Does a Mold Toxin Increase Testicular Cancer?
A Wake Forest University cancer researcher, Dr. Gary G. Schwartz, has proposed that a compound found in certain foods may be a cause of testicular cancer in young men proposes that exposure to a common carcinogen called ochratoxin A during childhood or even before birth may set up the testes so that testicular growth during puberty triggers the launch of testicular cancer.
Ochratoxin A results from molds that grow in grains and coffee beans and is found in animals that consume moldy grain, especially pigs. "Little is known about the etiology of testicular cancer, which is the most common cancer among young men," said Schwartz, associate professor of cancer biology and public health sciences. It strikes men mostly between 14 and 34. He said that epidemiologic data point to exposure either in the womb or early in life, "but the nature of the exposure is unknown." Schwartz's new theory calls for a process that takes several steps.
It begins with exposure to ochratoxin A during pregnancy or early childhood, which induces damage to testicular DNA. Ochratoxin A is transferred through the placenta to the fetus, and also is present in mothers' milk, so infants could be exposed through breastfeeding. The DNA changes remain dormant until testicular growth at puberty promotes these changes in testicular DNA into cancer. Testicular cancer is primarily a disease of young white men, and it shows marked geographic variation. For instance, the incidence is higher among northern Europeans than central or southern Europeans.
Schwartz noted that grains grown in northern Europe are more likely to be contaminated because weather conditions during harvest season promote mold. The highest rate in Europe is in Denmark, 7.8 cases per 100,000 per year. Consumption of pork products in Denmark is among the highest in the world, and Danes also eat the most rye, the cereal grain that is most often contaminated by ochratoxin A.
Another interesting element: testicular cancer is more common among people of higher socioeconomic levels. These are the groups most likely to breastfeed. "We propose that exposure to ochratoxin A contaminated food provides a coherent explanation for much of the descriptive epidemiology of testicular cancer," Schwartz said, adding that future studies of testicular cancer "should focus on breastfeeding practices and the consumption of ochratoxin A containing foods such as cereals, pork products, milk and coffee by mothers and their male children." If all this turns out to be correct, Schwartz offers several possible solutions.
Public health efforts may be able to reduce exposure to ochratoxin A. Alternatively, public health efforts may reduce the genotoxicity of ochratoxin A exposure. The toxicity of ochratoxin A could be reduced by giving pregnant women drugs like aspirin or indomethacin or vitamins A, C and E, he said. "These agents, in animals at least, markedly reduce the DNA damage caused by ochratoxin A," Schwartz said. Aspartame, the artificial sweeter, is similar structurally to ochratoxin A, and is a potent ochratoxin A antagonist.
Gary G. Schwartz, Ph.D., M.P.H., Cancer Causes and Control February / 2002 Wake Forest University Baptist Medical Center
My Thanks to This Helpful Researcher,