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Proceedings for Pain Management and Humane Endpoints

Arriving at a Biological Definition of Stress and Distress

Gary P. Moberg, PhD
Stress Research Unit, Department of Animal Science, University of California, Davis

We are well aware of the effects that stress has on the individual. Stress contributes to the development of infectious diseases, occurrence of heart disease, reproductive failure and psychological distress (Moberg, 1985). All negatively impact the quality of an individual's life, or its well-being. While we recognize that stress acts upon the individual and the consequences of severe stress, we still lack an understanding of what biologically differentiates stress from distress. There is nothing wrong with stress per se; stress is part of life. It is only when the burden of stress becomes so great that it negatively impacts an individual's well-being, that the animal suffers from distress. Our challenge is to identify biological indicators of when stress becomes distress (Moberg, 1987a; 1996).

In an effort to find biological indicators of distress, we have developed a model of animal stress to provide a framework for focusing our ideas about what constitutes distress. Since the detailed arguments for this model have been presented elsewhere (Moberg, 1985; 1987b), the focus of this discussion will be on those elements of the model that are relevant to identifying distress. The first step in the stress response is initiated by the central nervous system's recognition of a threat to homeostasis. Once this threat (or stressor) is perceived, the central nervous system organizes a biological defense. This defense consists of four general categories of biological response: behavior, the autonomic nervous system, the neuroendocrine axis and the immune system. Behavior provides the first line of defense and is, undoubtedly, the most biologically economical response. An individual may be able to simply remove itself from the stressor. The autonomic nervous system and the neuroendocrine system modulate many of the biological functions that are known to be severely impacted by stress; such as reproduction, immune competence, and metabolism (Moberg, 1985). It is the response of these two systems that may be most responsible for the undesirable changes in biological function associated with stress. Recently, we have come to recognize the significance of the immune system's separate response to stress and the implication for the health of the individual. Together, these four categories of responses constitute the biological defenses available to the animal for dealing with a stressor and are responsible for the biological changes, both desirable and undesirable, that occur during an animal's attempt to cope with stress.

In searching for indicators of distress, simple measurement of these defense responses would seem appropriate. But, there are several factors that prevent these four responses from serving as appropriate measures of distress. First, these systems respond to mild stressors that do not push an animal into a state of distress. In addition, there are a variety of modifiers that alter how each of these biological systems responds. Examples of such modifiers are experience, genetics, age and physiological state of the animal (Moberg, 1985). These modifiers influence not only perception of a stressor, but also influence the actual organization of the response (for a detailed discussion see Moberg, 1985). As a result, these modifiers make it difficult to rely on one simple measurement of these systems (such as increased concentrations of circulating glucocorticosteroids or expression of certain behaviors) as an indicator of distress. Because of these individual differences in the stress response, we must consider the next stage of the stress response for a clue as to when an animal enters distress.

Regardless of the combination of biological defenses the individual chooses in its response to a stressor, the result is a shift in the animal's normal biological function. That is, whatever the animal was doing prior to experiencing the stressor, once the stress occurs there is a change in biological function as the individual attempts to cope with the stressor. In most cases, this altered biological function has a minimal effect on the animal's well-being. Either the stressor is eliminated, or when the stressor is of brief duration, biological function soon returns to normal. As a simple example: during stress catecholamines mobilize stored glycogen providing the needed energy to deal with the stress. This response is followed by the secretion of glucocorticosteroids whose role is to induce gluconeogenesis needed for replenishing glycogen stores. For most stressors, such a response is relatively brief and non-threatening to the animal. Only when the stressor is not alleviated or if the stressor is of sufficient magnitude, is biological function so altered that the individual enters into a prepathological state. During the prepathological state, the individual is at risk of developing a pathology (Moberg, 1985, 1996), it's well-being is threatened and it can be argued that the individual is in distress.

One simple approach to identifying distress would be to observe whether the animals become sick or die, but such endpoints are unacceptable. Instead, a more reasonable approach would be for us to focus on the changes in biological function that result in the development of a prepathological state (Moberg, 1993a,b; 1996). Examples would be any suppression of immune competence that may lead to disease, any suppression of gonadotropin secretion that would prevent ovulation, or stress induced suppressions of normal growth. Each of these events can occur during severe stress and are clear indicators of distress.

Distress occurs when the stress is of such magnitude or duration that significant changes in biological function must occur for the animal to survive. Returning to the example of changes in metabolism during stress, a severe stressor would result in significant changes in metabolism as part of the biological attempt to provide the needed energy to cope with the stressor. Under such conditions, the biological cost could be so great, that the animal can not retain normal (i.e., pre-stress) function. Even if the stressor is eliminated, there will be an additional period of recovery before metabolic function would return to pre-stress status. In a growing animal, the result of such a stress response would be the failure of the animal to grow normally. I would argue that under such conditions, the animal is distressed. The biological cost of the stressor has shifted biological function sufficiently to enter a prepathologic state, which in turn results in the pathology of abnormal growth and the animal's well-being is threatened.

If we return to our model of stress, we see that in recognition of a threat to homeostasis, the individual mounts a biological defense consisting of a combination of four general biological responses: behavioral, autonomic, neuroendocrine, and immunological. The nature of this biological response varies between individuals. What is important is that the response alters biological function to cope with the stressor. This is the stress response, and this alteration of biological function is the consequence of the stress. For most stressors this change is minor, however, if the stress is of sufficient magnitude or duration, the individual is forced into a prepathological state which makes that individual vulnerable to pathology, whether this pathology is disease, abnormal behavior, reduced growth or some other type of undesirable shift in biological function. If we look for indicators of distress, we believe that those changes in biological function that lead to the development of the prepathological state are the key to identifying distress. The challenge for us is to develop measures of the prepathological state which will provide us indicators of an animal that is suffering from distress.


  • Moberg, G. P. (1985). Biological response to stress: key to assessment of animal well-being? In Animal stress (Ed. Moberg, G. P.) American Physiological Society, Bethesda, Maryland. 27-49.
  • Moberg, G. P. (1987a). Problems in defining stress and distress in animals. J. Am. Vet. Med. Assoc. 191:1207-1211 Moberg, G. P. (1987b). A model for assessing the impact of behavioral stress on domestic animals. J. Anim. Sci. 65:1228-1235.
  • Moberg, G.P. (1993a). Using risk assessment to define domestic animal welfare. J. Agri. and Envi. Ethics. 6 (Spec. Supp. 2):1-7.
  • Moberg, G. P. (1993b). Developing management strategies to reduce stress in swine: a new approach utilizing the biological cost of stress. In Proceedings of the Australasia Pig Science Association, Vol. 4. (Ed. by Batterham, E.S.), Australasia Pig Science Association. Attwood, Australia. 116-126.
  • Moberg, G. P. (1996). Suffering from stress: an approach for evaluating the welfare of an animal. Acta Agri. Scan., Sect. A, Ani. Sci. Supp. 27: 46-49.

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