stress
Health & Wellness / Lifestyle

Stress in the Modern Age: Impact on Homeostasis and What You Can Do (Part 1)

Jerry Jacobson, PhD, DMD, IOM

In 1926, Hans Selye first used the word stress in a biological context, referring to the nonspecific response of the body to any demand placed upon it.1 He performed experiments in the 1930s that later led to the view that stress refers to the condition in which an environmental demand exceeds the natural regulatory capacity of an organism.

Selye later published a model dividing stress into eustress, whereby stress enhances function, e.g., strength training or challenging work; and persistent stress that is unresolved through coping or adaptation, distress (leading to anxiety or depression).1-2 Indeed, homeostasis appears to lie at the core, and it was Walter Cannon who first used the term stress referring to external stimuli that disrupt homeostasis. But before examining how the body specifically responds to stress, let us consider why understanding the physiology of stress – and the potential for its effective management – are critically important.

Homeostasis and Stress

Homeostasis is the automatic maintenance of a steady state or state of balance within the bodies of all organisms. Living things possess inherited, or naturally built-in, feedback systems that help them to maintain a stable internal environment, even when the external environment changes, For example, after one dives into very cold water (change in external environment), the heart beats more rapidly than usual (change in internal environment) and the rate of breathing increases above normal. These are automatic responses to exposure to cold.

Stress is a key factor in the disruption of homeostatic functional equilibrium, in that living systems are in a constant state of flux, incessantly adjusting to the effects of environmental stimuli, both external and internal (emotional, chemical or physical). An organism's effort to restore homeostasis after an injury or life-threatening situation consumes energy and natural resources. Interestingly, Selye and others believed that,"stress, in addition to being itself, is also the cause of itself, and the result of itself."2-4

The central nervous system (CNS) plays a crucial role in the body's stress-related mechanisms, and the CNS works closely with the endocrine system to regulate these mechanisms. The sympathetic nervous system becomes primarily active during a stress response, regulating many of the body's physiological functions in ways that ought to make an organism more adaptive to its environment.

Stress: The Negative Consequences

Most Americans are familiar with stress and have come to accept the fact that everyday stress is a part of modern life. Modern life is full of hassles, deadlines, frustrations and demands.

But stress isn't always bad; in small doses, it can help you perform under pressure and motivate you to do your best. However, there is no clear-cut demarcation between good and bad stress; at best, we are faced with ambiguity.

For example, a young lady of 17 (with an IQ of 146) studied diligently for the SAT, hoping to perform especially well on the math section, as she looked forward to an acceptance from MIT. As the test papers were handed out, her sinuses swelled, she sneezed several times in a row, and her nose started to run like a faucet. Fortunately, she had come prepared with a box of tissues for what was ritualistic in a big test. She expected, as usual, to suffer through a stressful situation. She did get a 780 on the math section, putting her in the 99 percentile nationally, and was accepted to MIT.

We have all experienced sudden fright. The adrenaline surge through our bodies gives rise to that extra energy to escape from danger, the "fight or flight" response, producing stress, anxiety and nervousness. When stress becomes chronic and homeostasis is disrupted too long, overtaxing the body's adaptive mechanisms, our health suffers. Conditions that have been linked to chronic stress include angina, asthma, autoimmune disorders, cancer, the common cold, cardiovascular disease, depression, immune suppression, hypertension, type 2 diabetes, ulcerative colitis, ulcers, irritable bowel syndrome (IBS), menstrual irregularities, panic disorders, phobias, PTSD; the list goes on and on.

There are common warning signs and symptoms of stress overload, indicating a denigration of homeostatic function. Physical symptoms may include gastrointestinal irregularities, chest pain or rapid heartbeat, nausea or dizziness, loss of sex drive and frequent colds. Of course, the signs and symptoms of stress can also be caused by other psychological and medical problems.

Emotional symptoms of stress include moodiness, irritability or short temper, agitation or inability to relax, feeling overwhelmed, sense of loneliness, depression or general unhappiness.

As CNS structures are chronically maintained in non-homeostatic states, cognitive symptoms linked to stress include memory deficits, negative outlook, anxious or racing thoughts, and constant worrying. Your ability to tolerate stress depends on many factors, including the quality of your relationships, your basic outlook on life, your emotional intelligence and indubitably, genetics.

A strong network of supportive friends and family members is an enormous buffer against life's stressors. And the more lonely and isolated you are, the greater your vulnerability to stress. Common examples and categories of stressors include sensory output (pain, bright light, noise, and temperatures). Environmental issues include lack of control over environmental circumstances, such as food, air or water quality, housing, health, freedom or mobility. Stressors also include social problems, e.g., relationship conflict, deception or break ups, as well as major events such as birth, death, marriage and divorce.4-7

Stress and the Brain: Neural Communication Dysfunction

Understanding that the brain carries information about a stressful situation across various regions (from cortical sensory areas to more basal structures and vice versa) can help explain how stress and its negative consequences are heavily rooted in neural communication dysfunction. In order to illustrate how a stressful response is mediated, consider the basic hypothalamic-pituitary-adrenal axis (HPA).

