Brain tissue, both grey and white matter from the cerebral parietal region and the cerebellum, was obtained from 66 infants dying of sudden infant death syndrome. The fatty acid composition was analysed in these tissues by gas liquid chromatography after extraction and derivatisation. The subjects were divided according to their dietary history, either breast or formula feeding. Formula-fed infants were further subdivided according to the content of -linolenic acid in the formula milk. At the time of this study no formula milks analysed contained long chain polyunsaturated fatty acids. Dietary related differences were found in the accretion of polyunsaturated fatty acids into neural membranes. Docosahexaenoic acid concentrations were higher and conversely n-6 series fatty acids lower in breast-fed than formula-fed infants. In cerebral white matter, nervonic acid, the long-chain fatty acid associated with myelination, appeared in breast-fed in advance of formula-fed infants. Similar dietary related differences in polyunsaturated fatty acid compositions were found in the cerebella cortex and the cerebellar white matter was associated with an earlier accretion of nervonic and lignoceric acids when compared to the cerebrum. Analysis of the phospholipid and glycolipid composition of the cerebral and cerebellar white matter tissues was achieved by means of separation by high performance thin layer chromatography followed by scanning densitometry. The results of this study support the need for breast feeding for a minimum of four months. Formulation of manufactured milks should include long chain polyunsaturated fatty acids and nervonic acid at concentrations similar to those of breast milk.

The bacteria located within the human gastrointestinal tract (the gut microbiota) perform numerous protective, immunological and metabolic functions for the host. They are increasingly implicated in the pathogenesis of acquired inflammatory diseases of the gut in childhood, namely: necrotising enterocolitis (NEC) and inflammatory bowel disease (Crohn’s disease (CD) and ulcerative colitis (UC)). Study of the role that the microbiota may play in the development of such diseases may lead to new therapies to modulate or even cure them. However many current techniques depend on the ability to study such bacteria outwith their natural ecosystem. Although molecular techniques can identify species independent of standard cultures they can enlighten little on the metabolic activity of identified bacterial species, which may be important in the propagation of inflammatory responses. Little is known about the potential of novel therapeutic strategies, such as probiotics, to modulate diseases such as NEC. In addition inadequate scientific rigour has been applied to the science of probiotics. The aims of the study described in this dissertation were to test the following hypotheses. Hypotheses: 1. Probiotics prevent NEC in at risk infants of very low birth weight (VLBW). 2. The human gut microbiota can be labelled by stable isotope probing (SIP) to measure metabolic activity. 3. Quantitative measurement of the metabolic activity of the unculturable gut microbiota is a useful way of studying changes in the microbiota, compared with measures of bacterial diversity, and may enlighten our understanding of bacterially mediated inflammatory stimuli in inflammatory gut diseases of childhood.