This is the first study to provide evidence that an environmental influence - in this case diet - can affect the heart. It will also force researchers to rethink the diets of their laboratory mice. The results appear in the Journal of Clinical Investigation.
Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disease occurring in 1 in 500 individuals, and is characterized by shortness of breath, chest discomfort, and palpitations that may be a sign of life-threatening arrhythmias. While mutations in a number of genes have been linked to HCM, the variety of symptoms experienced by sufferers suggests that other genetic or environmental factors affect disease prognosis.
For years, soy-rich diets have been speculated to protect against heart disease. The biological consequences of a soy-diet have been attributed to the presence of phytoestrogens, which are plant-derived estrogen-like compounds that interact with the estrogen receptor. Leslie Leinwand and colleagues examined male and female mice that overexpressed a mutant form of the alpha myosin heavy chain gene, which is one known cause of HCM in humans. The researchers found significant growth (known as hypertrophy) of the heart of male mice fed a soy-based diet, in comparison to male and female mutant mice fed a soy-free diet.
The authors propose that the difference observed between the sexes is based on the fact that the female mice, who are constantly exposed to naturally circulating levels of estrogen compounds, are less sensitive than males to the change in estrogen level as a result of the soy diet. Interestingly, the authors observed a significant improvement in cardiac growth and function when the animals were switched to a soy-free diet. The new data provide a strong link between soy diet and the progression of cardiac disease, in mice.
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Potential causes of esophageal adenocarcinoma were identified by Mayne and her colleagues in a previously completed population-based, multi-center study of 1,095 cancer patients and 687 control subjects. As part of that study, they conducted a full dietary interview and had access to available data on consumption of both regular and diet soft drinks.
"Our team analyzed that data as the first direct test of the hypothesis that soft drinks might have contributed to the increase in this cancer," said Mayne. "We found that contrary to the hypothesis put forth by other researchers, carbonated soft drink consumption was inversely associated with esophageal adenocarcinoma risk, mainly attributable to diet soda, and that high intake did not increase risk of any esophageal or gastric cancer subtype in men or women."
Other Yale authors on the study included Harvey Risch, principal investigator of the grant that supported the work, Robert Dubrow, and Mayne's former student, Lauren Borchardt. Authors from other centers included Wong-Ho Chow, Marilie D. Gammon, Thomas L. Vaughan, Janet B. Schoenberg, Janet L. Stanford, A. Brian West, Heidi Rotterdam, William J. Blot and Joseph F. Fraumeni, Jr.
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