The HPA axis is a multi-step biochemical pathway wherein information is transmitted from one body part to another through a chemical messenger system. The electromagnetic and electrochemical communications networks are also viable aspects of the total stress-response mechanism. Each regional pathway passes information forward, as well as receiving feedback from regional messengers, such that the system is self-regulating to enhance or suppress messages.

The initiation of the stress-response occurs in the hypothalamus. The hypothalamus links together the body's nervous and endocrine systems, with numerous bidirectional neural inputs and outputs from and to various brain regions. The connections regulate the hypothalamic capacity to secrete hormones into the bloodstream, having far-reaching and long-lasting effects on physiologic processes such as metabolism.

The hypothalamus may receive signals from the cerebral cortex, the limbic system or visceral organs. The limbic system is composed of several structures, including the amygdala (processor of emotions and modulator of stress responses, including fear and anxiety); the hippocampus (playing a role in memory formation, cognitive processes such as prior memories that influence suppression or generation of stress-response); the locus ceruleus (synthesizer of norepinephrine, which plays an important role in the sympathetic nervous system's fight-or-flight response to stress, and projects to the spinal cord); and the raphe nucleus (synthesizer of serotonin, which is involved with mood regulation, especially with depression and anxiety).

Of course, the spinal cord plays a critical role in transferring stress response neural impulses from the brain to the rest of the body. In addition to the neuroendocrine blood hormone-signaling system mediated by the hypothalamus, the spinal cord communicates with the rest of the body by innervating the peripheral nervous system. (PNS). Certain nerves that belong to the sympathetic branch of the CNS exit the spinal cord and stimulate peripheral nerves, which in turn engage the body's major organs and muscles in a fight-or-flight manner.

When the hypothalamus receives signals from one of the many branches about conditions that deviate from an ideal homeostatic state, e.g., alarming sensory stimulus, emotionally charged occurrence or energy deficiency, this is interpreted as the initiation step of a stress-response cascade. The hypothalamus then secretes corticotropin-releasing hormone targeted for the pituitary gland, via a short blood vessel system.

When corticotropin-releasing hormone binds, it causes the pituitary gland to secrete adrenocorticotropic hormone (ACTH) into the body's bloodstream. The pituitary gland releases various hormones that play significant roles in regulating homeostasis. When ACTH binds to the adrenal gland, a key messenger in the cascade is then released: cortisol (having widespread effects in the body).

Signaling to the hypothalamus from primary sensory and limbic structures ultimately provides cortisol for the restoration of homeostasis, by redistributing energy (glucose) to critical organs like the heart and the brain, and away from digestive and reproductive organs. After the alarming stimulus has ameliorated, cortisol is then inhibited by the pituitary and hypothalamus, thus shutting down the HPA axis stress response cascade (via feedback inhibition). While the foregoing stress-response mechanism is normal, when challenge is not overcome, this system becomes overtaxed, and this can be harmful to the body and brain. This is so because cortisol suppresses the body's immune system during a stressful situation.

While not a major risk if a negative stimulus is short lived, under chronic stress the body becomes more vulnerable to disease. This is a biologically negative consequence of an exposure to a severe stressor, and is interpreted as stress in and of itself; an inadequate adaptation to changes in homeostasis. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1). IL-1 is especially useful in combating some diseases, e.g., endotoxic bacteria. In certain cases the result is leukocyte redistribution to lymph nodes, bone marrow and skin. Stress may also predispose the body to viral diseases, e.g., influenza.

Chronic stress takes a more significant toll on your body than acute stress does. It can raise blood pressure, increase vulnerability to anxiety and depression, contribute to infertility, and even hasten the aging process. People undergoing stressful life events, such as marital turmoil or bereavement, have a weaker lympho-proliferative response.

After antigens initiate an immune response, white blood cells send signals, composed of cytokines and hormonal proteins, to the brain and neuroendocrine system. Cytokines are crucial in cellular signaling. Cortisol prevents the production of cytokines, e.g., IL-1, such that fewer receptors are produced on immune cells (so that inflammation cannot be ended); and wound healing is negatively impacted. Stress promotes the accumulation of visceral fat, which in turn may cause hormonal and metabolic changes that contribute to heart disease.

The list of negative consequences from chronic, unresolved stress is seemingly endless. Clearly, communications networks (e.g., electrochemical and electromagnetic, of homeostatic function), must be renormalized through various methodological approaches initially external to the organism's natural adaptive mechanisms. However, these methods will enable the body's natural mechanisms to preferably regain the advantage of self-renormalization.8-10


Editor's note: Part 2 of this article appears in the May 15 issue and focuses on managing stress and strain with chiropractic care and electromagnetic therapy. Part 2 contains a complete reference list for the citations featured in both parts.

April 2014
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