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M R Law

Publications and source records attributed to M R Law.

At least 37 records · Page 2Linked to original sources
PubMed1998

Why is mortality higher in poorer areas and in more northern areas of England and Wales?

STUDY OBJECTIVE: To identify and quantify the factors responsible for the differences in mortality between affluent and deprived areas, the north and the south, and urban and rural areas in England and Wales. DESIGN: A multiple Poisson regression analysis of cause specific mortality in the 403 local authority districts, each classified by deprivation (using the Jarman Index), latitude (from 50 degrees to 55 degrees north) and urbanisation, adjusting for age, sex, and proportion of ethnic minorities. SETTING: England and Wales 1992. MAIN RESULTS: All cause mortality was 15% higher in the districts comprising the most compared with the least deprived tenth of the population, 23% higher in the most northern (55 degrees) than in the most southern (50 degrees) districts, and 4% higher in metropolitan (within large cities) than rural districts. Nationally these differences were associated with 40,000, 65,000, and 15,000 excess deaths respectively. More than two thirds of the overall excess mortality with deprivation, latitude, and urbanisation was from three diseases--ischaemic heart disease, lung cancer, and chronic bronchitis and emphysema. The excess mortality from these and other diseases closely matched that predicted from differences according to deprivation and latitude in smoking, heavy alcohol consumption, Helicobacter pylori infection, and temperature, and thus could be attributed to these causes. About 85% of the overall excess mortality with deprivation was attributable to heavier smoking and 6% to heavier alcohol consumption, but diet varied little. Deaths more directly related to deprivation (such as those caused by H pylori infection, drug misuse, psychoses) accounted for an estimated 12% of the excess deaths, but variation in provision and uptake of healthcare services only 1%. The direct effects of deprivation are more strongly related to morbidity than mortality. Of the difference in mortality with latitude, about 45% was attributable to differences in smoking, and 25% to climate (mainly the association of cardiovascular and respiratory disease with cold). The differences with urbanisation were mainly because of smoking. CONCLUSIONS: Differences in the prevalence of smoking account for much of the variation in mortality between areas. Alcohol accounts for some, diet little. The more direct material effect of deprivation contributes to the variation in mortality but is particularly important with respect to differences in morbidity.

Age Factors↗
PubMed1997

Helicobacter pylori infection and mortality from ischaemic heart disease: negative result from a large, prospective study.

OBJECTIVE: To determine whether there is an independent association between Helicobacter pylori infection of the stomach and ischaemic heart disease. DESIGN: Prospective study with measurement of IgG antibody titres specific to H pylori on stored serum samples from 648 men who died from ischaemic heart disease and 1296 age matched controls who did not (nested case-control design). SUBJECTS: 21,520 professional men aged 35-64 who attended the British United Provident Association (BUPA) medical centre in London between 1975 and 1982 for routine medical examination. MAIN OUTCOME MEASURE: Death from ischaemic heart disease. RESULTS: The odds of death from ischaemic heart disease in men with H pylori infection relative to that in men without infection was 1.06 (95% confidence interval 0.86 to 1.31). In a separate group of 206 people attending the centre, plasma fibrinogen was virtually the same in those who were positive for H pylori (2.62 g/l) and those who were negative (2.64 g/l). CONCLUSIONS: A study that by its size and design minimised both random error and socioeconomic bias found no relation between H pylori infection and ischaemic heart disease. The validity of the study was shown by its confirmation of the recognised association between H pylori infection and stomach cancer (odds ratio 4.0 (1.9 to 8.2); P < 0.001). Eradication of H pylori infection may greatly reduce the incidence of stomach cancer, one of the most common causes of death from cancer worldwide, but it cannot be expected to have any effect in preventing ischaemic heart disease.

Adult↗
PubMed1997

Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence.

