CT images reveal otherwise occult muscle depletion. Patients with cancer who are cachexic by the conventional criterion (involuntary weight loss) and by two additional criteria (muscle depletion and low muscle attenuation) share a poor prognosis, regardless of overall body weight.

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Human milk contains n-3 and n-6 LCPUFA (long chain polyunsaturated fatty acids), which are absent from many infant formulas. During neonatal life, there is a rapid accretion of AA (arachidonic acid) and DHA (docosahexaenoic acid) in infant brain, DHA in retina and of AA in the whole body. The DHA status of breast-fed infants is higher than that of formula-fed infants when formulas do not contain LCPUFA. Studies report that visual acuity of breast-fed infants is better than that of formula-fed infants, but other studies do not find a difference. Cognitive development of breast-fed infants is generally better, but many sociocultural confounding factors may also contribute to these differences. The effect of dietary LCPUFA on FA status, immune function, visual, cognitive, and motor functions has been evaluated in preterm and term infants. Plasma and RBC FA status of infants fed formulas supplemented with both n-3 and n-6 LCPUFA was closer to the status of breast-fed infants than to that of infants fed formulas containing no LCPUFA. Adding n-3 LCPUFA to preterm-infant formulas led to initial beneficial effects on visual acuity. Few data are available on cognitive function, but it seems that in preterm infants, feeding n-3 LCPUFA improved visual attention and cognitive development compared with infants receiving no LCPUFA. Term infants need an exogenous supply of AA and DHA to achieve similar accretion of fatty acid in plasma and RBC (red blood cell) in comparison to breast-fed infants. Fewer than half of all studies have found beneficial effects of LCPUFA on visual, mental, or psychomotor functions. Improved developmental scores at 18 mo of age have been reported for infants fed both AA and DHA. Growth, body weight, and anthropometrics of preterm and term infants fed formulas providing both n-3 and n-6 LCPUFA fatty acids is similar in most studies to that of infants fed formulas containing no LCPUFA. A larger double-blind multicenter randomized study has recently demonstrated improved growth and developmental scores in a long-term feeding study of preterm infants. Collectively, the body of literature suggests that LCPUFA is important to the growth and development of infants. Thus, for preterm infants we recommend LCPUFA intakes in the range provided by feeding of human milk typical of mothers in Western countries. This range can be achieved by a combination of AA and DHA, providing an AA to DHA ratio of approximately 1.5 and a DHA content of as much as 0.4%. Preterm infants may benefit from slightly higher levels of these fatty acids than term infants. In long-term studies, feeding more than 0.2% DHA and 0.3% AA improved the status of these fatty acids for many weeks after DHA; AA was no longer present in the formula, enabling a DHA and AA status more similar to that of infants fed human milk. The addition of LCPUFA in infant formulas for term infants, with appropriate regard for quantitative and qualitative qualities, is safe and will enable the formula-fed infant to achieve the same blood LCPUFA status as that of t...

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INTRODUCTIONNecrotizing enterocolitis (NEC) is an inflammatory bowel disease of neonates and remains one of the most common gastrointestinal emergencies in newborn infants [1] . Onset of NEC is often within the first three months of life and neonates who are of extremely low birth weight (< 1000 g) and under 28 wk gestation are the most susceptible [2] . Full term neonates account for 10% of all NEC cases while premature infants account for 90% [3] . With an incidence rate of 1%-5% for all newborns admitted to the NICU [1] , a prevalence of 7%-14% of very low birth weight infants (VLBW, 500-1500 g) [4] and a mortality rate approaching 20%-50% [5] , NEC continues to represent a significant clinical problem. In Canada, the incidence rate is 1.8 per 100 live births with a prevalence of 7% of VLBW infants [1] . Advances in obstetric and neonatal care have improved survival rates for smaller, more immature infants, and as more VLBW preterm infants survive the neonatal period, the population at risk for NEC increases [1] .No consistent association between sex, race, and rates of NEC has been identified. However, male VLBW infants and black infants are at greater risk of death [6] . Due to inadequate treatments and no effective preventative strategy, an estimated 20%-40% of babies with NEC require surgery [1] and 10%-30% experience significant morbidity including neurodevelopmental impairment, vision and hearing impairment, failure to thrive, feeding abnormalities, diarrhea, bowel obstruction, and short bowel syndrome [1,2,7] . The case fatality rate with surgical intervention is as high as 50% [1] . NEC is also a financial burden to the health care system with yearly hospital charges reported to be as high as $6.5 million in the US [8] . Thus, NEC continues to be an important health issue for preterm neonates. DIAGNOSIS Clinical signs and symptomsThe onset of NEC can occur suddenly within a few AbstractNecrotizing enterocolitis is an inflammatory bowel disease of neonates with significant morbidity and mortality in preterm infants. Due to the multifactorial nature of the disease and limitations in disease models, early diagnosis remains challenging and the pathogenesis elusive. Although preterm birth, hypoxic-ischemic events, formula feeding, and abnormal bacteria colonization are established risk factors, the role of genetics and vasoactive/inflammatory mediators is unclear. Consequently, treatments do not target the specific underlying disease processes and are symptomatic and surgically invasive. Breast-feeding is the most effective preventative measure. Recent advances in the prevention of necrotizing enterocolitis have focused on bioactive nutrients and trophic factors in human milk. Development of new disease models including the aspect of prematurity that consistently predisposes neonates to the disease with multiple risk factors will improve our understanding of the pathogenesis and lead to discovery of innovative therapeutics.

The complex lipid constituents of the eukaryotic plasma membrane are precisely controlled in a cell-type-specific manner, suggesting an important, but as yet, unknown cellular function. Neuronal membranes are enriched in long-chain polyunsaturated fatty acids (LC-PUFAs) and alterations in LC-PUFA metabolism cause debilitating neuronal pathologies. However, the physiological role of LC-PUFAs in neurons is unknown. We have characterized the neuronal phenotype of C. elegans mutants depleted of LC-PUFAs. The C. elegans genome encodes a single Δ6-desaturase gene (fat-3), an essential enzyme for LC-PUFA biosynthesis. Animals lacking fat-3 function do not synthesize LC-PUFAs and show movement and egg-laying abnormalities associated with neuronal impairment. Expression of functional fat-3 in neurons, or application of exogenous LC-PUFAs to adult animals rescues these defects. Pharmacological, ultrastructural and electrophysiological analyses demonstrate that fat-3 mutant animals are depleted of synaptic vesicles and release abnormally low levels of neurotransmitter at cholinergic and serotonergic neuromuscular junctions. These data indicate that LC-PUFAs are essential for efficient neurotransmission in C. elegans and may account for the clinical conditions associated with mis-regulation of LC-PUFAs in humans.

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Adding LCP to a preterm infant formula resulted in lymphocyte populations, phospholipid composition, cytokine production, and antigen maturity that are more consistent with that in human milk-fed infants. This may affect the ability of the infant to respond to immune challenges.