CB 7504 Raleigh, NC 27695
(919) 515-3470 phone
(919) 515-2556 fax
[email protected] http://www.ncsu.edu/news
Media Contact:
Sara Frisch, News Services, 919/515-3470 or [email protected]
May 26, 1999
NC State Professor Finds Possible Link Between Stress, Prostate Disease
FOR IMMEDIATE RELEASE
RALEIGH, N.C. -- Research at North Carolina State University is shedding new light on the relationship between stress and prostate disease. Scientists have begun characterizing the link between stress and increased inflammation of the prostate gland, a medical condition known as prostatitis. The missing piece could be the hormone prolactin, released by the body during stress and now believed to increase inflammation in the prostate.
Using lab rats with mild cases of prostatitis, veterinary pharmacologist and toxicologist Dr. C. Lee Robinette and a lab assistant showed that stress causes rats to produce higher levels of prolactin and to suffer sustained prostate inflammation.
Results of the study were presented at the Experimental Biology '99 meeting in Washington, D.C., in April. Robinette's co-author was Toni Weber, a research apprentice from a Raleigh-area high school at the time of the study and now a student at the University of North Carolina at Wilmington.
The findings suggest that stress may make prostatitis worse by causing the body to make more prolactin than usual. For adult men who suffer from inflamed prostates each year, this news could help doctors identify contributing factors and develop more effective treatments.
It's well-documented that stress induces prolactin release in both rats and humans, says Robinette. "Some human males who have chronic abacterial prostatitis indicate that their symptoms seem to become worse during periods of stress." But doctors don't know much about this form of prostatitis, and they don't agree on where it comes from, Robinette says. "Chronic prostatitis is the least studied and least understood of the major human prostate diseases."
Robinette, an associate professor at NC State's College of Veterinary Medicine, hopes his findings about prostatitis in rats will advance our understanding of the human condition. He says the extent to which the rat models human prostatitis is unknown. But, he says, the rat's lateral prostate lobe, which is most susceptible to inflammation, has similar origins to the areas of the human prostate that often become inflamed or cancerous.
In previous studies, Robinette had concluded that the hormone estradiol causes prostate inflammation in rats, and that prolactin was responsible for mediating this response. With the documented knowledge that stress induces prolactin release, he set out to explore the link between stress, prolactin and inflammation of the prostate.
Male rats were given short-term exposure to estradiol implants to induce mild cases of prostatitis. Then, researchers restrained the rats to stress them mildly. The rats endured 15-minute intervals of restraint stress twice daily, five days a week, for four consecutive weeks.
The restrained rats showed a two-fold increase in prolactin immediately after being stressed, Robinette says. The restraint also led to a greater degree of prostatitis, measured by discoloration and the number of inflammatory cells in the prostate gland. Most of the unstressed rats had a major resolution of their prostatitis symptoms during the same period.
Robinette says prolactin is likely to be the key link between stress and prostatitis, but further study is necessary to prove the link definitively. "We hope in future studies to show that if we block that stress-induced prolactin release, we also block the ability to sustain prostatitis," he says.
Meanwhile, the National Institutes of Health recently began its first major study on men with chronic prostatitis, and stress will be one of many factors doctors examine in the study.
--frisch--
NOTE TO EDITORS: Dr. Robinette is available to speak with reporters about the study. For assistance reaching him, contact Sara Frisch at NC State News Services at (919) 515-3470 or [email protected]. Following is Robinette's abstract from the presentation at Experimental Biology '99.
"Restraint Stress Sustains Hormone-induced Prostatitis in the Rat Lateral Prostate" Authors: C. Lee Robinette and Toni M. Weber, NC State University Presented at Experimental Biology '99, Washington, D.C., April 1999
ABSTRACT: Previous studies from this laboratory (Endocrinology 132:2407-2416,1993) have demonstrated that a profound inflammation can be induced in the rat lateral prostate by estradiol-17B (E2) and that this response is mediated by prolactin (PRL). Since restraint stress is known to stimulate PRL release, the purpose of this study was to determine if this type of stress could sustain E2-initiated prostatitis in the rat.
Prostatitis was induced in castrated, sexually mature, male Wistar rats by placing an E2 implant under the skin for one week. At the beginning of week 2, the E2 implant was removed and a dihydrotestosterone implant was placed subcutaneously to restore prostate wet weight. Periods of restraint lasting 15 minutes were administered Monday-Friday in the morning and afternoon during weeks 3-6. Control rats were similarly treated except that they were removed from and immediately returned to their cages in lieu of being restrained.
Rats subjected to restraint showed a greater degree of prostatitis and a higher level of serum PRL than did the unstressed controls. The inflammation, which consisted primarily of intraluminal neutrophils and stromal lymphocytes, was specific to the lateral prostate lobe. The rat thus provides a model for further characterizing the response of prostatitis to stress and its associated increases in serum PRL. Furthermore, these findings also set the stage for studies on the relationship between stress and prostatitis in humans where stress has been suggested to be a factor that contributes to chronic prostatitis problems.
###