In addition, the researchers also found that this relatively minimal amount of exposure may lead to higher body fat among males, when compared to those who were not exposed to caffeine. Although the study was in mice, the biological cause and effect described in the research paper is plausible in humans.

According to Scott Rivkees, Yale's Associate Chair of Pediatric Research and a senior researcher on the study, "Our studies raise potential concerns about caffeine exposure during very early pregnancy, but further studies are necessary to evaluate caffeine's safety during pregnancy."

To reach their conclusion researchers studied four groups of pregnant mice under two sets of conditions for 48 hours. The first two groups were studied in "room air," with one group having been injected with caffeine and another injected with saline solution. The second two groups were studied under conditions where ambient oxygen levels were halved, with one group receiving caffeine and the other receiving saline solution. They found that under both circumstances, mice given caffeine produced embryos with a thinner layer of tissue separating some of the heart's chambers than the group that was not given caffeine.

The researchers then examined the mice born from these groups to determine what long-term effects, if any, caffeine had on the offspring. They found that all of the adult males exposed to caffeine as fetuses had an increase in body fat of about 20 percent, and decreased cardiac function of 35�� percent when compared to mice not exposed to caffeine.

"Caffeine is everywhere: in what we drink, in what we eat, in pills that we use to relieve pain, and even in candy," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal . "This report shows that despite popular notions of safety, there's one place it probably shouldn't be: in the diet of an expectant mother."

faseb/

Low-calorie diets, which have been shown to increase lifespan and delay age-related disorders in nonhuman primates and other organisms, altered the way fats were processed in the yeast cells.

The researchers assessed calorie restriction along with a number of known mutations that extend yeast lifespan against a variety of age-related changes in fat metabolism and lipid transport.

To determine whether the diet-aging mechanism could be manipulated by a therapeutic drug, Titorenko and his colleagues developed a life-span assay for a high-throughput screening of multi-compound chemical libraries.

The assay identified five groups of novel anti-aging small molecules that significantly delayed yeast aging by remodeling lipid dynamics in the ER, peroxisomes and lipid bodies or by activating stress response-related processes in mitochondria.

These small molecules can be used as research tools to investigate the mechanisms of longevity, says Titorenko, and as possible pharmaceutical agents for age-related disorders that affect lipid metabolism such as heart disease, chronic inflammation, and Type 2 diabetes.

ascb/