Is NHS Direct meeting the needs of mental health callers?

Background: NHS Direct is a new service that offers 24-hour advice from trained nurses. The National Service Framework for Mental Health and the National Strategy for Carers both mention NHS Direct as an important source of support for people with mental health problems. Aims: This paper reports findings from an evaluation of the Department of Health's NHS Direct mental health initiative. This initiative was established to ensure that NHS Direct can meet the needs of callers with mental health problems by offering additional training to all staff and improving the database of mental health services. Method: The findings reported here are based on routine computer data provided by 12 out of 17 NHS Direct sites, 552 data forms completed by nurse advisers from the 17 sites, and 111 questionnaires administered over the telephone with callers to the 17 sites. Results: Mental health calls accounted for 3% of NHS Direct's workload, although these calls were often longer and more complex than other calls. The majority of callers to the service were in touch with other services for their mental health problems (59%), typically their GP. Most callers had 'moderate' mental health problems, as indicated by the Global Assessment of Functioning Scale. Generally callers were satisfied with the service they received, although satisfaction was lower in some areas than previous studies of NHS Direct. Conclusions: Improvements could be made in the mechanisms for referring callers on to other services, and training to increase nurse advisers' knowledge of mental health problems.

The Effect of Mental Health Problems on Children’s Ability to Discriminate Amongst Thoughts, Feelings and Behaviours

Many young children appear to have skills sufficient to engage in basic elements of cognitive behaviour therapy (CBT). Previous research has, however, typically used children from non-clinical populations. It is important to assess children with mental health problems on cognitive skills relevant to CBT and to compare their performance to children who are not identified as having mental health difficulties. In this study 193 6 and 7 year old children were assessed using a thought–feeling–behaviour discrimination task [Quakley et al. Behav. Res. Therapy 42 (2004) 343] and a brief IQ test (the WASI). Children were assigned to groups (at risk, borderline, low risk) according to ratings of their mental health made by their teachers and parents on the Strengths and Difficulties Questionnaire [Goodman, J. Am. Acad. Child Adolescent Psych. 40 (2001) 1337]. After controlling for IQ, children ‘at risk’ of mental health problems performed significantly less well than children with a ‘low risk’ of mental health problems. Before receiving CBT, children’s meta-cognitive development should be assessed and additional help provided to those with meta-cognitive difficulties.

Infant Attachment Security and the Timing of Puberty: Testing an Evolutionary Hypothesis

Life-history theories of the early programming of human reproductive strategy stipulate that early rearing experience, including that reflected in infant-parent attachment security, regulates psychological, behavioral, and reproductive development. We tested the hypothesis that infant attachment insecurity, compared with infant attachment security, at the age of 15 months predicts earlier pubertal maturation. Focusing on 373 White females enrolled in the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development, we gathered data from annual physical exams from the ages of 9½ years to 15½ years and from self-reported age of menarche. Results revealed that individuals who had been insecure infants initiated and completed pubertal development earlier and had an earlier age of menarche compared with individuals who had been secure infants, even after accounting for age of menarche in the infants’ mothers. These results support a conditional-adaptational view of individual differences in attachment security and raise questions about the biological mechanisms responsible for the attachment effects we discerned.

Effects of phthalic acid esters on the liver and thyroid

The effects, over periods from 3 days to 9 months of administration, of diets containing di-2-ethylhexyl phthalate are very similar to those observed in rats administered diets containing hypolipidemic drugs such as clofibrate. Changes occur in a characteristic order commencing with alterations in the distribution of lipid within the liver, quickly followed by proliferation of hepatic peroxisomes and induction of the specialized P-450 isoenzyme(s) catalyzing omega oxidation of fatty acids. There follows a phase of mild liver damage indicated by induction of glucose-6-phosphatase activity and a loss of glycogen, eventually leading to the formation of enlarged lysosomes through autophagy and the accumulation of lipofuscin. Associated changes are found in the kidney and thyroid. The renal changes are limited to the proximal convoluted tubules and are generally similar to changes found in the liver. The effects on the thyroid are more marked. Although the levels of thyroxine in plasma fail to about half normal values, serum triiodothyronine remains close to normal values while the appearance of the thyroid varies, very marked hyperactivity being noted 7 days after commencement of treatment, this is less marked at 14 days, but even after 9 months treatment there is clear cut evidence for hyperactivity with colloid changes which indicate this has persisted for some time. Straight chain analogs of di-2-ethylhexyl phthalate, di-n-hexyl phthalate and di-n-oxtyl phthalate differ entirely in their short-term effects on the liver and kidney but have similar effects on the thyroid. The short-term in vivo hepatic effects of the three phthalate esters can be reproduced in hepatocytes in tissue culture. All three phthalate esters, as well as clofibrate, have early marked effects on the metabolism of fatty acids in isolated hepatocytes. The nature of these changes is such as to increase storage of lipid in the liver. A hypothesis is presented to explain the progress from these initial metabolic effects to the final formation of liver tumors.