and poor asthma control (Lemmens et al, 2009).

It has also been associated with a tendency to overperceive dyspnea (shortness of breath or “air hunger”) and other respiratory symptoms (Wisnivesky et al, 2010). Overperceiving asthma symptoms only further exacerbates those symptoms. Thus, one crucial aspect of asthma management is developing the ability to discriminate between actual asthma symptoms and the emotion-related sensations, thoughts and feelings that we associate with them. (As you’ll see Part 2, meditation can help.)

So stress accentuates the body’s immune response to environmental asthma triggers and the body effectively treats stress as if it were an external environmental trigger (e.g., tobacco smoke or air pollution). Stress – and the body’s automatic response to it – taps three critical biological pathways that directly influence airway inflammation and bronchoconstriction  (Chen, Miller, 2007):

  • hypothalamic-pituitary-adrenal (HPA) axis
  • sympathetic-adrenal-medullary (SAM) axis
  • sympathetic and parasympathetic arms of the autonomic nervous system.

Stress also directly affects other biological systems such as the immune-brain loop, which directly links the brain to the immune system via the vagus nerve, causing bronchoconstriction and increased sensitivity to external triggers. (For more about the immune-brain loop, see How Stress Impacts the Immune System.)

The HPA Axis

Certain types of emotional distress are known to be powerful triggers of the HPA axis. For example, acute situations that involve high levels of social evaluation and trigger self-conscious emotions like shame reliably boost output of ACTH (adrenocorticotropin hormone) and stress hormones (e.g., cortisol, epinephrine, norepinephrine), especially when the stressors threaten the person’s physical integrity and are completely out of the person’s control (Miller, Chen, Zhou, 2007). Under chronic, prolonged exposure to high levels of cortisol, our white blood cells eventually mount a counter-regulatory protest by downregulating the receptors that bind cortisol. The result is that immune cells become less sensitive to glucocorticoid signals that would normally trigger an anti-inflammatory, immune response (Miller et al, 2002). So, the next time a person with asthma is exposed to a trigger and needs the immune systems to kick into gear, it may be more difficult to regulate the amount and duration of airway inflammation, and over the longer term, they may even find that glucocorticoid medications have become less effective.


Stressors activate the sympathetic nervous system (SNS), which increases the release of epinephrine (adrenaline) from the adrenal medulla and activates noradrenergic (containing noradrenaline or norepinephrine) nerve fibers that supply lung and lymphoid tissue. This tissue produces antibodies and white blood cells (lymphocytes) that fight allergens and infection. SNS activation also dilates bronchi in the lungs and triggers an exaggerated antibody response. Now, you may be thinking that an exaggerated antibody response sounds like a good thing for asthma sufferers, but the problem is that prolonged, chronic exposure to stress hormones triggers that immune system counter-regulatory protest mentioned earlier. The body’s immune response to an asthma trigger becomes exaggerated and dysregulated, flooding the airways with Th-2 cytokines, eosinophils and leukotrienes. The airways become obstructed and constricted (Miller, Chen, 2007).


While stress typically decreases parasympathetic nervous system (PNS) activity in non-asthmatic people, some studies have found that in people with asthma, stress causes parasympathetic pathways to kick into overdrive or hyperresponsiveness (Lehrer et al, 1993). Parasympathetic nerve fibers descending from the vagus nerve release the neurotransmitter acetylcholine and signal smooth muscle cells and mucus glands in the airways, which triggers asthma symptoms such as bronchoconstriction and mucus secretion.

Negative Emotions Exacerbate Asthma and Affect Lung Function

While all humans experience a physical reaction to negative emotions, people with asthma may be more sensitive, autonomically speaking. Several studies have linked acute negative emotions to autonomic nervous system reactivity in people with asthma. In one study where children with asthma watched a sad film, the more emotional the children reported feeling over the film, the greater their airway reactivity, as measured by a standard methacholine chemical test.

A follow-up study of these children showed that sadness, compared with happiness and neutral feelings, also produced the greatest heart rate variability (indicating greater parasympathetic activation) and unstable oxygen saturation (indicating airway instability). These findings show that in people with asthma, negative emotional responses typically associated with stressful life experiences may elicit autonomic (in this case, parasympathetic) responses that cause or worsen asthma symptoms and contribute to bronchoconstriction (Miller, Wood, 1994).

There’s evidence that lung function in people with asthma is negatively affected by all sorts of strong negative mood states (anger, anxiety, sadness and especially depression) in daily life.

For example, one study of asthma patients showed that negative mood states (compared to positive or neutral states) were heavily associated with bronchoconstriction — a reduction in forced expiratory volume (FEV) and changes in Ros (respiratory resistance). Lung function was not significantly affected by mood in non-asthmatic control subjects, suggesting that it is especially important for people with asthma to be able to manage their emotions (Ritz, Steptoe, 2000).

Other research suggests that living with chronic anger may impair lung function and exacerbate asthma symptoms; one moving example involved a study of children at summer asthma camp with anger-induced asthma exacerbation who received an intervention course in assertion training. Researchers found that when children were allowed to express anger in constructive ways, asthma deteriorated (Hock et al, 1987).

