277 with schizophrenia that
one or both the parents of schizooften themselves to a greater or schizophrenic phrenics lesser degree. Other siblings may be affected by the disease. This is to be expected by the nature of the genetics of the disease, thought by a number of authorities to be the expression of a single dominant gene (Slater thinks it to have partial penetrance). Because the behaviour of a parent is disturbed in no way means this behaviour is the cause of the children’s illness, but it does mean that psychiatrists must be alert and be prepared to diagnose and treat all the ill members of any family. They must in no way apportion blame for a disease state, but in no way underestimate the explosive situations which may arise in a household in which two or more paranoid schizophrenics are living. There is no point in pretending terrible situations do not arise. They do. Laing et al. were almost certainly aware of these intense situations but misinterpreted them by not realising that schizophrenia is a genetically inherited disease. It is the biochemical error which results from the faulty gene that we want to find most urgently if we are to help sufferers from schizophrenia and their families. are
G. P. HEMMINGS, Llanfair Hall, Caernarvon LL55 1TT.
Hon. Secretary, Schizophrenia Association of Great Britain.
DIETARY TREATMENT OF MATURITY-ONSET DIABETES MELLITUS SIR,-Any critical study of diabetic therapy is to be welcomed, and Dr Doar and his colleagueshave demonstrated again the value of diet alone in the treatment of
maturity-onset diabetes and have rightly emphasised its importance as initial therapy. However, their conclusion that glucose tolerance was in fact improved in the great majority of their 119 patients after two months of dieting is debatable-it depends how glucose tolerance is defined. We have stated2 thatgood’ glucose tolerance may be typified in descriptive terms by a blood glucose curve which is allowed to rise for only a short time before being rapidly returned to the fasting level-that is, the ’peak’ glucose level occurs early and the raised glucose level occurs for only a short time. Conversely, ’bad’ glucose tolerance is typified by a blood glucose which is allowed to continue rising for much longer-a delayed peak-and which stays much longer above the fasting level ". We have attempted to evaluate glucose tolerance in quantitative terms according to this concept by a simple index-the H index.2 Dr Doar and his colleagues do mean
W. H., Thompson, M. E., Wilde, C. E., Sewell, P. F. J. Lancet, 1975, i, 1263. 2. Billewicz, W. Z., Anderson, J., Lind, T. Br. med. J. 1973, i, 573.
Endocrine Unit, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP. M.R.C. Reproduction and Growth Unit, Princess Mary Maternity Hospital, Newcastle upon Tyne.
J. ANDERSON. T. LIND W. Z. BILLEWICZ.
DRUGS FOR ARRHYTHMIAS
enjoyment your editorial for arrhythmias. We have (May 17, p. 1125) drugs some of the mechanisms of digitalis-induced investigated arrhythmias and found that the adrenergic nervous system plays a decisive role in digitalis-induced ventricular tachyarrhythmias.5-1s Thus, we cannot agree when you SIR,-We
define what they as always, is just taken that they assessed their not
for granted-they simply tell us oral glucose-tolerance test (o.G.T.T.) plasma-sugar curves in terms of the area between the curve and the abscissa. This area is, however, heavily influenced by the portion under the fasting blood-glucose level so that a. small change in that level has a disproportionately large effect on the total area. This is clearly seen in the upper pair of graphs in fig. 1 in their paper-the second O.G.T.T. sugar results look " better " in that they are pitched lower, but the shape of the glucose response curve is identical. In fact, H indices calculated on the basis of figures derived from these graphs give values of 19-7 for the first set of mean values and 18-8 for the second (post-treatment) setboth highly abnormal by our criteria and hardly showing a significant difference. All that has happened after treatment is that the fasting level has fallen-" glucose tolerance " remains much the same. We should point out that in this context the H indices are given simply in an illustrative 1.
strictly speaking H indices cannot be used the means. The result of an oral glucose-tolerance test includes two distinct components: the fasting level and the response to the glucose load. In theory either component can be normal or abnormal in its own right.33 The prognostic significance of the fasting level and of deterioration or improvement in the shape of the response curve should perhaps be considered separately. We do not deny that dieting is probably the first line of attack in mild to moderate maturity-onset diabetes, certainly if significant obesity is present. Dieting is safe and if correctly followed is very effective in " controlling the diabetes. Here we agree with Dr Doar and his colleagues. We disagree, on the data presented in this series, with the conclusion that dieting " improves " glucose tolerance-it lowers the fasting blood-sugar level (and the prognostic significance of this is unknown) but does not in this study appear to alter the response curve-in the terms that we have defined it, glucose tolerance is unchanged. It is, of course, doubtful whether any purely statistical manipulations will indicate which method of assessing O.G.T.T. results is " better " than those of another, although the statistical properties of one index may be more useful than those of another, depending on the context. For evaluation in clinical terms we need a clearly defined goal, to which any given index can be related. Nevertheless, we suspect from the data given that if the authors had calculated incremental indices or H values for their patients, their conclusions might have been different. However, it is only fair to state that many patients with obesity and maturity-onset diabetes in whom we have performed O.G.T.T. before and after successful dieting (in terms of weight loss) do in fact show an improvement in the glucose-response curve, which can deteriorate again if dieting is allowed to lapse.4 Except in a small number of patients with mild diabetes, we have not so far observed such improvement in the H index in patients treated with sulphonylurea drugs. sense, since
read with great on
Billewicz, W. Z. Clin. Endocr. 1975, 4, 49. Anderson, J. Unpublished. Levitt, B., Cagin, N., Somberg, J., Bounous, H., Mittage, T., Raines, A. J. Pharmac. exp. Ther. 1973, 185, 24. 6. Cagin, N., Somberg, J., Bounous, H., Mittage, T., Raines, A., Levitt, B. Archs int. Pharmacodyn. Thér. 1974, 207, 340. 7. Gillis, R., Raines, A., Sohn, Y., Levitt, B., Standaert, F. J. Pharmac. exp. Ther. 1972, 183, 154. 8. Levitt, B., Raines, A., Roberts, J., Standaert, F. Pharmacologist, 1967, 26, 3. 9. Raines, A., Levitt, B., Standaert, F. Archs int. Pharmacodyn. Thér. 1967, 170, 485. 10. Roberts, J., Levitt, B., Standaert, F. Nature, 1967, 214, 912. 11. Gillis, R., Levitt, B., Raines, A. Pharmacologist, 1969, 11, 244. 12. Levitt, B. ibid. 1969, 11, 217. 13. Standaert, F., Levitt, B., Roberts, J., Raines, A. Eur. J. Pharmac. 1969, 6, 209. 14. Levitt, B., Raines, A., Sohy, Y., Standaert, F., Hirshfeld, J. J. Mt Sinai Hosp. 1970, 37, 227. 15. Cagin, N., Freeman, E., Somberg, J., Mittage, T., Raines, A. Levitt, B. Archs int. Pharmacodyn. Thér. 1974, 207, 162. 3. 4. 5.