This is a review of biological stress from interviews with UC Berkeley’s Department of Integrative Biology professors, Dr. Michael Shapira and Dr. George Bentley, for Berkeley Scientific Journal’s 18^th volume. The information below summarizes what I learned not only from talking with the researchers but also from the pre-interview preparation. Combined, of course, with what I felt were the big picture “take home” points that would (on the most part) overlook the molecular biology, but instead focus on larger concepts and implications of how stress can affect biological systems.

Acute Stress vs. Chronic Stress

Exposure to acute stress, a response to a single traumatic event, highlights a paradox that is vital to how we have evolved and to our day-to-day lifestyle. Biologically speaking, the immediate response is a suppression of the immune system due to the anti-inflammatory effects of the hormones involved. One would believe that this seems rather counter-intuitive because we are suppressing a system that would be useful in cases of wound healing. This is the very essence of acute stress’ adaptive effects on the immune system through evolution! The mechanism allows for a compromise between immunosuppression and susceptibility to infectious diseases because instant inflammation, an instant immune response, would leave the organism exposed and prevent healing of the wound.

This beneficial adaptive stress response is lost in chronic stress (the continuous exposure to acute stress) because the need for being constantly prepared for pathogen exposure inevitably takes its toll on the body’s ability to maintain important metabolic pathways. Chronic stress overtime dampens the stress responses and the potentially beneficial effects of acute stress are lost due to this repetition. Thereby, a pro-inflammatory response ensues that also leads to slower wound healing. Chronic activation of these stress hormones prevents the proper flow of mechanisms that organisms have developed throughout evolution to counter instances of acute stress.

The Model Organism

Professor Shapira summed it up rather nicely for us: “C. elegans is one of the best models to study [immune responses due to stress] … because many of the mechanisms characterized in them are also found to be very important for mammals.”

Caenorhabditis elegans (C. elegans) serves as the classic model organism for investigation into the interplay between stress and immunity. Professor Shapira defines it as a “step towards the ‘real world’ of multicellular organism” whose multi-tissue physiology can serve to provide greater knowledge.

Researchers can decrease the expression of any gene of interest to examine its function. Additionally, a lack of circulatory system is accounted for by a very impressive nervous system that is in charge of maintaining the important metabolic pathways. For the above reasons, C. elegans serve as the model organism because they essentially are a middle ground between the well-defined genetically tractable model and a complex organism. Therefore, genome scale responses are easily accessible!

Effects of Stress on Reproduction

How stress and immunity play a significant role in biological systems is well demonstrated by their effects on reproduction. The trade-off lies between maintenance of life and production of offspring. Organisms have adapted through time to turn off reproductive potential during stress in order to sustain themselves and cope with the stress.

If reproduction is halted, there is a greater investment in maintenance. But it is important to realize that the strength of natural selection decreases as we age and consequences of stress appearing past the reproductive age have no effect on fitness. And it if for this reason that species have tended to select for mechanisms that are beneficial at the beginning of life, even if they might be bad later on!

This is observed in the reproductive cycle of worms. If conditions are not favorable (starvation-stress), worms will leave the normal developmental course leading to reproduction.

In birds, a principle hormone that is activated by stress inhibits reproductive physiology in mammals!

Based on Professor Bentley’s research, what you see on the ‘SPRING’ histograms is that the hormone is produced abundantly in stressed animals. This, as already seen in worms, is an adaptive response because animals under such stressors want to direct physiological resources and energy towards metabolic demands that help them deal with stress rather than waste them on reproductive efforts.

The difference, or rather the lack of a difference, in the hormone level response at the end of the breeding season, ‘FALL’,  is best explained by the systematic increase of the hormone during the non-breeding season to focus on other aspects of maintenance. Therefore, no increase is detected during this time period because they are already maxed out.

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