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a British babies were given a formula in which the fat component came from cow's milk. b Dutch babies were given a formula in which the fat component was provided by a vegetable oil.

a British babies were given a formula in which the fat component came from cow's milk. b Dutch babies were given a formula in which the fat component was provided by a vegetable oil.

widespread. Reasons for the superiority of the LCPUFA may be the significantly higher P-oxida-tion of 18:3n-3 compared with LCPUFA and limited activity in the elongation/desaturation pathway.

An adequate supply of LCPUFA in milk is even more important in infants born prematurely, since these acids would normally have been supplied to the foetus from the mother's blood or metabolized from parent acids in foetal tissues. There is limited evidence that giving formula enriched with fish oil improves the 22:6n-3 status and visual function of premature babies, but their 20:4n-6 status deteriorates. Thus, the optimum amounts of parental essential fatty acids and their elongation/desa-turation products, and the optimal ratios between n-3 and n-6 families remain crucial topics in pae-diatric nutrition research. Box 4.1 illustrates some of the debate about the appropriate fatty acid composition of infant formulas in more detail.

4.2.3 Dietary lipids supply essential fatty acids that are essential to life but cannot be made in the animal body Historical background: discovery of essential fatty acid deficiency

In 1929 the Americans Burr and Burr described how acute deficiency states could be produced in rats by feeding fat-free diets and that these defi ciencies could be eliminated by adding only certain specific fatty acids to the diet. Until that time it had been thought that fat was important only in so far as its energy contribution was concerned. It was shown that linoleic and later arachidonic acid were responsible for this effect and the term vitamin F was coined for them. They are now known universally as 'essential fatty acids' (EFA).

EFA deficiency can be produced in a variety of animals, including man, but data for the rat are the best documented (Table 4.8). The disease is characterized by skin symptoms, such as dermatosis and the skin becomes more 'leaky' to water. Growth is retarded, reproduction is impaired and there is degeneration or impairment of function in many organs of the body. Biochemically, EFA deficiency is characterized by changes in the fatty acid composition of many tissues, especially their biological membranes, whose function is impaired and, in the mitochondria, the efficiency of oxidative phosphorylation is much reduced. Well-documented EFA deficiency in man is rare, but was first seen in children fed virtually fat-free diets. Four hundred infants were fed milk formulas containing different amounts of linoleic acid. When the formulas contained less than 0.1% of the dietary energy as linoleic acid, clinical and chemical signs of EFA deficiency ensued. The skin abnormalities were very similar to those described in rats and these and other signs of EFA deficiency disappeared when linoleic acid was added to the diet.

Box 4.1 Are long-chain n-3 polyunsaturates necessary constituents of infant feeds?

Long-chain polyunsaturated fatty acids (LCPUFA) such as 20:4n-6 (AA) and 22:6n-3 (DHA) make up about a third of brain lipids. DHA seems to have a key role in the structure of retinal, neural and synaptic membranes and AA may have a neurotransmitter role. Human brain development begins in foetal life and continues for some months after birth. The mother's circulation supplies the foetus with preformed LCPUFA or parent acids that the foetus can desaturate and elongate. After birth, breast milk supplies parent acids and small amounts of LCPUFA. Infant formula milks normally supply parent acids (albeit in widely differing amounts depending on the brand), but not LCPUFA. During the latter part of the 1990s some manufacturers started to provide products containing LCPUFA

The need for a supply of LCPUFA has been a topic of controversy mainly due to lack of sufficient information. Limited data suggest that:

• visual and neural abnormalities develop in infant monkeys given feeds with a low concentration of 18:3n-3;

• similar deficiencies have been observed in premature human infants;

• infants randomly allocated to formula containing DHA displayed even better visual development than those whose sole source of n-3PUFA was 18:3.

• n-3PUFA may suppress growth in premature babies.

Furthermore, there is substantial evidence that breast feeding confers significant advantages compared with normal formula in respect of neural development. However, such findings are almost impossible to interpret because breast milk differs from formula milk in many aspects other than its LCPUFA content. Nevertheless, a consensus seemed to have developed that the addition of LCPUFA to infant formula was beneficial, if not essential.

A study published in December 1999 has caused this view to be less secure. Its authors concluded that:

There was no evidence of a beneficial or adverse effect on cognitive or motor development ... Our trial does not provide support for the addition of LCPUFA to standard infant formula but we are now doing further follow-up of this cohort. (A. Lucas et al. (1999) Lancet, 354, 1948-1954).

The study was a double-blind, randomized, controlled trial of formula with (n=154) and without (n=155) LCPUFA and a reference group that was breast-fed (n=138). The outcome measures were several tests of mental and psychomotor development.

The authors were careful also to include tests that would assess the safety of consuming feeds rich in LCPUFA, since there had been previous evidence of adverse effects on growth. These included tests for allergic reactions, infections, growth and gastrointestinal tolerance. There was no evidence of adverse effects.

What can we conclude? Although addition of LCPUFA to infant formula at a concentration of 0.2 g l-1 (the amount used by Lucas and colleagues) can be regarded as safe, there is insufficient evidence to conclude that the development of infants is improved by LCPUFA supplements. Any benefits are likely to be modest and smaller than the advantage of breast milk over formula feeds.

In 1971, the first unequivocal case of EFA deficiency in an adult was reported. The patient, a man of 44, had all but 60 cm of his bowel surgically removed. He was then given intravenous feeding only, with preparations containing no fat, and after 100 days he developed scaly dermatitis. In a London hospital in 1974, three patients with chronic disease of the small bowel, who had been treated with low fat diets, but not given intravenous feeding, were suspected of having EFA deficiency. They responded successfully to the application to the skin of lipids containing a high proportion of lino-leic acid, demonstrating that EFA need not necessarily be absorbed through the conventional route to be effective. Biochemical basis for EFA deficiency

Once EFA deficiency had been demonstrated, the hunt was on to discover which fatty acids had EFA

Table 4.8 Major effects of n-6 essential fatty acid deficiency in rats


Dermatosis, water permeability

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Many women who have recently given birth are always interested in attempting to lose some of that extra weight that traditionally accompanies having a baby. What many of these women do not entirely realize is the fact that breast-feeding can not only help provide the baby with essential vitamins and nutrients, but can also help in the weight-loss process.

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