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Dive into the research topics where Barry Lewis is active.

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Arteriosclerosis, Thrombosis, and Vascular Biology | 1999

Coronary Heart Disease: Reducing the Risk: The Scientific Background to Primary and Secondary Prevention of Coronary Heart Disease A Worldwide View

Gerd Assmann; Paul Cullen; Fabrizio Jossa; Barry Lewis; Mario Mancini

Coronary heart disease (CHD) is the major cause of death in most developed countries and in many developing countries. The clinical complications of CHD lead to substantial disability and are a main source of the rising cost of health care. While CHD incidence is decreasing in western Europe, the United States, and Australia, it is steeply increasing in central and eastern Europe and, to some extent, in Asia and Africa.1 2 3 4 Worldwide, the need for more effective preventive strategies against CHD has become urgent and cannot be postponed. Much has been learned about preventive policies, both at the population and the individual level, in the past decade. The International Task Force for Prevention of CHD has developed an updated document that takes into account the results of the recent, major, lipid-lowering trials of primary and secondary prevention. Clinical and quantitative approaches are provided to assess the global risk of CHD according to classic and newly recognized risk factors and thereby to assign an appropriate level of intervention against risk factors. This targeted strategy maximizes the use of dietary methods and provides clear indications for drug treatment.nnThe primary importance of improving health-related behavior in the population as a whole is emphasized. In the present document, the undervalued scope for preventive care at the individual clinical level is the major theme; it is based on the selection and management …


Circulation | 1999

Coronary Heart Disease: Reducing The Risk A Worldwide View

Gerd Assmann; Rafael Carmena; Paul Cullen; Jean-Charles Fruchart; Fabrizio Jossa; Barry Lewis; Mario Mancini; Rodolfo Paoletti

Worldwide, cardiovascular diseases are now the most common cause of death and a substantial source of chronic disability and health costs. In the light of new data from clinical trials and a fuller understanding of risk factors, the International Task Force for the Prevention of Coronary Heart Disease, in cooperation with the International Atherosclerosis Society, prepared a revised and comprehensive statement regarding the scientific basis of the primary and secondary prevention of cardiovascular disease. The following is a short account of the clinical implications of this statement. It is best read in conjunction with the full document, which can be found at http://www.chd-taskforce.comnnAssessing a patient’s overall or global risk of cardiovascular disease is the first step in preventive care, for it enables the physician to identify and provide the appropriate level of treatment for risk factors. Much can be learned from measuring even a few risk factors. The fuller the knowledge of the patient’s risk status, the sounder the treatment decisions. Initial costs may be offset by long-term rational treatment. The goals of treatment and, hence, the extent of dietary change and the need for (and choice and dosage of) drug treatment all depend on global risk assessment. Two methods for determining global risk follow.nnNote and tabulate the following risk factors, including those laboratory investigations that are available.nn### Age, Sex, and Menopausal StatusnnRisk increases progressively with adult age, and coronary heart disease (CHD) is most common after the age of 60 years. In premenopausal women, CHD is rare (except in those who use oral contraceptives and smoke). After menopause, risk increases steeply, approaching that of men after the age of 70 years.nn### History of Cardiovascular DiseasennThe risk of further CHD events or stroke is much higher in persons with a history of myocardial infarction, angina, stroke, or intermittent claudication and in those who have ischemic …


The Lancet | 1972

CLINICAL AND METABOLIC STUDY OF ALCOHOLIC HYPERLIPIDÆMIA

Alan Chait; AubreyW February; Mario Mancini; Barry Lewis

Abstract In a survey of identifiable causes of hypertriglyceridaemia, alcoholic excess seemed to be remarkably common. Accordingly, the mechanism and clinical features of alcoholic lipaemia have been studied in thirteen patients. Alcohol did not decrease peripheral uptake of triglyceride from plasma, as assessed by the intravenous fat-tolerance test. It is suggested that alcohol increases hepatic secretion of lipoprotein, inducing hyperlipidaemia in individuals predisposed by having a relatively low ability to clear triglyceride from plasma.


The Lancet | 1971

Serum lipids and lipoproteins in peripheral vascular disease.

RogerM. Greenhalgh; David S. Rosengarten; Ivan Mervart; Barry Lewis; J.S. Calnan; Peter Martin

Abstract Fasting serum-lipid concentrations were abnormally high in 44% of a consecutive series of 116 patients with proven peripheral vascular disease. In 39% of patients with peripheral vascular disease the serum-triglyceride level was raised. In 15% of patients the serum-cholesterol level was increased. Lipoprotein abnormalities were identified in 39% of patients, with a preponderance of increased prebeta-lipoprotein over other abnormalities.


European Journal of Clinical Investigation | 1972

Plasma Triglyceride and Fatty Acid Metabolism in Diabetes mellitus

Barry Lewis; Mario Mancini; Martin Mattock; Alan Chait; T. Russell Fraser

Abstract. Free fatty acid and triglyceride metabolism was studied in diet‐responsive and insulin‐dependent diabetics and in non‐diabetic obese patients before and during treatment. Free fatty acid turnover was elevated in diabetics and in most obese patients, and was decreased by diabetic control; it showed no significant change in the obese patients during caloric restriction. Plasma triglyceride levels exceeded 160 mg/100 ml in 20 of the 34 diabetics, and gross lipaemia occurred both in insulin‐requiring and diet‐responsive patients. The fractional turnover of injected triglyceride was low in 20 of 33 measurements on untreated diabetics, and was negatively correlated with endogenous triglyceride levels. The fractional turnover increased significantly during diabetic control. These findings are compatible with the view that diabetic hypertrigly ceridaemia may be due in part to impaired removal of triglyceride from plasma.


