from where i sit, not surprisingly it all comes back to zinc as a lowest common denominator of sorts. maternal zinc status informs whether or not you have congenital malformations, for starters:
Congenital Malformations Resulting from Zinc Deficiency in Ratshttp://ebm.rsmjournals.com/content/123/3/692.abstract
A mild but specific zinc deficiency was produced in female rats by the use of a purified diet lacking the element and by stringent elimination of sources of zinc contamination from the environment. Almost all of the full-term fetuses produced under such conditions showed gross congenital malformations encompassing a wide variety of organ systems, including skeletal, brain, eye, heart, lung, and urogenital defects
. The fetuses from zinc-deficient females contained less zinc than did their controls, suggesting that the congenital anomalies resulted from a direct effect of lack of zinc in the fetal tissues.
Congenital malformations of the central nervous system in rats produced by maternal zinc deficiencyhttp://onlinelibrary.wiley.com/doi/10.1
Teratogenic effects of maternal zinc deficiency in rats have been observed, confirming previous reports. The deficient diet differed in several respects from that used by Hurley and coworkers but the results were essentially the same. Special attention was given to malformations of the central nervous system and to tissue anomalies not recognizable by gross inspection of the fetuses
Maternal zinc status: a determination of central nervous system malformationhttp://onlinelibrary.wiley.com/doi/10.1
Maternal serum zinc concentrations were estimated during 244 normal pregnancies and 15 abnormal pregnancies. The serum zinc concentrations were lower in the anencephalic pregnancies than in the normal control subjects.
going forward zinc levels help determine genetic expression based on predisposition, zinc levels help determine susceptibility to infection by bacteria and viruses, etc.:
Possible roles of zinc nutriture in the fetal origins of diseasehttp://www.sciencedirect.com/science/ar
Risk of diseases of metabolism such as atherosclerosis and adult onset diabetes mellitus is increased by fetal malnutrition. Deficiencies of micronutrients essential for methylation are believed to contribute to the phenomenon in part through epigenetic abnormalities. Zinc is one of the nutrients essential for the epigenome
. Because the worldwide prevalence of zinc deficiency is at least 20% (JL: by 'normal' standards
), fetal zinc deficiency is common. We suggest fetal zinc deficiency contributes to the pathogenesis of metabolic diseases in adults. In support of our thesis, research in experimental models and humans established the essentiality of zinc at all stages of intrauterine and infant life. Experiments in rodents and/or non-human primates found that fetal and/or suckling zinc deficiency impairs neuropsychological functions of progeny and that the effects persist in spite of nutritional rehabilitation. In addition, maternal zinc deficiency in mice is reported to impair immunity of progeny
; effects persist in spite of nutritional rehabilitation into the next generation. We suspect that zinc deficiency is a far greater human health problem than is generally recognized.
i suspect that too