Title: Zinc Deficiency and Conception

Key words: Embryo, foetus, foetal development, zinc absorption, zinc depletion, malformations, premature delivery, teratogenic, growth retardation, chromosomal damage

Date: June 1999

Category: 11. Life Changes

Type: Article

Author: Dr Van Rhijn

 

Zinc Deficiency and Conception

 

 

Introduction

The development of the embryo and foetus follow a genetic programme which is particularly susceptible to inadequacy of dietary nutrients1. This article looks at the consequences of zinc deficiency in this delicate process.

Secondary Zinc Deficiency

Elements such as iron, cadmium, and to a certain extent calcium, copper, folic acid and oxalic acid as well as phytates (grains & legumes), alcohol and drug interactions may compromise zinc absorption with the risk of inducing foetal zinc depletion2. Excessive quantities of zinc can be excreted from the body during diarrhoea (Crohn’s), or as a result of excess caffeine and Vitamin C. Supplementation with zinc (15 mg/day)3 is recommended during high levels of iron intake and bouts of diarrhoea. Zinc status may be compromised due to genetic defective malabsorption (acrodermatitis enteropathica4). Plasma zinc is reduced in an acute phase response due to stress, injury or infection, secondary to cytokine release and sequestration in the liver, resulting in decreased embryonic uptake.

Role of Zinc

The biochemical role of zinc can basically be divided into catalytic (metabolic enzymes), structural (zinc-finger proteins) and regulatory (MT-like proteins) functions5. Zinc deficiency, therefore, may adversely affect numerous physiological functions in the developing foetus, including lipid peroxidation, apoptosis, cell proliferation, replication and differentiation. Zinc promotes the function of amino acids (cysteine, taurine and tryptophan) and is a cofactor for Prostaglandin synthesis. It has various enhancing effects on the hormonal system, including the production of Human Growth Hormone (hGH), Insulin-like Growth Factor-1 and Triiodothyronine (T3), storage and secretion of insulin and also facilitates binding to insulin receptors. Zinc is essential for effective functioning of the immune system. It increases numbers of circulating Helper T-Cells, T-Lymphocytes and increases production of antibodies, Interferon Gamma and Interleukin 2.

Zinc is therefore considered essential for foetal development6 throughout pregnancy.

Implications for the Foetus

Severe maternal zinc deficiency during embryogenesis may be teratogenic, causing serious congenital malformations. This has been demonstrated in rats7, but its role in humans remains controversial8, 9. Zinc deficiencies have been associated with stillbirths, congenital malformations, intrauterine growth retardation, low birth-weight10 and primary height growth failure of the foetus. There is good experimental evidence in animals11 but equivocal data in humans12 for these associations.

There is also evidence of premature delivery, prolonged labour and vaginal bleeding in women with low zinc levels13. The results of supplementary studies remain controversial14, 15, and it seems likely that the benefits of intervention with zinc may only be seen in pregnancies at risk of delivering small for gestational age (SGA) babies16, 17, 18. Zinc deficiency may also result in chromosomal damage, reduced DNA replication, transcription19, binding of growth factors to receptors and oxidative damage (promote diabetes) as well as altered cell death patterns.

Conclusion

The role of zinc deficiency in preventing normal foetal development cannot be discounted20. Although marginal deficiencies seem21 less likely to lead to foetal malformations, there is uncertainty regarding the amount of zinc required. Fortification should be considered, as it is difficult to obtain 15 mg/day from the diet.

 

References

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