Search PubMed⌕ Search

Biomedical subjects

G C Watt

Publications and source records attributed to G C Watt.

15 recordsLinked to original sources
PubMed1992

Abnormalities of glucocorticoid metabolism and the renin-angiotensin system: a four-corners approach to the identification of genetic determinants of blood pressure.

AIM: To assess the feasibility and utility of a new method to identify factors associated with increased predisposition to high blood pressure in young people. SUBJECTS: Eight hundred and sixty-four people aged 16-24 years and their parents. SETTING: Ladywell Medical Centre, Edinburgh, Scotland, UK. METHOD: Blood pressure was measured in 864 young adults and in both of their parents. Four groups of approximately 50 offspring were selected from the corners of a scatter diagram, with offspring blood pressure scores on one axis and combined parental blood pressure scores on the other. Blood and urine samples were taken for biochemical and genetic analyses. RESULTS: Two groups of offspring had parents with high blood pressure and two groups had parents with low blood pressure. When parental blood pressure was low, comparison of offspring with high and low blood pressure revealed significantly higher mean body mass index in offspring with high blood pressure, but no significant elevation of biochemical or hormonal variables. When parental blood pressure was high, comparison of offspring with high and low blood pressure also revealed a significant difference in body mass index, but in addition, offspring with high blood pressure and high parental blood pressure had higher levels of angiotensinogen, cortisol and 18-OH corticosterone. Restriction fragment length polymorphism analysis revealed that 27% of offspring at the greatest genetic risk (high personal and parental blood pressure) were homozygous for the larger allele of the glucocorticoid receptor gene compared with only 9% of those at lowest genetic risk (low personal and parental blood pressure). CONCLUSION: The combined biochemical and genetic findings suggest that abnormalities of glucocorticoid metabolism and the renin-angiotensin system may help to explain genetic predisposition to high blood pressure. The new sampling method is practicable and could be applied to the investigation of other continuously distributed variables which show familial aggregation.

Adolescent↗
PubMed1992

Potential impact of emergency intervention on sudden deaths from coronary heart disease in Glasgow.

OBJECTIVE: To determine the potential impact of emergency intervention strategies to prevent deaths from coronary heart disease outside hospital. DESIGN: Analysis of routine medical and legal records of all persons dying of coronary heart disease in a defined population. SETTING: Glasgow City, north of the river Clyde, 1984. SUBJECTS: 420 people under 65 years for whom the underlying cause of death on the death certificate was coronary heart disease (ICD 410-414, 9th Revision). RESULTS: Of the 296 deaths outside hospital, 73% occurred at home. The deaths of 40% of those who died outside hospital were not witnessed and these people could not have received prompt cardiopulmonary resuscitation. Only 16% of the witnesses of a death attempted cardiopulmonary resuscitation before the arrival of a doctor or an ambulance crew. Over half (53%) of the cases in which cardiopulmonary resuscitation could have been attempted by a witness, but was not attempted, death occurred in the presence of the spouse or other close relative. Death occurred in the presence of a duty doctor or the ambulance crew in a maximum of 5% of deaths outside hospital. Ninety one per cent of people were dead before a call for help was made. CONCLUSION: Unless a greater proportion of patients receive cardiopulmonary resuscitation before emergency staff arrive at the scene the provision of emergency care staff with defibrillators is unlikely to have a significant impact on deaths outside hospital caused by coronary heart disease.

Adult↗
PubMed1992

Mortality in Glasgow and Edinburgh: a paradigm of inequality in health.

STUDY OBJECTIVE: The aim was to describe, predict, and interpret mortality in Glasgow and Edinburgh. DESIGN: The study was an analysis of all cause and cause specific mortality data for quinquennia based on census years between 1931 and 1981, linking age and sex specific mortality rates by year of birth, for people dying between the ages of 25 and 74 years. SETTING: Glasgow and Edinburgh, Scotland. MAIN RESULTS: Age and sex specific mortality rates declined steadily in Edinburgh and Glasgow during the period 1931-1981, with rates always being lower in Edinburgh than in Glasgow. Since 1961 log mortality rates have tended to rise linearly with age in both cities. In 1979-83, the population of Glasgow reached a given all cause mortality rate 3.9 years earlier in men and 3.6 years earlier in women than did the population of Edinburgh. These differences have increased, and are predicted to increase further, especially in men. CONCLUSIONS: The current 40% cross sectional difference in mortality rates between the cities is largely determined by levels of mortality in early adulthood which provide a baseline for the subsequent rise in log mortality. Disease specific epidemiology provides a limited view of inequalities in health, and a partial basis for health promotion. Campaigns to alter disease risk profiles in adults should be complemented by measures operating earlier in life to reduce susceptibility to risk. Maternal and child health require greater priority in public health policy, particularly in areas of socioeconomic disadvantage.

Adult↗
PubMed1991

Prediction of high blood pressure in young people: the limited usefulness of parental blood pressure data.

Blood pressure was measured in 864 young people aged 16-24 years, 8 years after both of their parents had their blood pressures measured as part of the screening phase of the Medical Research Council Mild Hypertension Trial. Only 29% of offspring with a conventional 'family history of hypertension', defined in terms of having at least one parent with a score in the top 10% of the distribution, had a blood pressure score in the top 20% after 8 years. The positive predictive value was increased to 38% in offspring with two parents in the top 20%, but only 4% of offspring met this definition and only 7% of offspring in the top 20% after 8 years were identified by this method. Sensitivity was increased to 46% in offspring with at least one parent in the top 20%, but 33% of offspring met this definition and 74% of them did not have a blood pressure level in the top 20% after 8 years. It is concluded that parental blood pressure data are of limited value for the prediction of high blood pressure in young people and provide no scientific basis for a high risk strategy of prevention.

Adolescent↗
PubMed1988

Does "susceptibility" explain the weak epidemiological relationship between dietary sodium and blood pressure?

It is often suggested that the weak epidemiological relationship between dietary sodium and blood pressure may reflect a stronger relationship within a susceptible subgroup. The evidence in favour of this explanation is reviewed, and found to be insubstantial. A more consistent explanation of the available data is that there is a weak general effect of dietary sodium on blood pressure acting on the general population. This conclusion has important practical implications for food and health policies.

Blood Pressure↗
PubMed1985

Dietary sodium and arterial blood pressure: evidence against genetic susceptibility.

Thirty five subjects with both parents in the top third of their age specific blood pressure distributions and 31 subjects with both parents in the bottom third of their blood pressure distributions restricted their intake of sodium for eight weeks while taking part in a double blind, randomised crossover trial of supplements of sodium and placebo. A comparison of two periods of four weeks at different intakes of sodium showed no differences in blood pressure in either the groups as a whole or the subgroups who complied best with the diet and tablets. In the compliant subgroups mean urinary sodium excretions were above 120 mmol(mEq) and below 50 mmol/day. The study provides evidence against the hypothesis that people with a family history of high blood pressure are more susceptible in their blood pressure response to dietary sodium.

Adult↗