The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of the metabolic syndrome, result from the effects of poor nutrition in early life. The present review however, considers an opposite explanation. We hypothesize that fetal over-nutrition plays a major role in the development of the metabolic syndrome. We found evidence that the thrifty phenotype may be the consequence of fetal hyperglutamatemia. Maternal glutamate (GLU) reaches the fetal circulation, as part of the materno-fetal glutamine-glutamate exchange. Glutamine is absorbed from the maternal circulation, and deaminated for nitrogen utilization, resulting in a fetal production of GLU. GLU is extracted as it returns to the placenta. When the umbilical plasma flow is low, GLU may be trapped in the fetal circulation, and reaches neurotoxic levels. Administering GLU to newborn rodents completely destructs arcuate nucleus neurons, and results in permanently elevated plasma leptin levels that fail to adequately counter-regulate food intake. Chronic fetal exposure to elevated levels of GLU may be caused by chronic maternal over-nutrition or by reduced umbilical plasma flow. We strongly suggest abandoing the flavoring agent monosodium glutamate and reconsidering the recommended daily allowances of protein and amino acids during pregnancy.