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In this article, we review the evidence on the effects of poverty and low income on children's development and well-being. We argue that poverty is an important indicator of societal and child well-being, but that poverty is more than just an indicator. Poverty and low income are causally related to worse child development outcomes, particularly cognitive developmental and educational outcomes. Mechanisms through which poverty affects these outcomes include material hardship, family stress, parental and cognitive inputs, and the developmental context to which children are exposed. The timing, duration, and community context of poverty also appear to matter for children's outcomes-with early experiences of poverty, longer durations of poverty, and higher concentrations of poverty in the community leading to worse child outcomes.

Concentrations of fatty acids (FA) in prostatic tissue of patients with either benign or malignant prostatic disease have previously been shown to be significantly different. In particular, there was a significant reduction in arachidonic acid (AA, C20:4n-6) and docosapentaenoic acid (DPA, C22:5n-6) concentrations in malignant prostatic tissue (PCa) phospholipids (PL). It was suggested that the decreased AA concentration in PCa may be due to its increased metabolism via the cyclooxygenase (CO) and/or lipoxygenase (LO) pathways to produce eicosanoids such as prostaglandins (PGs) and/or leukotrienes (LTs) rather than an impairment in desaturase activity in situ. The eicosanoid production in benign prostatic tissue (BPH) and PCa was determined using [3H]AA. The only eicosanoid produced in significant amounts by either tissue was PGE2 and PCa converted radiolabelled AA to PGE2 at an almost 10-fold higher rate than BPH. PGE2 production from [3H]AA by PCa was investigated in the presence of oleic acid (OA, C18:1n-9), eicosapentaenoic acid (EPA, C20:5n-3), docosahexaenoic acid (DHA, C22:6n-3), dihomo-gamma-linolenic acid (DGLA, C20:3n-6), eicosatetraynoic acid (ETYA) and ketoprofen (KPN) respectively. OA was found to be the most effective inhibitor of PGE2 production by PCa compared with DHA, EPA, ETYA and KPN, while DGLA was the least effective. Diacylglycerol (DAG) formation from labelled AA by PCa was about 4-fold greater than in BPH. Such high levels of DAG may be a means of promoting tumorigenesis through activation of protein kinase C as found with phorbol esters which can be regarded as DAG analogues.

There is increasing evidence that essential fatty acids (EFA) may have a role to play in the aetiology of some types of cancer although their precise mode of action is unknown. Differences in the metabolism of EFA between patients with benign or malignant prostatic disease may help to elucidate their role in the latter. We have, therefore, measured the concentration of the essential fatty acids, and their metabolites, in the phospholipid fractions of both plasma and tissue, in patients with either benign or malignant prostatic disease. Comparison of the median concentration of fatty acids in each group (n = 10) revealed significant differences between them. The phospholipid component of total lipid was greater in malignant (P less than 0.04, unpaired t-test) than in benign tissue. The concentrations of linoleic acid (LA) and di-homo gamma linolenic acid (DGLA) in plasma and tissue were not different between the two groups of patients, but a significant reduction in arachidonic acid (ARA) (P less than 0.002, Mann-Whitney U-test) and docosapentaenoic acid (DPA) (P = 0.009) concentrations was observed in malignant tissue as compared to benign. Patients with malignant prostatic disease also had a significantly higher concentration of oleic acid in phospholipids from both plasma and prostatic tissue. The stearic to oleic acid ratio was similar in plasma but was significantly reduced in malignant tissue (P = 0.006). We suggest that the decreased arachidonic acid concentration in malignant tissue may be due to its increased metabolism, via the lipoxygenase and cyclooxygenase pathways to produce higher concentrations of eicosanoids, rather than an impairment in desaturase activity in situ.

Child poverty rates have remained high since the middle of the 1970s. While several trends, including declines in the number of children per family and increases in parental years of schooling, worked to reduce child poverty rates, several others, including show economic growth, widening economic inequality, and increases in the proportion of children living in mother-only families, had the opposite effect, pushing more children into poverty. Poverty is a common risk: One-third of all children will be poor for at least one year. For many, poverty lasts only a short while, but for a small percentage, poverty persists both throughout childhood and into the adult years. Poverty is not shared equally across different demographic groups. African-American children. Latino children, and children in mother-only families are disproportionately poor. Long-term poverty is even more concentrated than single-year poverty. In 1992, almost 90% of long-term poor children were African-American as compared to all poor children (single-year and long-term poor), of whom 60% were white. Both family structure and the labor market are implicated in long-term childhood poverty. Changes in employment of family members and changes in family composition are each strongly associated with transitions into and out of childhood poverty. Of these, changes in employment are the most important.