Plant-based fats may cut the risk of prostate cancer by reducing the levels of both testosterone and certain enzymes that metabolize testosterone into more active forms, a new study by University at Buffalo nutrition researchers has shown.
The study, published recently in the Journal of Nutritional Biochemistry, reported that feeding rats a diet rich in phytosterols, the type of fat found in plants, reduced testosterone in the blood stream by 33 percent. A high level of testosterone has been implicated as a risk factor for developing prostate cancer.
The levels of two enzymes — 5-a reductase and aromatase — that metabolize testosterone into end products that also are implicated in the development of prostate cancer were reduced by 44 percent and 55 percent respectively, results showed.
Lead researcher Atif Awad, Ph.D., director of UB’s Nutrition Program, and colleagues have been trying to understand the mechanisms responsible for vegetarians’ lower rates of hormone-dependent cancers, and for the lower mortality rate from prostate cancer in Asian countries, where populations eat little meat. Awad is an associate professor in the Department of Physical Therapy, Exercise and Nutrition Sciences in the UB School of Health Related Professions.
With fats known to play a role in the development of several cancers, Awad’s group has been focusing on the phytosterols for possible answers. He reported at an international conference on cancer research in Greece last October that the phytosterol B-sitosterol appears to play a role in inhibiting the growth of human prostate-cancer cells by strengthening an intracellular signaling system that inhibits cell division. (See previous news release, “PLANT-BASED FAT INHIBITS CANCER-CELL GROWTH BY ENHANCING CELL’S SIGNALING SYSTEM, UB RESEARCHERS SHOW,” at .)
The objective of the current study was to examine the influence of vegetable fats on the metabolism of testosterone in liver, testis and prostate tissue in rats.
The fact that prostate cancer doesn’t develop in men castrated before puberty or in men who have low levels of 5-a reductase suggested to Awad’s group that suppressing the action of the enzyme might be useful in preventing prostate cancer in high-risk groups. The enzyme aromatase converts testosterone to estrogen, also considered a possible risk factor for prostate cancer.
To determine if high levels of phytosterols could inhibit these enzymes, the researchers fed one group of rats a standard, or basal, diet. A second group, designated the control group, ate the standard diet plus cholic acid, which stimulates the absorption of vegetable fats. A third group ate a standard diet enhanced with a mixture of phytosterols, plus cholic acid. The trial lasted 22 days.
Results showed that rats fed the phytosterol diet had between 33 and 48 percent less testosterone than the animals that received no additional phytosterols. There was no difference in serum testosterone levels between the basal and control groups.
The enhanced diet reduced the activity of 5-a reductase by 44 percent in the liver and by 33 percent in the prostate, but did not affect the enzyme’s activity in the testis, results showed. Phytosterols reduced the activity of aromatase by 57 percent in the prostate, but had no effect in the liver or testis.
Awad said his research team continues to examine exactly how phytosterols bring about these changes, but he believes one pathway involves the “fluidity” of membranes that harbor the enzymes. “Every enzyme requires a specific fluidity in the membrane in which it resides in order to be activated,” he said. “If the membrane is too fluid, the enzymes may not function properly.”
Other options include the possibility that phytosterols compete with testosterone and its products of metabolism for the enzyme’s active receptors, or that they reduce production of the enzymes themselves.
“At any rate, the combined effect of reducing levels of testosterone and the activity of its two main enzymes suggests that a diet high in foods containing phytosterols could help reduce the risk of prostate cancer,” Awad said.
Additional researchers on the study were Maria Sri Hartati, a master’s degree student, and Carol S. Fink, Ph.D., UB clinical assistant professor of nutrition.
The research was supported by a grant from the Allen Foundation.
ScienceDaily (Feb. 25, 1999