The Lancet | 1973

TRIGLYCERIDE METABOLISM IN THYROID DISEASE

B.R. Tulloch; Barry Lewis; T. Russell Fraser

Abstract The fasting levels of plasma-triglyceride were increased in nine out of ten primary hypothyroid subjects, and they returned towards normal after thyroxine therapy. In seven thyrotoxic patients, fasting triglyceride levels were low normal and the mean levels did not change after antithyroid therapy. The clearance-rate of an infused triglyceride load showed abnormalities more striking than the changes observed in circulating triglyceride level. The clearance-rate in hypothyroid subjects was low and in the thyrotoxic patients it was either high or normal. After treatment of either state the fractional clearance-rates tended towards normal. There were parallel changes in free-fatty-acid flux. In the hypothyroid subjects, a slow clearance of exogenous triglyceride was associated with low post-heparin lipolytic activity (P.H.L.A.), but in the thyrotoxic subjects the rapid clearance of triglyceride was associated with unexpected low or low normal P.H.L.A. levels. It is suggested that in thyroid disease the tissue clearance of circulating triglycerides may be an important determinant of fasting plasma-triglyceride values.


Clinica Chimica Acta | 1971

The binding of cholic acid and its taurine conjugate to serum proteins

C.W. Burke; Barry Lewis; D. Panveliwalla; Soad Tabaqchali

Abstract By the method of steady-state gel filtration, cholic and taurocholic acids have been shown to be strongly bound by plasma albumin. Cholic acid is more avidly bound than its taurine conjugate. There is probably one primary binding site per albumin molecule, and approximately 7 secondary sites of weaker affinity. Plasma has a very high binding capacity for bile acids and the binding shows rapid equilibration. In the stagnant loop syndrome, protein binding of unconjugated, bile acids may be a factor contributing to their high concentration in plasma.


BMJ | 1980

Dietary prevention of ischaemic heart disease--a policy for the '80s.

Barry Lewis

The two daughters of the Greek god of healing, Asklepios, represent contrasting attitudes to medical care: Panaceas name has been translated as Cure-all and Hygieias as Health. Neither approach alone could overcome the problem of ischaemic heart disease, which led to 156 000 deaths in England and Wales in 1976, proportionately more in Scotland, and much acute and chronic sickness. The valued contributions of coronary care units and of coronary artery surgery in individual management of patients have been estimated to reduce overall mortality from ischaemic heart disease by 4% and (on generous assumptions) 4-5% respectively.12 Medium term trials indicate a place for drug treatment with beta adrenergic blockers,3 and sulphinpyrazone4 and aspirin5 may possibly reduce the risk of reinfarction in patients with ischaemic heart disease. But the need for primary prevention is inescapable.


BMJ | 1974

Experience with simplified scheme of treatment of hyperlipidaemia.

Soad Tabaqchali; Alan Chait; Rosamund Harrison; Barry Lewis

A series of 57 hyperlipidaemic patients have been investigated clinically and by measurement of cholesterol and triglyceride levels and inspection of stored serum. Two had secondary (alcoholic) hyperlipidaemia. Those with primary disorders were allocated to three groups believed to require different optimal therapy. At one year 51 of these 55 patients had lipid levels within a predetermined normal range and two others showed improvement. Despite the large number of primary hyperlipidaemic states our results suggest that in most patients successful treatment can be given according to simple classification into three therapeutic categories.


BMJ | 1980

Dietary prevention of ischaemic heart disease.

Barry Lewis

industry, membership of the board appears to consist almost entirely of biochemists and nutritionists with no cardiologist and little representation of epidemiology: much of the great body of epidemiological data was not considered. Perhaps the most striking aspect of the report is its inconsistency: the board considers it unwise to make specific recommendations in the absence of conclusive evidence and yet it has found itself able to make firm recommendations conceming a reduction in salt intake. Sir John claims furthermore that none of the best-conducted and statistically controlled trials of lipid-reducing polyunsaturated-fat diets or drugs have shown any preventive effects on the incidence or progress of coronary heart disease. There is no doubt that the recent WHO clofibrate trial showed a reduction in coronary heart disease incidence related to the cholesterol lowering property of this drug (the therapeutic implications of this study have been widely discussed, but this very finding has not been disputed).4 We have reviewed in some detail the dietary studies of coronary heart disease prevention4 and concluded that while absolute proof of a beneficial effect of dietary modification will probably never be produced in any single clinical trial, the results of the trials are encouraging. It is of interest that one of the two studies quoted by Sir John was indeed well conducted but certainly not controlled in the true statistical sense.5 It is difficult indeed to resolve thiis ssue in the correspondence columns of your journal, but we cannot help but wonder whether those who oppose dietary change may not at times be even more open to criticism than the polyunsaturated fat evangelists. We would not count ourselves among the latter since the dietary modification which we recommend does not represent a substantial increase in polyunsaturated fat but rather a reduction in saturated fat which marginally changes the polyunsaturated to saturated fat ratio.

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Mario Mancini

University of Naples Federico II

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Fabrizio Jossa

University of Naples Federico II

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Paul Cullen

University of Münster

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