Scientists at the Weizmann Institute prevented the onset of eating disorders through dietary intervention.
A new study by scientists at the Weizmann Institute of Science, published in the journal Cell Metabolism, establishes, for the first time, a clear causal link between prenatal stress and the onset of eating disorders. Furthermore, in a study in mice, researchers successfully prevented the onset of a compulsive eating disorder by the sole means of a unique diet.

Moderate exposure to stress during pregnancy is not necessarily negative. The effect of stress on the fetus makes evolutionary sense with regard to survival – by providing mothers with a way to communicate with her unborn offspring about the world into which they are about to emerge. For example, when the mother inhabits an area of poor food availability, she would want to prompt the embryo to develop its body in an efficient and frugal manner and slow down its metabolic rate. Such maternal messages transmitted to the embryo are also termed fetal “programming.” Problems arise when the “programming” does not match actual conditions and demands; for example, a child who is “programmed” to slow metabolism down but is actually born into a culture with an abundance of high calorie foods, may develop obesity and metabolic syndrome.

Prof. Alon Chen and his team in the Neurobiology Department used a genetic system they developed to simulate the biological stress mechanisms in mice. The findings were clear: females born to mothers exposed to stress during pregnancy tended to develop a compulsive eating disorder following exposure to the environmental challenge. The study was led by postdoctoral fellow Dr. Mariana Schroeder, with the participation of Drs. Maya Sharon Lebow, Yonat Drori and Mira Jakovcevski; research students Tamar Polacheck and Mareen Engel; and Dr. Shifra Ben–Dor from the Department of Life Sciences Core Facilities.

Beyond identifying the link between stress during pregnancy and compulsive eating disorder, the research team sought to understand and uncover the mechanisms through which the brains of those females who tended to develop an eating disorder were programmed. They repeated the experiment, but instead of waiting for the offspring to reach adulthood, they examined the embryonic brain prenatally. Chen: “We discovered a very interesting thing: Looking at embryos’ brains, we saw large molecular differences between offspring whose mothers’ stress mechanism was activated and those in whose mothers it was not activated. However, in adulthood, the differences disappear. The differences will be expressed only when the mice are exposed to some form of challenge. This signifies that an epigenetic, rather than a genetic, marker was introduced at the embryonic stage as there was no change in the genes.”

Epigenetics (literally: on top of genetics) research addresses the molecular mechanisms that mediate environmental messages and how these messages influence and shape our genome’s expression – without changing the genes themselves or the DNA sequence. In this case, messages that originated in the mother caused changes in the brains of the female embryos. One of the most important epigenetic mechanisms is DNA methylation, a simple biochemical process in which a methyl group binds to a genetic segment, thereby determining the transcription level of a particular gene. In this research, scientists have shown, for the first time, that exposure to stress is expressed in sub–methylation in the hypothalamus, a brain region that regulates metabolic processes, hormone production, and stress reactions. But the most surprising part of the study lay ahead. The researchers found that by administering a diet of foods that affect the body’s methylation processes, such as folic acid, choline, methionine, and vitamins B12 and B6, they could prevent the ”predisposed” mice from developing a compulsive eating disorder.