The physical complications of anorexia nervosa are common and can be life threatening, but psychiatrists and the increasing number of non-medical therapists involved in treatment programmes often overlook these complications. Cardiovascular complications are the most common, and the most likely to result in fatalities, particularly in those patients who vomit, purge or abuse diuretics, because of the electrolyte abnormalities induced. Osteoporosis is an early and perhaps irreversible consequence of severe weight loss. Further, there are dangers in rapid intravenous hyperalimentation.

The total direct cost of treating schizophrenia in the UK is £397 million, or 1.6% of the total health care budget. Hospital-based and community-based residential care accounts for nearly three-quarters of these costs, while drugs account for only 5%. A conservative estimate of the indirect annual costs of lost production is in the region of £1.7 billion. The heterogeneity of the disease and its outcome means that average treatment costs per person with schizophrenia should be treated with caution; 97% of direct costs are incurred by less than half the patients. Therefore, treatments which reduce the dependence and disability of those most severely affected by schizophrenia are likely to have a large effect on the total cost of the disease to society and may therefore be cost-effective, even though they appear expensive initially.

Anxiety neurosis has been the subject of intensive study during the past ten years. Renewed interest in this syndrome has arisen both from the stimulus of new methods of treatment and from attempts to classify anxiety more accurately. Recently Pitts and McClure (1967) reported that anxiety symptoms and anxiety attacks could be produced by a specific biochemical stimulus: sodium lactate. This work was prompted by the finding that 'standard exercise’ tends to produce an excess amount of lactic acid in patients with anxiety neurosis (Cohen and White, 1950; Jones and Mellersh, 1946; Linko, 1950; Holmgren and Strom, 1959). Pitts and McClure found that an intravenous infusion of 10 ml. of half-Molar sodium (DL) lactate per kilogram of body weight, given over a twenty minute period, produced an anxiety attack in patients suffering from anxiety neurosis. The symptoms began a minute or two after the infusion was started and developed rapidly, and some patients reported ‘exacerbations of their characteristic symptom profiles for two to five days after the sodium lactate infusion’. In their double-blind study, many fewer symptoms were produced when calcium ion was added to the lactate infusion, and almost no symptoms were produced by an infusion of glucose in saline of similar osmolarity. Many fewer and less severe symptoms were produced in normal controls than in the patient group, both in response to sodium lactate and to lactate with added calcium, and almost no symptoms during the glucose and saline infusion. Pitts and McClure postulated that anxiety symptoms may have a common determining biochemical end-mechanism, involving the complexing of ionized calcium at the surface of excitable membranes by lactate ion with resulting interference ‘with the normal functioning of calcium in transmitting nerve impulses' (Pitts, 1969). They concluded that ‘there may be something highly specific about lactate ion in producing the naturally occurring hypocalcaemic anxiety symptoms in human beings'.

Among a consecutive unselected series of 29 patients with Cushing's syndrome 21 had bilateral adrenal hyperplasia and 8 had tumours. Twenty-five (86 per cent) were significantly depressed; three of the tumour patients, but only one of the hyperplasia group were free of symptoms so that if there are no psychiatric symptoms there is a three in four chance that the patient has a tumour. There was a family history of depression or suicide or a history of early bereavement or separation in half the cases. In six of the hyperplasia patients a major emotional disturbance had preceded the onset, and in five this was a loss. The severity of the depression was not related to the level of circulating Cortisol. The depression was rapidly relieved when the tumour or hyperplastic glands were removed. Depression in Cushing's syndrome might result from a substance other than Cortisol produced by the adrenal under excessive pituitary and/or hypothalamic stimulation, which could play a part in the aetiology of depressive illness in general.

The evidence for a genetic contribution to schizophrenia is compelling. However, the pattern of inheritance is complex and it is usually assumed that environmental factors also have a role that will eventually be identified. We argue that this is not necessarily the case. While a hypothesis combining genetic diathesis with environmental stress cannot be disproved, it is also possible that ‘non-genetic’ factors consist entirely of stochastic events affecting gene expression or structure.

