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Immunity

Meditation and Immunity

How Stress Impacts the Immune System

For the past couple of decades, researchers have known that behavioral and psychological events can influence the immune system. The mind-body stress response can be activated by everyday physical and psychological stress; or rather, by our inability to effectively manage that stress. Stress-related illnesses are triggered by chronic, prolonged activation of that neuroendocrine (brain and hormones) stress response. So, while stress doesn’t guarantee that you’ll get sick, it definitely increases the risk.

Studies in the field of Psychoneuroimmunology have revealed the mechanisms through which stress compromises the immune system, shedding light on the complex relationships between DNA, stress hormones and the immune system. Psychoneuroimmunology is the study of the interactions between the brain, body, emotions, and the immune system; that is: the mind’s effect on our ability to ward off illness.

The Relationship Between Stress and Illness

When the body’s stress response is triggered, its emergency resources are immediately mobilized for action. For example, secretion of the stress hormone cortisol ramps up to help the body support its fight-or-flight response. But while our hormones are preparing for battle, energy-consuming components of the immune system (e.g., white blood cell production), must temporarily shut down. In shutting down some of the body’s critical defenses, stress makes us more vulnerable to disease; for example, stress decreases secretion of antimicrobial peptides, the body’s natural broad spectrum antibiotics that kill bacteria.

In compromising the immune system, stress also diminishes our ability to heal properly and recover from illness.

People who have suffered heart attacks, for example, tend to have a much harder time bouncing back while simultaneously experiencing major stressors, such as financial worries. On the other hand, an ability to effectively manage stress can significantly speed recovery from conditions such as cardiac disease or cancer.

Acute, short-term stress revs up the immune system, an adaptive response that  prepares our bodies for injury or infection. But chronic, prolonged stress inflicts too much wear and tear on the immune system, and the system breaks down. It’s cortisol’s job to help regulate inflammation, the body’s natural response to injury or infection. But chronic stress triggers chronically elevated cortisone levels, which damage the immune system, cell by cell. In fact, research has shown that over a prolonged period of chronic stress, body tissue becomes desensitized to cortisol and the hormone loses its ability to effectively regulate inflammation (Cohen, 2012; Laboratory for the Study of Stress, Immunity and Disease at Carnegie Mellon University).

This chronic wear and tear of stress is sometimes referred to as allostatic load, which is the cumulative “cost” or damage inflicted on the body as a result of chronic exposure to a heightened or wildly fluctuating neuroendocrine stress response, particularly the repeated triggering of the hypothalamus-pituitary-adrenal (HPA) axis. (For more about how meditation influences the (HPA) Axis, see: How Altered Consciousness Happens.)

Allostatis

Allostasis is the process through which the body responds to stressors in order to regain homeostasis or physiological equilibrium. Allostatic load is measurable and includes variables such as: hormones (e.g., epinephrine, norepinephrine and cortisol), catecholamines (e.g., epinephrine, dopamine), immune system components (e.g., interleukins, leukocytes), and cardiovascular parameters (e.g., blood pressure).

Allostatic overload occurs when the HPA axis is unable to counter-regulate the immune system. A study of cancer patients with stress disorders (e.g., PTSD), anxiety and depression found that their allostatic overload was triggered by (Ronson, 2006):

  • the proliferation of stressors over time
  • an inability to adapt even to stressors that don’t pose a threat (e.g., public speaking)
  • an inability to extinguish stress and anxiety for past threats that are no longer threatening
  • faulty regulatory feedback loops (e.g., cortisol regulates its own production by negative feedback loops in the hippocampus, hypothalamus and pituitary), which leads to a prolonged stress response — overworked immune and autonomic nervous systems

The Immune-Brain Loop

How does the brain know there’s an infection in the first place?

The immune system sends signals to the brain that significantly alter neural activity, thus altering all activity that flows from the brain, such as behavior, thought, emotions and mood. Signals from the brain (the hypothalamus, in particular), trigger what we think of as the “sickness response,” which triggers a series of physiological and behavioral changes such as fever, changes in liver metabolism, reduced food and water intake, reduced motivation or increased anxiety.

And, of course, the classic stress response occurs: cortisol is released.

Macrophages, which are the first responders on the scene of any infection, trigger the sickness response by creating pro-inflammatory cytokines. The presence of cytokines is, in fact, a marker for inflammation. Cytokines are potent chemical messengers that bind to the receptors of infected target cells (e.g., cancer cells or virus-infected cells). Cytokines serve as the chief communication conduit between immune cells (e.g., T cells), encouraging cell growth, promoting cell activation, directing cellular traffic, and destroying infected cells. Cytokines include interleukins, growth factors, and interferons.

