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Soy Lecithin and Development

Also see
PUFA and Development
Baby Formula, Soy, and Immunosuppression

Dev Psychobiol. 1985 Jan;18(1):59-66.
Effects of a commercial soy lecithin preparation on development of sensorimotor behavior and brain biochemistry in the rat.
Bell JM, Lundberg PK.
Pregnant rat dams and offspring were exposed to a 5 or 2% soy lecithin preparation or a control diet. Enrichment was either lifelong beginning at gestation, limited to the time preceding, or the time following weaning, or absent (constituting a “pure” control group). The most marked early sensorimotor deficits (reflex righting and swimming development) were seen in the 5% soy lecithin preparation group, although all soy lecithin preparation-exposed offspring had elevated brain/body weight ratios and choline acetyltransferase levels. Later, animals exposed to lifelong 5 or 2% soy lecithin preparations were hypoactive, had poor postural reflexes, and showed attenuated morphine analgesia. The results indicate that dietary soy lecithin preparation enrichment during development leads to behavioral and neurochemical abnormalities in the exposed offspring.

Dev Psychobiol. 1985 Sep;18(5):383-94.
Perinatal dietary supplementation with a commercial soy lecithin preparation: effects on behavior and brain biochemistry in the developing rat.
Bell JM, Slotkin TA.
Rats exposed perinatally to dietary commercial soy lecithin preparation (SLP) showed alterations in sensorimotor development and brain cell maturation. Latencies for righting responses (measured on postnatal Days 1-4) and negative qeotaxis (measured on postnatal Days 5-8) were shorter in the SLP treated animals. This pattern was accompanied by specific alterations in cerebellar development; biochemical markers for cellular maturation indicated a compression of the ontogenetic time course, as assessed by ornithine decarboxylase (ODC) activity, and levels of nucleic acids and proteins. In contrast, cellular development in the cerebral cortex indicated a generalized slowing of the time course of maturation and a deficit in the number of cells which persisted into adulthood. Behavioral abnormalities also did not disappear in adulthood, as morphine analgesia was markedly reduced in the SLP group. These results indicate that exposure of the fetus and neonate to dietary SLP during development leads to regionally specific alterations in brain cell maturation associated with disruption or behavioral patterns.

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