OBJECTIVES: To estimate the risk of ischaemic heart disease caused by exposure to environmental tobacco smoke and to explain why the associated excess risk is almost half that of smoking 20 cigarettes per day when the exposure is only about 1% that of smoking. DESIGN: Meta-analysis of all 19 acceptable published studies of risk of ischaemic heart disease in lifelong non-smokers who live with a smoker and in those who live with a non-smoker, five large prospective studies of smoking and ischaemic heart disease, and studies of platelet aggregation and studies of diet according to exposure to tobacco smoke. RESULTS: The relative risk of ischaemic heart disease associated with exposure to environmental tobacco smoke was 1.30 (95% confidence interval 1.22 to 1.38) at age 65. At the same age the estimated relative risk associated with smoking one cigarette per day was similar (1.39 (1.18 to 1.64)), while for 20 per day it was 1.78 (1.31 to 2.44). Two separate analyses indicated that non-smokers who live with smokers eat a diet that places them at a 6% higher risk of ischaemic heart disease, so the direct effect of environmental tobacco smoke is to increase risk by 23% (14% to 33%), since 1.30/1.06 = 1.23. Platelet aggregation provides a plausible and quantitatively consistent mechanism for the low dose effect. The increase in platelet aggregation produced experimentally by exposure to environmental tobacco smoke would be expected to have acute effects increasing the risk of ischaemic heart disease by 34%. CONCLUSION: Breathing other people's smoke is an important and avoidable cause of ischaemic heart disease, increasing a person's risk by a quarter.

Aged↗
PubMed1997

The accumulated evidence on lung cancer and environmental tobacco smoke.

OBJECTIVE: To estimate the risk of lung cancer in lifelong non-smokers exposed to environmental tobacco smoke. DESIGN: Analysis of 37 published epidemiological studies of the risk of lung cancer (4626 cases) in non-smokers who did and did not live with a smoker. The risk estimate was compared with that from linear extrapolation of the risk in smokers using seven studies of biochemical markers of tobacco smoke intake. MAIN OUTCOME MEASURE: Relative risk of lung cancer in lifelong non-smokers according to whether the spouse currently smoked or had never smoked. RESULTS: The excess risk of lung cancer was 24% (95% confidence interval 13% to 36%) in non-smokers who lived with a smoker (P < 0.001). Adjustment for the effects of bias (positive and negative) and dietary confounding had little overall effect; the adjusted excess risk was 26% (7% to 47%). The dose-response relation of the risk of lung cancer with both the number of cigarettes smoked by the spouse and the duration of exposure was significant. The excess risk derived by linear extrapolation from that in smokers was 19%, similar to the direct estimate of 26%. CONCLUSION: The epidemiological and biochemical evidence on exposure to environmental tobacco smoke, with the supporting evidence of tobacco specific carcinogens in the blood and urine of non-smokers exposed to environmental tobacco smoke, provides compelling confirmation that breathing other people's tobacco smoke is a cause of lung cancer.

Adenocarcinoma↗
PubMed1997

A meta-analysis of cigarette smoking, bone mineral density and risk of hip fracture: recognition of a major effect.

OBJECTIVE: To determine the magnitude and importance of the relation between smoking, bone mineral density, and risk of hip fracture according to age. DESIGN: Meta-analysis of 29 published cross sectional studies reporting the difference in bone density in 2156 smokers and 9705 non-smokers according to age, and of 19 cohort and case-control studies recording 3889 hip fractures reporting risk in smokers relative to non-smokers. RESULTS: In premenopausal women bone density was similar in smokers and non-smokers. Postmenopausal bone loss was greater in current smokers than non-smokers, bone density diminishing by about an additional 2% for every 10 year increase in age, with a difference of 6% at age 80. In current smokers relative to non-smokers the risk of hip fracture was similar at age 50 but greater thereafter by an estimated 17% at age 60, 41% at 70, 71% at 80, and 108% at 90. These estimates of relative risk by age, derived directly from a regression analysis of the studies of smoking and hip fracture, were close to estimates using the difference in bone density between smokers and non-smokers and the association between bone density and risk of hip fracture. The estimated cumulative risk of hip fracture in women in England was 19% in smokers and 12% in non-smokers to age 85; 37% and 22% to age 90. Among all women, one hip fracture in eight is attributable to smoking. Limited data in men suggest a similar proportionate effect of smoking as in women. The association was not explained by smokers being thinner, younger at menopause, and exercising less nor by actions of smoking on oestrogen, but smoking may have a direct action on bone. CONCLUSIONS: Hip fracture in old age is a major adverse effect of smoking after the menopause. The cumulative excess bone loss over decades is substantial, increasing the lifetime risk of hip fracture by about half.

