Soy research is complicated because there’s considerable variation in isoflavone exposure among people classified as soy consumers. Agronomic factors (such as the soybean cultivar and the environmental conditions under which the crop grew) affect a food’s isoflavone profile, as does the way a soy food is processed. For example, soy protein concentrate produced by alcohol extraction may have only 12.5 milligrams (mg) total isoflavones per 100 g, in contrast to the nearly 199.0 mg total isoflavones per 100 g of full-fat roasted soy flour. Additionally, the fact that most of the isoflavones in food occur bound to sugar affects how they are digested.
Once genistin enters the digestive tract, it releases its sugar and becomes “free” genistein. Some of this free genistein is absorbed. However, most is reconjugated into glucuronides or sulfates, the primary circulating forms of genistein, which are thought to have either low or no biological activity. Only a very small amount of free genistein escapes conjugation by the liver and circulates in that form.
“People need to know that as it occurs in soy and other plant products, genistin is the compound that’s there. The amount of actual genistein is very low, one percent or less probably,” says Michael Shelby, director of the National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction (CERHR). Key exceptions are fermented products, such as miso and tempeh, which may contain up to 40% free genistein.
Several researchers say that figuring out the pharmacokinetics of genistin and genistein is a vital piece of missing information. “It’s a matter of finding out how much genistin is converted to genistein in the digestive system, and that information is not known,” says Jefferson. “I don’t think a lot of this was understood years ago when some of the animal experiments started, and at that time we didn’t have a clear understanding of the metabolism and fate of these chemicals. We did the best we could, as a community, to try to use the compound we thought would be the one we should look at. I think it’s given us some excellent starting types of data, where we know that these compounds are capable of causing reproductive and developmental effects.”
According to Thomas Badger, director and senior investigator at the Arkansas Children’s Nutrition Center in Little Rock, however, these effects are seen only under certain experimental conditions that are not likely to occur in humans—and therein lies the crux of the debate. Criticisms of many studies of genistein’s effects on reproduction and development have centered on exposure occurring by injection and consequently bypassing the usual metabolic pathways. There is also disagreement about the use of neonatal mice—commonly used in studies of reproduction and development—as a suitable model for predicting effects in human infants.
Despite these criticisms, Newbold stands by her data. “There was some confusion on the fact that in all of our work we have injected genistein,” she says. “We went back and did some of the pharmacokinetics with that to show that the total circulating amounts of genistein are very similar to what’s been reported in feeding rats and also in infants. Metabolism doesn’t have to be the same, but you have to know that the active compounds are getting to the target tissue. Ultimately, a mouse and a rat are not the human, though. You just have to accept it and be as careful with your extrapolations as possible.”
Soy research is complicated because there’s considerable variation in isoflavone exposure among people classified as soy consumers. Agronomic factors (such as the soybean cultivar and the environmental conditions under which the crop grew) affect a food’s isoflavone profile, as does the way a soy food is processed. For example, soy protein concentrate produced by alcohol extraction may have only 12.5 milligrams (mg) total isoflavones per 100 g, in contrast to the nearly 199.0 mg total isoflavones per 100 g of full-fat roasted soy flour. Additionally, the fact that most of the isoflavones in food occur bound to sugar affects how they are digested.Once genistin enters the digestive tract, it releases its sugar and becomes “free” genistein. Some of this free genistein is absorbed. However, most is reconjugated into glucuronides or sulfates, the primary circulating forms of genistein, which are thought to have either low or no biological activity. Only a very small amount of free genistein escapes conjugation by the liver and circulates in that form.“People need to know that as it occurs in soy and other plant products, genistin is the compound that’s there. The amount of actual genistein is very low, one percent or less probably,” says Michael Shelby, director of the National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction (CERHR). Key exceptions are fermented products, such as miso and tempeh, which may contain up to 40% free genistein.Several researchers say that figuring out the pharmacokinetics of genistin and genistein is a vital piece of missing information. “It’s a matter of finding out how much genistin is converted to genistein in the digestive system, and that information is not known,” says Jefferson. “I don’t think a lot of this was understood years ago when some of the animal experiments started, and at that time we didn’t have a clear understanding of the metabolism and fate of these chemicals. We did the best we could, as a community, to try to use the compound we thought would be the one we should look at. I think it’s given us some excellent starting types of data, where we know that these compounds are capable of causing reproductive and developmental effects.”According to Thomas Badger, director and senior investigator at the Arkansas Children’s Nutrition Center in Little Rock, however, these effects are seen only under certain experimental conditions that are not likely to occur in humans—and therein lies the crux of the debate. Criticisms of many studies of genistein’s effects on reproduction and development have centered on exposure occurring by injection and consequently bypassing the usual metabolic pathways. There is also disagreement about the use of neonatal mice—commonly used in studies of reproduction and development—as a suitable model for predicting effects in human infants.Despite these criticisms, Newbold stands by her data. “There was some confusion on the fact that in all of our work we have injected genistein,” she says. “We went back and did some of the pharmacokinetics with that to show that the total circulating amounts of genistein are very similar to what’s been reported in feeding rats and also in infants. Metabolism doesn’t have to be the same, but you have to know that the active compounds are getting to the target tissue. Ultimately, a mouse and a rat are not the human, though. You just have to accept it and be as careful with your extrapolations as possible.”
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