Stress

Effects of Genetics, Gender, Age, and Previous Stressor Exposure
by National Institute of Health

(Page 4 of 6)

Genetic Differences

Both the psychological and physiological responses to a given stressor may vary greatly between individuals, thereby influencing the type of pathology to which a person is vulnerable. Such vulnerability may be influenced by genetic factors.

In mice and rats, behavioral, hormonal, immunological, and neurochemical effects of a given environmental stressor may differ significantly between different genetic strains. For example, some rodent strains exposed to a stressor may display marked HPA alterations or variations of brain neurotransmitter levels, whereas other strains may display fewer or less profound effects. Similarly, the same stressful event may induce opposite effects on certain aspects of immune functioning in different rodent strains. Rather than regarding such interindividual or interstrain variations as a "noise factor," the experimenter can use them to help identify both the factors that predict the response to a stressor and the occurrence of a pathological state related to the stressor.

Individual or genetic differences in the stress response may indicate either an overall increase of reactivity or a highly specific increase in the reactivity of a particular biological system. Similarly, alterations of transmitter function in one brain region, or alterations of one aspect of immune functioning, do not suggest similar alterations in other brain regions or in other aspects of immunity. Interindividual differences in the fragility of different biological systems may determine why a stressor increases the vulnerability to a particular pathology in one individual but a different pathology in another individual. In addition, if the organism is endowed with increased vulnerability to stressor effects on neurochemical processes as well as increased genetic vulnerability to a particular pathology, then the stressor would be expected to increase the risk for this particular pathology. In the case of alcoholism, genetic factors favoring increased alcohol intake, coupled with an inherited disposition toward excessive stressor reactivity or inappropriate coping styles, could potentially contribute to alcohol abuse.

Gender

Data concerning gender-dependent effects of stressors are relatively limited, although researchers have found that the HPA response to stressors is greater in female rats than in male rats. This effect appears to occur at almost every level of HPA functioning, and the responses, to some extent, are regulated by interaction among the hypothalamus, pituitary gland, and gonadal organs. Such factors may contribute to the gender differences often seen with respect to some behavioral disturbances (mood disorders), but the contribution of these factors to AOD consumption is not yet clear.

Age

In humans, the age-dependent effects of stressors intertwine with numerous psychosocial factors (reduced physical abilities; financial constraints; and loss of coping resources, social support, and psychological flexibility). Animal studies further suggest that certain neurochemical systems that are sensitive to stressors react differently in aged compared with young individuals. In aged rats, stressor-provoked neurochemical alterations are induced more readily than in young rats, and the return to basal levels of neuronal functioning requires a relatively sustained period of time. Theoretically, stressors should generate rapid neurochemical responses that readily normalize upon stressor termination. Thus, the sustained neuronal activation of aged animals may reflect a lack of adaptability of functioning. Aged animals might therefore be more vulnerable to stressor-provoked pathology. In humans, where aging is frequently associated with reduced coping abilities or opportunities (owing, for example, to diminished social supports following loss of friends and loved ones, reduced physical abilities, and possibly financial concerns), the effects of stressors on pathological processes may be particularly marked. Given that developmental, social, and cultural factors influence not only stressor perception but also individual coping styles. Ultimately, such variables probably contribute to pathological states and should be considered in relating stress to alcoholism.

Similar to an aged animal, however, a very young organism may lack or may not have developed the behavioral and neurochemical repertoire to cope with stressors effectively and thus may be at increased risk for pathology. As discussed shortly, stressors in young animals may act to program (or reprogram) neuronal functioning to increase vulnerability to neurochemical disturbances encountered later in life.

Effects of Prior Life Events or Stressor Exposure

Sensitization. Stressful events not only have marked immediate effects but also may influence one's response to later stressor experiences. Such a sensitization effect may be responsible for the high rates of relapse associated with psychiatric disorders, such as depression. Studies in animals have indicated that exposure to stressors typically induces physiological changes that persist for a relatively brief duration. However, if animals are reexposed to the same stressor at a later time, then the neurochemical changes in the brain occur more readily. Such effects have been noted with respect to several neurotransmitters, but particular attention has been devoted to the analysis of norepinephrine and dopamine. Interestingly, these effects have not only been observed when the reexposure session involves the same stressor, but also when it involves an entirely different stressor. Furthermore, such crosssensitization effects have been witnessed between processive stressors and drug treatments. Thus, treatment with amphetamine or cocaine may enhance the response introduced by subsequent exposure to a stressor.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.