So early in arriving, so late in catching up

molecule of the month: until recently, all formula milk lacked arachidonic acid, putting premature babies at a disadvantage. John Emsley reports

Despite all the care lavished on them, premature babies are still smaller than normal babies, even when they are one year old. They also have a high risk of disabilities such as cerebral palsy and blindness. Recent research shows that they are disadvantaged because their diet lacks a nutrient essential for the growth of blood vessels and brain cells: arachidonic acid (AA).

Professor Michael Crawford of the Institute of Brain Chemistry at Hackney Hospital, east London, has been researching the effect of AA on brain development for more than 20 years, and this month his work has been recognised by the International Award for Modern Nutrition. In 1992 Crawford showed that lack of AA was associated with premature birth and low birth weights. The blood level of AA in such babies falls rapidly to less than a half that of a baby still in the womb.

A pregnant woman's placenta provides her foetus with plenty of AA, and her milk continues the supply after she has given birth. A premature baby is cut off from AA, which has now been proved to be essential for its development. Most milk substitutes do not provide any AA.

Crawford urges that AA be added to formula feeds: "We need these to be as close to placenta production as possible, because premature babies collapse into a serious deficit of AA immediately after they are born. Arachidonic acid, and the related fatty acid, DHA, are essential for the growth and function of blood vessels within the brain, and for the brain itself."

The European Society for Paediatric Gastroenterology and Nutrition reported on the fat content of formula feeds in 1991. It recommended that these should supply long-chain fatty acids like those in human milk, and in particular supply those polyunsaturated fats that a baby cannot make for itself. Humans make the AA they need from another, more common, fatty acid, linoleic acid, which we get from our food. Eventually a baby is able to do the same, once it has developed the necessary enzymes. Until then it has to rely on its mother for AA but, if it is premature, it has to be tube-fed using formula feed. It may be fed its own mother's milk, but not milk from other mothers because of the risk of HIV infection. Because the rate of brain and blood vessel development is so great, Crawford believes that even formulas for normal-term babies should also be fortified with these essential fatty acids.

Linoleic acid (LA), the precursor to AA, is especially abundant in seed oils such as sunflower oil (50 per cent), in peanuts (14 per cent) and smoked bacon (5 per cent), while the much maligned lard has 10 per cent. AA is not abundant in plants or animals, and its scarcity has thrown the formula feed makers into turmoil. So far, the only manufacturer to come up with an answer is the Dutch company Milupa, whose UK subsidiary is at Uxbridge in Middlesex.

Milupa is using egg yolks, which contain AA and DHA, and has patented a process for extracting them and blending them into its formula. Niamh Rice, Milupa's scientific director, says: "We add AA and DHA to the feed for premature babies in amounts and ratios similar to those of breast milk. We also add the blend to our starter infant formula as there is compelling evidence that normal, healthy babies benefit from these fatty acids."

Arachidonic acid was discovered about 50 years ago and is present in the liver, brain and various glands of the body. It is essential because we need it to make prostaglandins, hormones and cell membranes. More than half the brain's structure is composed of cell membranes. Arachidonic acid may have other roles and it has been shown that without LA and AA, rats develop eczema. Provided we get about five grams (a fifth of an ounce) of acids such as LA each day we have enough to keep our skin in good condition.

Sometimes the cells of our body produce AA when we would rather they did not. A strained muscle, an infection or an arthritic joint can cause this to happen, and is the first step in the formation of prostaglandins, an excess of which cause inflammation and pain at the site of the damage. When this happens we can take aspirin or paracetamol, and while these do not remove the AA, they block the enzyme that turns the acid into prostaglandins.

The author is the prize-winning science writer in residence at Imperial College, London's Department of Chemistry.

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