Charles Fletcher
Medical Research Council
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Journal of the Royal Statistical Society. Series A (General) | 1978
B. Benjamin; Charles Fletcher; Richard Peto; Cecily Tinker; Frank E. Spiezer
Describing the largest prospective study of the preclinical stages of chronic bronchitis yet reported, this book is remarkable in two ways. First, it illustrates the value of relatively simple observations continued over a number of years by a dedicated team of workers in elucidating the natural history of a common disease. Secondly, it shows that if a study ofthis type is carefully planned and diligently executed expert statistical analysis can produce straightforward, unambiguous, and often unexpected conclusions. The authors have employed these techniques most effectively in their study of chronic bronchitis and have made a cogent case for a drastic reappraisal of traditional views on the pathogenesis of that disease. Of particular importance is the distinction made between the obstructive and hypersecretory forms of chronic bronchitis, and their. conclusion that acute infective exacerbations of chronic obstructive lung disease do not, contrary to popular belief, cause a permanent loss of ventilatory capacity. Another pertinent observation is that some cigarette smokers are more liable than others to develop airflow obstruction. Smoking is clearly responsible for most cases of chronic bronchitis, and the incidence of the disease would undoubtedly diminish dramatically if, by some miracle, the habit were to be abandoned by the majority of the population. It would appear, however, that other as yet undertermined factors are implicated in the production of airflow obstruction and mucus hypersecretion. If we could identify those which predetermine the increased susceptibility of some smokers to chronic bronchitis, particularly the obstructive form of the disorder, this knowledge would, as the authors point out, be of considerable value in predicting the course of the disease, and it might also provide the basis for a more rational approach to the practical aspects of prevention and treatment. This book could well be a milestone in the bibliography of chronic bronchitis and related disorders. It deserves to be widely read not only in Britain but also in those countries where the problems posed by this common disease are even less clearly understood.
BMJ | 1986
Peter Maguire; Susan Fairbairn; Charles Fletcher
Thirty six young doctors who as medical students had been randomly allocated to either video feedback training or conventional teaching in interviewing skills during a psychiatry clerkship were reassessed five years later. Each doctor interviewed one patient with a psychiatric illness and two with a physical illness. Each interview was rated independently. Both groups had improved since the fourth year clerkship, but those given feedback training had maintained their superiority in the skills associated with accurate diagnosis. This superiority was as evident in their interviews with physically ill patients as it was with psychiatric patients. Both groups, however, still used closed questions and were more reluctant to cover psychosocial problems in physically ill patients. Those trained conventionally were clinically inadequate in both these aspects and in clarifying their patients statements. Given these lasting benefits, all medical students should have feedback training in interviewing skills.
BMJ | 1948
Charles Fletcher
processes by which this fibrous tissue may disappear have been discussed briefly. A high-protein diet, containing 35% protein but low in methionine, was not as beneficial as a ration containing 20% of similar protein to which adequate supplements of. choline or methionine had been added. A high-protein diet which contained an adequate amount of naturally occurring methionine produced results as favourable as those which were secured when suitable amounts of choline or methionine were added to diets of lower protein content. While the experimental evidence indicates that the presence of the lipotropic agents is essential for the repair of the damaged liver under the conditions of our experiments, it does not suggest that the addition of choline or its precursor, methionine, to diets already containing adequate amounts of these factors will enhance the therapeutic effect unless some interference with the absorption or action of the lipotropic agents exists. No evidence has been secured that inositol exerts a favourable effect on experimental cirrhosis. On the basis of the experimental findings it is suggested that the favourable clinical results which have been obtained in patients with liver damage when an effective therapeutic diet is provided may be attributable in large part to the lipotropic factors which the diet supplies.