Adult↗
PubMed1997

Cigarette smoking, sex hormones and bone density in women.

It is known that among women over the age of 65, bone mineral density is lower, and the risk of hip fracture higher, in smokers than non-smokers. We report a study in 1334 health pre- and post-menopausal women aged 35-64 years, to determine whether this effect can be attributed to lower oestrogen levels in smokers. Among 676 premenopausal women forearm bone density was no lower in smokers (95% confidence interval 1% lower, 4% higher). Among 543 postmenopausal women who had not used hormone replacement therapy (HRT) for more than a year there was no statistically significant difference, but the lower confidence interval was consistent with a lower bone density in older smokers (by 8% at age 55-59, 16% at age 60-64). Measurements in 194 postmenopausal women not taking HRT showed that oestrone and oestradiol were similar in smokers and non-smokers, as were cortisol and FSH, LH and prolactin. Meta-analysis of the present study and previous studies confirmed significantly higher levels in smokers of the androgens DHEAS (by 37%) and androstenedione (by 34%). Oestrogens were no lower in smokers, and the lower confidence limit excluded more than a trivial effect of smoking in lowering oestrogen. These results indicate that the recognised lower bone density in elderly smokers cannot be explained by an effect of smoking on oestrogen, since in premenopausal women bone density is no lower in smokers and in postmenopausal women oestrogens are no lower in smokers. The data suggest a balance between higher androgen levels but lower rates of conversion of androgens to oestrogens in smokers. The effect of smoking on bone may be due to impaired response of bone and other target organs to oestrogen, or to actions independent of oestrogen.

Adult↗
PubMed1997

The dose-response relationship between cigarette consumption, biochemical markers and risk of lung cancer.

The relationship between the number of cigarettes smoked per day and the incidence of lung cancer is linear but, from the multistage model of carcinogenesis, it should be quadratic (upwards curving). We investigated this anomaly in a study of 11,403 male never smokers and current smokers in whom carboxyhaemoglobin (COHb) was measured in all and serum cotinine in 1175. The relationship between the biochemical markers and the reported number of cigarettes per day was approximately linear up to 20 cigarettes per day as expected. But above 20 cigarettes per day the marker levels increased less steeply and were 35% lower than expected in men who smoked more than 40 cigarettes per day. Less smoke is inhaled from each cigarette by men with high daily cigarette consumption than by men with lower consumption. Allowance for this transforms the observed linear dose-response relationship into one consistent with the expected quadratic relationship. The anomaly is explained by the observation that heavier smokers inhale less smoke from each cigarette.

Adult↗
PubMed1996

Environmental tobacco smoke.

Environmental tobacco smoke is an important contaminant of indoor air. For a non-smoker living with a smoker the exposure is equivalent to about 1% of that from actively smoking 20 cigarettes a day (based on plasma cotinine). There is strong and consistent evidence that passive smoking increases the risk of lung cancer. It is estimated that there is an increase in risk of 24% (95% confidence interval 11-38%) compared to unexposed non-smokers, and several hundred lung cancer deaths per year in Britain are attributable to environmental tobacco smoke exposure. Passive smoking is associated with an increase in risk of chronic respiratory disease in adults of 25% (10-43%), and increases the risk of acute respiratory illness in children, by 50-100%. It is likely that passive smoking increases the risk of ischaemic heart disease, and that exposure in pregnancy lowers birthweight, but there is inconsistency between different estimates of the magnitude of risk. The overall hazard is sufficient to justify measures to restrict smoking in public places and workplaces, and to discourage people from smoking in their homes.

Adult↗
PubMed1995

Increasing incidence of tuberculosis in England and Wales: a study of the likely causes.

