Chronic low intakes of micronutrients cause classic vitamin and mineral deficiencies. These micronutrient deficiencies are well characterised for most micronutrients and include scurvy for vitamin C, beriberi for thiamine, pellagra for niacin and anaemia for iron. Historically, deficiencies of micronutrients were problematic, but more recently a better understanding of nutrition and a greater access to food has decreased the incidence of the classic deficiency diseases in the developed nations. In fact, outside of the third world such classic nutrient deficiencies are now confined to specialist medical cases and are exceedingly rare. However, while micronutrient deficiencies are now rare in Western nations, insufficiencies are surprisingly common. Defined as an intake low enough to cause significant detrimental subclinical physiological changes, but high enough to prevent an outright deficiency and death, insufficiencies are now recognised in their own nutritional classification by some nutritionists.
Deficiencies of vitamin D are well characterised, and are known to produce rickets in children and osteomalacia in adults. Recent research has however shown that chronic low intakes of vitamin D high enough to prevent these disease can lead to insulin resistance, weight gain, diabetes, cancer and cardiovascular disease. The changes associated with these subclinical deficiencies (insufficiencies) are subtle and result in clinically undetectable alterations in metabolism, most of which would have no obvious cause upon inspection. However, apart from vitamin D, few of the micronutrient insufficiencies are characterised or understood outside of the specialist nutritional literature, and the medical establishment has paid little attention to or concern for the problem. Much research has been performed on the micronutrient intakes of the developed nations and consistently borderline low intakes of most micronutrients are reported. In particular, zinc intake is reported to be low in populations who consume the Western diet regularly.
Increases in stress such as through exercise or work related commitments can increase the requirement for micronutrients and push individuals into an insufficient state. This is also true for pregnancy. However, in the case of pregnancy, the additional mineral requirements of the foetus will necessitate further increased minerals intake in the mother. Therefore marginal intakes can cause insufficiencies in the mother through a combination of stress and foetal mineral requirements. This is difficult to study in humans because of the ethical implications of depriving pregnant women of essential minerals. However, experiments have been performed on monkeys to assess the impact of chronic low zinc status1. Rhesus monkeys were fed a diet containing the amount of zinc (4 parts per million zinc) that was low but did not produce deficiency symptoms in non-pregnant monkeys when fed for 10 weeks. Control animals were fed a diet of 100 parts per million zinc and either given ad libitum access to food, or a restricted dietary intake.
By the third trimester of the pregnancy, the low zinc monkeys has developed some of the classic signs of zinc deficiency including dermatitis, anorexia and also has low plasma levels of zinc and serum alkaline phosphatase concentrations. Differences in the plasma levels of zinc were dependent on the weight gain or loss in the animals. Those who lost weight maintained plasma zinc levels to a higher degree than those who gained weight during pregnancy, suggesting that the zinc status might have been related to food intake. In other words, parapoxically the more the monkeys ate of the low zinc food, the lower their plasma zinc levels became depressed. Monkey deprived of zinc also developed low levels of vitamin A, but other micronutrients were reported to be normal. Haematological changes were also reported in the zinc deficient animals including reductions in cell packed volumes, reduced corpuscular volumes and reduced haemoglobin. Immunological changes were also evidenced by a reduction in lymphocyte mitogen response.
Therefore in pregnant rhesus monkeys, marginal zinc status during pregnancy causes detrimental changes to immunohaematological function, which would almost certainly cause detrimental health to the mother and foetus. The ability of low zinc status to depress the immune response is well reported, and this may increase the risk of infection. The fact that zinc supplements reduce the severity and duration of common colds is not because of a pharmacological effect of zinc, but results from repleting an individual of zinc once an insufficiency has developed. This explains the inconsistent results of such studies, because only those with a marginal deficiency will respond with improvements. Interestingly, no signs of zinc deficiency were detected in the zinc deprived monkeys in the first half of pregnancy, suggesting that the mineral needs of the foetus and mother were able to be met by the 4 parts per million zinc intake. As the stress of pregnancy continued and the mineral needs of the foetus grew, zinc insufficiencies became evident, followed by deficiencies.
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