Cytokines mobilize T cells, those amazing natural killer cells that have the ability to spontaneously recognize and selectively target and kill certain tumor cells and virus-infected cells. Always on “surveillance” duty, T cells bind to their targets on contact and deliver a burst of lethal chemicals.

This cellular immune system, which allows the body to attack invading organisms on a cellular level, is paired with the humoral immune system, which releases antibodies that tag and target invader cells. The term “humoral immunity” was derived from 1800s medical theories that immunity was mediated by cells which float in bodily fluids such as blood and lymph, or “humors.” We’re all born with some innate antibodies that recognize broad types of harmful cells and organisms and we acquire additional antibodies through exposure to viruses and microbial toxins.

Antibodies are proteins that exist in bodily fluids. They originate in bone marrow B cells and mature in plasma cells. These plasma cells effectively become little antibody factories floating throughout the bloodstream. Each B cell clone produces a single species of antibody, each with a unique antigen-binding site at its tips. (A typical antibody molecule is Y-shaped, with two identical antigen-binding sites at the tips of the Y.) Thus each antibody can effectively target and bind only with an antigen with which it has high affinity. The strength of an antibody-antigen interaction depends on both the number and the affinity or compatibility of the antigen-binding sites.

While some antibodies are capable of neutralizing antigens themselves, generally, antibodies only recognize and tag antigens (toxins) for destruction then alert other defensive cells, such as killer T cells, to do the dirty work of attacking these antigens. Antibodies tag antigens for destruction by binding with those antigens. The interaction of antibody with antigen also activates the complementary cellular immune system, recruiting help from, for example, killer T cells.

Now, back to the immune-brain loop… how does the body translate a blood-borne signal into a neural signal? Through the vagus nerve, which links the brain to the immune system. Neurotransmitters on the vagus nerve called paraganglia contain receptors for interleukin-1, a cytokine released by the macrophages. So, a macrophage releases interleukin-1 into its neighboring space. The interleukin-1 binds to receptors on the paraganglia, which send neurotransmitters to activate the vagus nerve, which signals the brain to make more interleukin-1, a signal that sets off the sickness response and sends signals back to the immune system, activating other immune cells. It’s a complete, bidirectional immune-to-brain circuit (Maier, 2001).

Now, stress travels this very same immune-brain circuit (which is how stress can make us physically, physiologically sick), except that it begins in the brain rather than the immune system. And worse, stress and infection each sensitize the body’s reaction to the other. Infection primes the circuit so that it will be predisposed to experience an exaggerated response to later stress, and vice versa (Maier, 2001). To the immune system, stress is, in effect, just another form of infection — its impact is that physiological.

This dual-function stress-sickness circuitry may help explain in part why mental health problems such as depression are so often inextricably linked to physical illnesses such as cardiovascular disease or cancer. For example, studies of patients receiving interleukin-1 to fight cancer found that these patients developed severe depression and, vice versa: people with depression also had elevated cytokine levels. And clinical studies have also associated cytokines with cognitive impairments, such as memory and learning problems (Maier, 2001), suggesting that the immune-brain loop even impacts our mental abilities.

Immunity and DNA

The Tiny Clock: The Telomere

The cell is the basic building block of the human body, the smallest structural and functional unit of every living organism. Every human cell contains a tiny clock called a telomere, a protective cap on the end of our chromosomes that shortens each time the cell divides. A cellular enzyme within cells called telomerase keeps immune cells young by preserving their telomere length and their ability to continue dividing. Telomere shortening, in other words, is counteracted by telomerase — reduced telomerase activity is a precursor to telomere shortening.

Telomere shortening and reduced telomerase activity have emerged as prognostic markers of disease risk, progression, and premature mortality, and have been associated with accelerated aging and many serious illnesses, including, for example, depression (Simon et al, 2006) and several cancers (breast, prostate, colorectal, bladder, head and neck, lung, and renal cell) (Ornish, 2008). Short telomeres have also been heavily linked to stressful life circumstances such as prolonged caregiving (Epel, 2004) and lower socioeconomic status (Cherkas et al, 2006).

What causes telomere shortening?

It has been linked to factors such as:

  • chronically elevated cortisol (especially at night), which suppresses immune cells’ ability to activate telomerase (Effros, 2008)
  • chronic inflammation
  • chronic oxidative stress
  • Trait (pervasive) negative mood is associated with lower telomerase activity and telomere shortening (Epel et al, 2009)
  • A perceived inability to cope with stress — primarily, an inability to cope with demands and feeling a lack of control (Epel et al, 2009)

Oxidative Stress

Chronic stress increases the body’s level of oxidative stress (Liu, Mori, 1999), a destructive process in which free radicals or reactive oxygen molecules react with the components of cells (e.g., proteins or fats and nucleic acids such as DNA), ultimately damaging those cells. Oxidative stress leads to chronic inflammation and the immune system loses its ability to detoxify these reactive molecules or easily repair the resulting damage. The reality is that much of what we eat, drink, or breathe may contain cytotoxic oxidants and free radicals, but we count on our immune systems to combat them.