A more recent study of anger’s wear and tear on the lungs found that chronic anger and hostility were associated with poorer lung function and more rapid rates of decline in 680 older men. And spirometric tests showed that the greater their hostility, the more rapid their decline in lung function (Kubzansky, 2006). The results suggest that chronic anger may lead to chronic dysregulation. The psychophysiology of anger overlaps with that of stress. Anger, after all, is part of the “fight” component in our fight‐flight reflex. (For an in-depth look at how Sahaja helps us eliminate or manage anger, see Anger and the Inner Energy System.)

Certain psychological disorders are unusually common among people with asthma, such as anxiety disorders (especially panic attacks, panic disorder and specific phobia) (Hasler et al, 2005; Goodwin et al, 2003) and major depression, dysthmia and bipolar disorders, (Goodwin et al, 2003). Researchers have found that treating panic attacks has the potential to decrease future asthma attacks, reduce the need for medication, asthma treatments, emergency room visits and hospitalization (Hasler et al, 2005).

Anxiety and depression can exacerbate asthma in several critical ways; for example: by reducing self‐care, through the direct physiological effects of emotional dysrelgulation and distress on the airways, and through the effect that suffering from chronic physical illness has on a person’s emotional state (Lehrer, 2006). (For comprehensive information about anxiety and depressive disorders, including specific ways that Sahaja meditation can help, see our anxiety and depressive disorders sections.)

Meditation may not only help relieve the psychological burden of asthma, there is evidence to suggest that it may also impact the physiological roots of asthma as well.


Asthma and Allergy Foundation of America, aafa.org, 2012.

  1. Boulet LP, Bateman ED, Voves R, et al. A randomized study comparing ciclesonide and fluticasone propionate in patients with moderate persistent asthma. Respir Med 2007;101:1677–86.

Centers for Disease Control and Prevention, U.S. Department Of Health And Human Services. Summary Health Statistics for U.S. Adults: National Health Interview Survey, 2011. Vital and Health Statistics Series 10, Number 256. December 2012.

Chen, Edith, Miller, Gregory E.. Stress and Inflammation in Exacerbations of Asthma. Brain Behav Immun. 207 November: 21(8); 993-999.

Goodwin R D, Jacobi F, Thefeld W. Mental disorders and asthma in the community. Arch Gen Psychiatry 2003. 601125–1130.1130.

Greenwood, V.. Why Are Asthma Rates Soaring? Scientific American. April, 14, 2011.

Hasler G, Gergen P J, Kleinbaum D G. et al Asthma and panic in young adults: a 20‐year prospective community study. Am J Respir Crit Care Med 2005. 1711224–1230.1230.

Hock R A, Rodgers C H, Reddi C. et al Medico‐psychological interventions in male asthmatic children: an evaluation of physiological change. Psychosom Med 1987. 40210–215.215.

  1. Holgate ST, Chuchalin AG, Hebert J, et al. Efficacy and safety of a recombinant anti-immunoglobulin E antibody (omalizumab) in severe allergic asthma. Clin Exp Allergy 2004;34:632-8
  2. Kelan G. Tantisira, M.D., Jessica Lasky-Su, Sc.D., Michishige Harada, Ph.D., et al. Genomewide Association between GLCCI1 and Response to Glucocorticoid Therapy in Asthma. N Engl J Med 2011; 365:1173-1183September 29, 2011.


Kubzansky L D, Sparrow D, Jackson B. et al Angry breathing: a prospective study of hostility and lung function in the Normative Aging Study. Thorax 2006. 61863–868.868.

Lehrer PM, Isenberg S, Hochron SM. Asthma and emotion: A review. Journal of Asthma. 1993; 30: 5–21.

Lemmens KM, Nieboer AP, Huijsman R. A systematic review of integrated use of disease-management interventions in asthma and COPD. Respir Med 2009; 103:670–91.

Mamta Sharma, Jyotsna Batra1, Ulaganathan Mabalirajan1, Shilpy Sharma1, Rana Nagarkatti1, Jyotirmoi Aich1, Surendra K. Sharma2, Pramod V. Niphadkar3 and Balaram Ghosh1. A Genetic Variation in Inositol Polyphosphate 4 Phosphatase A Enhances Susceptibility to Asthma. Am. J. Respir. Crit. Care Med. April 1, 2008 vol. 177 no. 7.

Martinez FD (2007). Genes, environments, development and asthma: a reappraisal. Eur Respir J 29 (1): 179–84.

Markham AW, Wilkinson JM. Complementary and alternative medicines (CAM) in the management of asthma: an examination of the evidence. J Asthma 2004; 41:131–9.

Miller GE, Chen E, Zhou ES.. If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. Psychol Bull. 2007 Jan;133(1):25-45.

Miller GE, Cohen S, Ritchey AK. Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid resistance model. Health Psychology. 2002;21:531–541.

Miriam F. Moffatt, Michael Kabesch, Liming Liang,  et al. Genetic variants regulating ORMDL3 expression contribute to the risk of childhood asthma. Nature 448, 470-473 (26 July 2007).

Sandberg S, Paton JY, Ahola S, McCann DC, McGuinness D, Hillary CR. The role of acute and chronic stress in asthma attacks in children. Lancet. 2000; 356: 982–987.

Sleiman PM, Flory J, Imielinski M, Bradfield JP, et al. Variants of DENND1B associated with asthma in children. N Engl J Med. 2010 Jan 7;362(1):36-44.

Ritz T, Steptoe A. Emotion and pulmonary function in asthma: reactivity in the field and relationship with laboratory induction of emotion. Psychosom Med 2000. 62808–815.815.