Unprecedented numbers of cases of MPD have been diagnosed, mainly in North America, since 1957. Widespread publicity for the concept makes it uncertain whether any case can now arise without being promoted by suggestion or prior preparation. In order to determine if there is any evidence that MPD was ever a spontaneous phenomenon, a series of cases of MPD from the earlier literature has been examined, with particular attention given to alternative diagnoses which could account for the phenomena reported and to the way in which the first alternate personality emerged. The earlier cases involved amnesia, striking fluctuations in mood, and sometimes cerebral organic disorder. The secondary personalities frequently appeared with hypnosis. Several amnesic patients were trained with new identities. Others showed overt iatrogenesis. No report fully excluded the possibility of artificial production. This indicates that the concept has been elaborated from the study of consciousness and its relation to the idea of the self. The diagnosis of MPD represents a misdirection of effort which hinders the resolution of serious psychological problems in the lives of patients.

Among 84 adoptees, 18 years of age and older, separated at birth from their biological parents and without further contact with them, alcoholism was found more frequently in those whose relatives included an individual with alcoholism or in whom heavy drinking had been noted. Adoptee alcoholism did not correlate with any other diagnosis in a biological parent.

Childhood socialized conduct disorder was significantly higher in those adoptees who later received a diagnosis of alcoholism or suspected alcoholism, and was positively, but not significantly, related to heavy drinking or alcoholism in parents.

Age of adoptee, time spent in foster care, age of biological mother at the time of the birth, socio-economic status of adoptive home, psychopathology other than alcoholism in the biological background, and psychiatric or behavioural problems in the adoptive family (parents or sibs) were all unrelated to adult alcoholism in the adoptee.

We present a prevalence study of psychiatric morbidity in people over 50 years of age with learning disability (LD), using a new semistructured clinical interview specifically for use with people who have LD (the ‘PAS-ADD’). Assessment involved parallel interviewing of subject and informant, these two sets of information being combined to reach a final diagnosis using ICD-9 and DSM-III-R criteria. Detection of dementia involved interviews with informants, plus investigation of loss of cognitive function over a three-year period. The experimental sample was a mixed community and institutional group (n = 105), including, as far as possible, all people in a single administrative district (Oldham) matching the age and ability criteria. Prevalence of psychiatric disorder excluding dementia was 11.4% (n = 12), most of which were depression and anxiety. Seventy-five per cent of these cases were unknown to mental health services. However, immediate care staff were usually aware of the symptoms, although often unaware of their clinical significance. Prevalence of dementia was also 11.4% (n = 12), with a combined case prevalence of 21.0% (n = 22). The PAS-ADD proved a flexible interview, effective in use with people of varying linguistic level and intellectual ability: 61.9% (n = 65) of the sample were able to be interviewed, fully adequate clinical interviews being obtained with a group of 38 people whose mean IQ was only 39. In the remaining 38.1% (n = 40), diagnosis relied exclusively on informant data. Overall, the combination of subject and informant data was essential for sensitive case detection.

The measurement of agreement between ratings of patient symptomatology by two or more psychiatrists is discussed. It is noted that coefficients which allow for possible chance agreement are to be preferred, but they involve assumptions about the way in which chance factors may operate. Assumptions which involve prior probabilities of the incidence of a symptom appear to be too stringent, and a new coefficient, called the RE coefficient, is recommended in which chance is assumed to operate in a purely random way. Binary scales are discussed in detail, but methods of dealing with scales of wider range are also referred to.

Two clinicians scored the ICD–10 Research Criteria Checklist either while observing or after administering CIDI interviews to a sample of 20 subjects. Overall diagnostic concordance between clinical and CIDI assessments was found to be good (overall kappa = 0.77). Assessment of the specific diagnoses could be done only for the three most commonly represented in the studied sample: anxiety/phobic disorders (kappa = 0.73), depressive disorders (kappa = 0.78), and psychoactive substance use disorders (kappa = 0.83). While the lack of independence of the two assessments and the small, non-randomly selected sample might have exaggerated the concordance, this study shows that the CIDI provides all the data needed to score diagnoses in the ICD–10 nomenclature, as indicated by the small number of questions clinicians needed to ask following completion of the CIDI.

This editorial summarises what is known about accelerating the transfer of discoveries in the health sciences into implementation in routine clinical practice. Three phases are described: adoption in principle, early implementation, and persistence of implementation. Facilitators and barriers to the implementation across these phases are discussed.