Oxidative stress may be linked to at least 100 serious diseases (Fisher-Wellman, 2009), including, for example, cancer, Alzheimer’s Disease, cardiovascular disease and hypertension, diabetes, Parkinson’s Disease, anxiety and bipolar disorders.

Inability to cope and negative mood

A pair of studies found that experiencing more stressors as threats rather than challenges was associated with shorter telomere length (Epel et al, 2004, 2009), demonstrating that coping helps buffer against the long-term wear and tear effects of stress on the immune system.

Whenever we’re confronted with a stressful situation, we immediately perform a cognitive appraisal to determine whether we feel equipped to handle the situation. That appraisal will determine whether we experience the stressor as eustress (positive stress that we perceive to be within our coping ability) or distress (negative stress that we perceive to fall outside our coping ability). Notice that a key aspect of the appraisal process is evaluation of our ability to control the outcome.

So, we may feel distressed when we appraise a situation that harms or threatens goals that matter to us and don’t feel that we have the resources to cope with those demands. This is known as a “threat appraisal.” A “challenge appraisal” occurs if we appraise a stressful situation and perceive ourselves as capable of coping with it and thus perceive the stressor as a challenge. (For an in-depth look at the appraisal process and how to cope with stress, see: Practical Cognitive Strategies for Coping with Stress.)

Our cognitive appraisals of our stressors drive our emotional states. Threat appraisals drive negative emotions such as fear and anxiety, whereas challenge appraisals can foster positive emotions (e.g., feeling energized or elated), even if they also foster some degree of anxiety in the short term. If the stressful situation is resolved favorably, a positive emotional state (e.g., relief, satisfaction) results. But if the event is resolved unfavorably or remains unresolved, a negative emotional state results (e.g., anger, guilt, anxiety) and the coping process loops through reappraisals and continued rounds of coping. This looping can easily slip into rumination, repetitive thought that is not goal-directed or constructive and is heavily associated with depression. Rumination has also been associated with higher cortisol levels (McCullough et al, 2007), which of course, eventually ravage the immune system.

By enhancing coping skills and resilience and boosting the immune system down to the cellular level, meditation may be an antidote to such cognitive stress states.

To learn how, see How Meditation Boosts Immunity.

References

Cherkas LF, Aviv A, Valdes AM, et al. The effects of social status on biological aging as measured by white-blood-cell telomere length. Aging Cell Oct;2006 5(5):361–365.

Cohen Sheldon ; Janicki-Deverts Denise ; Doyle William J. ; et al.. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proceedings Of The National Academy Of Sciences Of The United States Of America. Volume: 109,  Issue: 16   Pages: 5995-5999. April 17, 2012.

Effros, Rita. Mechanism Behind Mind-body Connection Discovered. Brain, Behavior and Immunity, May, 2008.

 

Epel ES, Blackburn EH, Lin J, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci U S A Dec 7; 2004 101(49):17312–17315.

Elissa Epel, PhD., Jennifer Daubenmier, Ph.D., Judith T. Moskowitz, Ph.D., Susan Folkman, PhD., and Elizabeth Blackburn, PhD. Can meditation slow rate of cellular aging? Cognitive stress, mindfulness, and telomeres. Ann N Y Acad Sci. 2009 August ; 1172: 34–53.

Kelsey Fisher-Wellman, Heather K Bell, and Richard J Bloomer. Oxidative stress and antioxidant defense mechanisms linked to exercise during cardiopulmonary and metabolic disorders. Oxid Med Cell Longev. 2009 Jan-Mar; 2(1): 43–51.

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Liu J, Mori A. Stress, aging, and brain oxidative damage. Neurochem Res Nov;1999 24(11):1479– 1497.

Maier, S. A new take on psychoneuroimmunology. Monitor on Psychology, American Psychological Association. December 2001, Vol 32, No. 11; 34.

McCullough ME, Orsulak P, Brandon A, Akers L. Rumination, fear, and cortisol: an in vivo study of interpersonal transgressions. Health Psychol Jan;2007 26(1):126–132.

Ronson, Alain. Bull Cancer. Psychological stress in oncology: the role of glucocorticoids. 2006 Jul;93(7):699-708.

Simon NM, Smoller JW, McNamara KL, et al. Telomere Shortening and Mood Disorders: Preliminary Support for a Chronic Stress Model of Accelerated Aging. Biol Psychiatry Mar 31; 2006 60:432–435.