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14.1.1: Stress and Homeostasis

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    136468
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    All organisms, including humans, must maintain a baseline of normal functions within their cells, tissues, and organs to survive. This constancy of internal functions is referred to as homeostasis; however, homeostatic regulation may be challenged by a variety of both external and internal factors. These stimuli are referred to as stressors, exposure to which leads to a period in which there is a potential for the disruption of homeostasis. Within limits, all organisms have evolved certain physiological mechanisms to respond to stressors in an effort to maintain homeostasis. For example, some organisms, such as dogs, will develop a thicker coat of fur during cooler periods and they will shed this additional fur during warmer periods. This cyclical fur development linked to seasonal weather changes is but one way that these organisms maintain their homeostasis. The range of changes in the physiology (function), morphology (form), and/or behavior of organisms in response to their environments and the potential stressors of those environments is regulated by its phenotypic plasticity. A special case of phenotypic plasticity, polyphenism, is broadly defined as the ability of a single genotype within the organism to produce multiple phenotypes when exposed to different environmental conditions or stressors. Changes to the organism’s physiology, morphology, and/or behavior that are linked to its underlying phenotypic plasticity may result in changes that are merely temporary or those that are permanent. With respect to human phenotypic plasticity as well as evolutionary history, there are several primary mechanisms that have led to variations among individuals and between populations. These mechanisms, which are referred to as adjustments (behavioral, acclimatory, and developmental) and adaptations, are explained in detail in the following sections.


    14.1.1: Stress and Homeostasis is shared under a CC BY-NC license and was authored, remixed, and/or curated by LibreTexts.