OBJECTIVE: To examine factors responsible for the recent increase in tuberculosis in England and Wales. DESIGN: Study of the incidence of tuberculosis (a) in the 403 local authority districts in England and Wales, ranked according to Jarman score, and (b) in one deprived inner city district, according to ethnic origin and other factors. SETTING: (a) England and Wales 1980-92, and (b) the London borough of Hackney 1986-93. MAIN OUTCOME MEASURE: Age and sex adjusted rate of tuberculosis. RESULTS: In England and Wales notifications of tuberculosis increased by 12% between 1988 and 1992. The increase was 35% in the poorest 10th of the population and 13% in the next two; and in the remaining 70% there was no increase. In Hackney the increase affected traditionally high risk and low risk ethnic groups to a similar extent. In the "low risk" white and West Indian communities the incidence increased by 58% from 1986-8 (78 cases) to 1991-3 (123), whereas in residents of Indian subcontinent origin the increase was 41% (from 51 cases to 72). Tuberculosis in recently arrived immigrants--refugees (11% of the Hackney population) and Africans (6%)--accounted for less than half of the overall increase, and the proportion of such residents was much higher than in most socioeconomically deprived districts. The local increase was not due to an increase in the proportion of cases notified, to HIV infection, nor to an increase in homeless people. CONCLUSIONS: The national rise in tuberculosis affects only the poorest areas. Within one such area all residents (white and established ethnic minorities) were affected to a similar extent. The evidence indicates a major role for socioeconomic factors in the increase in tuberculosis and only a minor role for recent immigration from endemic areas.

Asia↗
PubMed1995

Serum cholesterol and ischaemic heart disease.

A systematic examination of the evidence on the relationship between serum cholesterol and ischaemic heart disease shows conclusively that serum cholesterol reduction in populations with high rates of heart disease is an effective and safe method of reducing ischaemic heart disease rates. The relative protective effect is greater at younger ages (50% reduction at age 40 for a 0.6 mmol/l reduction in serum cholesterol declining to about 20% at age 70 or more). The absolute protective effect is greater if the disease is common because the effect of a give serum cholesterol reduction is proportional to the prevailing heart disease rate. The full effect of a serum cholesterol reduction is evident after about 5 years. The use of drugs of the 'statin' type can lower serum cholesterol by about 1.8 mmol/l, yielding a reduction in risk of about 60% at age 60. A diet typical in Japan would lower serum cholesterol by about 1.2 mmol/l and lead to a halving of the risk. Only modest serum cholesterol reductions (about 0.3 mmol/l) are generally achievable by individuals altering their diet independently of others and this is expected to lead to a 15% reduction in the risk of ischaemic heart disease at age 60. Larger reductions (about 0.6 mmol/l) require collective action over the supply and preparation of food which could reduce the risk by about 30%. Achieving the full impact of serum cholesterol reduction in a population will require a national nutritional policy. It is not something that can be effectively left to individual action.

Adult↗
PubMed1994

Systematic underestimation of association between serum cholesterol concentration and ischaemic heart disease in observational studies: data from the BUPA study.

OBJECTIVE: To estimate the size of the association between serum concentration of low density lipoprotein cholesterol and mortality from ischaemic heart disease. DESIGN: Prospective study of total serum cholesterol concentration and mortality from ischaemic heart disease in 21,515 men (538 deaths) and study of total cholesterol concentration measured on two occasions an average of three years apart in 5696 men in whom low density lipoprotein cholesterol concentration was also measured on the second occasion. SUBJECTS: Men who attended the medical centre of the British United Provident Association (BUPA) in London between 1975 and 1982. MAIN OUTCOME MEASURE: The difference in mortality from ischaemic heart disease for a 0.6 mmol/l difference in concentration of low density lipoprotein cholesterol after adjustment for, firstly, regression dilution bias, which arises from the random fluctuation of serum cholesterol concentration in people over time, and, secondly, the surrogate dilution effect, which arises because differences in total cholesterol concentration between people reflect smaller differences in low density lipoprotein cholesterol concentration. RESULTS: The observed difference in mortality from ischaemic heart disease associated with a difference of 0.6 mmol/l in total serum cholesterol concentration was 17% but increased to 24% after correction for the regression dilution bias and to 27% (95% confidence interval 21% to 33%) after adjustment for both sources of underestimation, which provides an estimate of the difference in mortality for a true difference of 0.6 mmol/l in low density lipoprotein cholesterol concentration. The association was greater at younger ages. The estimated decrease in mortality from all causes was 6% before and 10% (1% to 17%) after adjustment for the two sources of underestimation. There was no excess mortality from any cause associated with low cholesterol concentration. CONCLUSIONS: The association between serum cholesterol concentration and ischaemic heart disease is materially stronger than directly inferred from prospective studies. This has important implications for the health benefit of achieving low cholesterol concentrations.

Adult↗