Occupational and Environmental Medicine | 1951
A. L. Cochrane; Charles Fletcher; J. C. Gilson; P. Hugh-Jones
There can be no doubt that coalworkers pneumoconiosis presents one of the most serious problems in industrial medicine in Britain, at least in respect of the numbers of men affected. From 1931 up to the end of 1949 some 36,000 men had been officially diagnosed by the Silicosis Medical Board or the Pneumoconiosis Panels of the Ministry of National Insurance as being disabled by the disease. Over 80% of these cases had arisen in the South Wales coalfield. The social consequences of the disease in South Wales have been reviewed by Hugh-Jones and Fletcher (1950). The cost of the disease in terms of compensation has been enormous and in terms of human suffering immeasurable. The disease is one that has been shown to be due to the inhalation of coal dust (Hart and Aslett, 1942) and its ultimate control and prevention will come from dust suppression. Airborne dust concentrations underground must be reduced to levels at which they will not cause pneumoconiosis in men exposed to them throughout a normal working life. Coal dust in some mines appears to be less dangerous than in others. But since the factors which may make coal dust dangerous are not yet known, the precise levels of dust concentration in different pits which may be regarded as safe are uncertain, and indeed they cannot be established until a generation of coal miners has been exposed to them for their working life and has been shown to remain healthy. At present the Ministry of Fuel and Power and the National Coal Board have accepted as provisional levels for approved dust conditions under which men may be expected to work with reasonable safety, 650 particles/cc.* between 1 and 5 microns in anthracite pits and 850 particles/cc., within the same size range, in steam and bituminous coal pits. This expectation is, however, based on scanty evidence (Bedford and Warner, 1942), and the approved dust levels
Sovetskoe zdravookhranenie / Ministerstvo zdravookhranenii︠a︡ SSSR | 1971
Charles Fletcher; D. Horn
A new development in the 20th century has been the increasing use of cigarettes manufactured primarily from flue-cured tobaccos. It has been clearly shown during the last 20 years that cigarette smoking impairs health to such a serious degree that means for its control must be developed. Cigarette smoking has been found to have a major part in the development of many diseases the most important of which are ischemic heart disease lung cancer chronic bronchitis and emphysema. Apart from these diseases which are major causes of death cigarette smoking is responsible for widespread and distressing disability from chest and heart diseases and increases the mortality and disability from several other conditions. The more recent adoption of cigarette smoking by women in developed countries is already associated with increasing mortality and morbidity from lung cancer and other illnesses. The health effects of smoking are largely confined to the individual smoker and although severe become manifest only after many years of smoking and are therefore not obviously connected with the habit. In countries where deaths and disability associated with cigarette smoking are already at high levels more preventive action is necessary. It is essential to take action that will promote the reduction or discontinuance of smoking and that will discourage young people from starting to smoke. Focus in the remainder of the discussion is on evidence connecting smoking with disease smoking habits and total mortality diseases causing excess mortality of cigarette smokers cigarette smoking as a cause of excess mortality cigarette smoking as a cause of excess morbidity specific diseases related to cigarette smoking approaches to prevention and experience in the United States.
BMJ | 1987
Charles Fletcher
recommends 1500 mg of calcium daily for women with osteoporosis it seems to imply a major role for calcium in the management of this condition. The section on fluoride is ambiguous but that on vitamin D is positively misleading. No mention is made of calcium malabsorption, which is a common feature of established osteoporosis, or of the fact that this malabsorption responds dramatically to alfacalcidol or calcitriol.5 Nor is any attempt made to distinguish between the use of low dose calcitriol for correcting calcium malabsorption, which is almost certainly beneficial, and high dose calcitriol for stimulating bone turnover, which causes hypercalcaemia and is almost certainly harmful. The section on anabolic steroids is also mistaken in its emphasis, particularly in relation to side effects. The grim picture it paints ofatherogenesis, liver dysfunction, and possible liver tumours arises from a failure to distinguish between orally administered steroids, which pass through the liver and may have major effects on liver function and lipids, and parenteral steroids, which have only a marginal adverse effect on the lipids. Although even parenteral anabolic steroids given to whole populations over long periods might produce a detectable rise in cardiovascular mortality, the risk to an individual given six to 12 months of such treatment must be negligible. Above all, the weakness of the report (as noted by Dr Tony Smith (p 872)) is its failure to identify which women should be given the oestrogen treatment that the panel so strongly advocates. The average reader may not realise that the main determinant of bone density for many years after the menopause is the initial value at the time of menopause. This is because the range of bone densities in premenopausal women (±22% of the mean6) is large compared with the rates ofbone loss (1-2% a year). The women who require preventive treatment are therefore those whose bone density at the time of menopause is low; they are at increased risk of fracture from the beginning and cannot afford to lose bone. From this it follows that women should be screened by bone densitometry (a forearm measurement is almost certainly adequate7) at about the time of the menopause. Our policy is to reassure and dismiss those above the 75th centile, to investigate and treat those below the 25th centile, and to ask those in the middle of the range to return for remeasurement after a year or so, or to estimate their bone loss from blood and urine measurements.8 Finally, could we stop hearing about the traditional risk factors invoked by Dr Smith? There is no evidence that small stature is a risk factor for osteoporosis and little evidence of a family history in osteoporotic women. There is some evidence that thin people lose bone faster than fat people but nothing to suggest that the all important peak bone density is determined by body weight. Of course, women with an early menopause start losing bone early but because the rate of loss slows down with time and because women lose bone at different rates the bone density in women over 60 is independent of their age at menopause.9 In our experience the menopausal age of osteoporotic women is also no different from that of normal subjects matched for chronological age.
Annals of Internal Medicine | 1968
Charles Fletcher; Cecily Tinker; I. David Hill; Frank S. Speizer
Excerpt The study was designed to test the hypothesis that in the development of chronic airway obstruction mucous hypersecretion encourages bronchial infection which causes bronchiolar damage, or ...
BMJ | 1977
Charles Fletcher; Richard Peto
BMJ | 1986
Peter Maguire; S Fairbairn; Charles Fletcher
BMJ | 1984
Charles Fletcher