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Biomedical subjects

R Doll

Publications and source records attributed to R Doll.

At least 55 records · Page 3Linked to original sources
PubMed1999

Possible protective effect of milk, meat and fish for cerebrovascular disease mortality in Japan.

Cerebrovascular disease was a leading cause of death from 1955 to 1980 in Japan. The mortality rate from this disease has decreased sharply in recent decades. This downward trend seems to correspond to the dietary habits of Japanese. Data from a large prospective cohort study were analyzed to examine the association between dietary habits and cerebrovascular disease mortality in Japan. The subjects for this analysis were 223,170 men and women aged 40 to 69 at baseline in December 1965. There were 6,168 deaths in men and 4,862 deaths in women due to cerebrovascular disease (ICD7: 330-334) during the follow-up period from January 1966 to December 1981. Rate ratio (RR) and 95% confidence interval (95% CI) adjusted for sex, attained age, follow-up period, prefecture, cigarette smoking, alcohol drinking and occupation was used for comparison. In this study, the risk of mortality from cerebrovascular disease was inversely associated with dairy milk, meat and fish consumption. Therefore the joint effect of dairy milk, meat and fish (DMF) as animal fat and protein was of interest. In the binary analysis, DMF (D, M, F) means the combination of dairy milk (1-3 times/week or more), meat (1-3 times/week or more) and fish (4 times/week or more). Thus DMF (d, m, f) was the reference group having dairy milk (less than 1 time/week), meat (less than 1 time/week) and fish (less than 4 times/week). For the disease, the RR of DMF (D, M, F) was 0.68 with 95% CI of 0.63 to 0.74, relative to the reference group. Furthermore the joint effect of DMF was more strongly associated with cerebral haemorrhage (ICD7: 331, DMF (D, M, F); RR: 0.63, 95% CI: 0.55-0.70) than with cerebral embolism and thrombosis (ICD7: 332, DMF (D, M, F); RR: 0.79, 95% CI: 0.70-0.89). These findings suggest that the increasing intake of animal fat and/or protein may have played a key role in reducing cerebrovascular disease in Japan.

Adult↗
PubMed1999

Risk from tobacco and potentials for health gain.

Evidence that smoking tobacco harms health has accumulated over 200 years, but was largely ignored before 1950, when five case-control studies associated smoking with the development of lung cancer. The idea that it might cause the disease was greeted with scepticism, and it was nearly 10 years before it became generally accepted. By then there had been additional evidence from cohort studies, and known carcinogens had been identified in tobacco tars. Cigarette smoking has now been positively associated with some 40 causes of death and negatively associated with eight or nine. A few of the associations are due to confounding, but the great majority reflect causality. In several instances cigarette smoking increases the risk of death ten-fold, and altogether it doubles the annual risk of death at all ages combined, in both sexes. Tobacco smoke in the environment also has a small effect on the health of non-smokers, particularly in infancy and childhood, but also to some extent later in life. Nearly a quarter of all deaths in men and a tenth in women in industrialised countries in 1990 were attributed to smoking, giving a total of 1.8 million a year. In 20-30 years' time the total is estimated to rise to 10 million a year, with 7 million in low income countries, if smoking habits persist unchanged.

Humans↗
PubMed1999

Cancer patients' expectations of the role of family physicians in communication about complementary therapies.

OBJECTIVE: To explore cancer patients' experiences with and expectations of the role of family physicians in communication about complementary therapies. DESIGN: Focus group interviews. SETTING: British Columbia Cancer Agency and the University of Calgary. PARTICIPANTS: Sample of 14 cancer patients using complementary therapies comprising 3 focus groups (2 in BC and 1 in Alberta). RESULTS: The role of family physicians in discussing complementary therapies varied from being extraneous to patients' decision making to being a partner in making decisions about cancer treatments. Patients expected their physicians to be supportive, caring, kind and to show an interest in them. They also expected their physicians to be accepting and nonjudgmental regarding complementary therapy use and to reinforce a sense of hope. Most patients did not expect their doctors to have extensive knowledge about these therapies. All patients strongly felt the need to seek information themselves. In addition, they felt that believing in the type of therapies they were using was very important. CONCLUSION: Family physicians can play an important role in exploring and discussing complementary therapies with their patients. It is important that they are made aware of their patients' needs in this area.

Aged↗
PubMed1998

Epidemiological evidence of the effects of behaviour and the environment on the risk of human cancer.

The incidence of cancer in middle and old age can, in principle, be reduced by 80%-90% and the risks worldwide could be halved, although the methods required are not always socially acceptable. The proportions of fatal cancers attributable to different causes are examined under 17 headings: smoking, alcohol, pharmaceutical products, infection (parasites, bacteria, viruses) electromagnetic radiation (ionizing, ultraviolet, lower frequency) occupation, industrial products, pollution (air, water, food), physical inactivity, reproductive hormones, and diet. Smoking is the most important factor. It contributes to the production of seven types of cancer in addition to the eight that were recognized by the International Agency for Research on Cancer in 1986 and is estimated to have been responsible for 38% of cancers in men and 6% in women in Germany in 1985. Firm estimates can also be made of the proportions of fatal cancers attributable to alcohol and ionizing radiation, and reasonable guesses can be made at the maximum effect of some of the other categories. Many of the factors act synergistically with one another, so that the risk of developing specific cancers can be modified in different ways. When all the avoidable causes are known, the sum of the proportions avoidable in different ways may add up to several hundred per cent.

Diet↗
PubMed1998

Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine.

The time course of expression of TNF-alpha in myocardial wound healing following ischemic injury was investigated in the porcine heart. Microembolization was used to induce focal ischemia and necrosis in hearts of 39 adult pigs. The animals were sacrificed after 3, 6, 12, 24 h, 3 and 7 days, and after 4 weeks, and the myocardial tissue was studied by immunofluorescence using specific antibodies. TNF-alpha containing cells were identified as monocytes/macrophages by double staining with a muramidase antibody. Monocytes/macrophages were the only source of TNF-alpha. Microembolization caused multiple necrotic foci with loss of myocytes in the left ventricular myocardium. These foci contained numerous monocytes/macrophages and showed an inflammatory reaction typical of wound healing followed by replacement with scar tissue. The number of TNF-alpha positive cells increased after 24 h, peaked between 3-7 days and slowly decreased thereafter. Expression of TNF-alpha in monocytes/macrophages was significantly reduced after pretreatment of pigs with cyclosporine or dexamethasone. It is concluded that 1.) in myocardial tissue monocytes/macrophages are the only cell type expressing TNF-alpha, 2.) TNF-alpha is involved in wound healing after ischemia, and 3.) synthesis of TNF-alpha and inflammatory angiogenesis can be inhibited be treatment with either cyclosporine or dexamethasone.

Animals↗
PubMed1998

Risk of lung cancer associated with residential radon exposure in south-west England: a case-control study.

Studies of underground miners occupationally exposed to radon have consistently demonstrated an increased risk of lung cancer in both smokers and non-smokers. Radon exposure also occurs elsewhere, especially in houses, and estimates based on the findings for miners suggest that residential radon is responsible for about one in 20 lung cancers in the UK, most being caused in combination with smoking. These calculations depend, however, on several assumptions and more direct evidence on the magnitude of the risk is needed. To obtain such evidence, a case-control study was carried out in south-west England in which 982 subjects with lung cancer and 3185 control subjects were interviewed. In addition, radon concentrations were measured at the addresses at which subjects had lived during the 30-year period ending 5 years before the interview. Lung cancer risk was examined in relation to residential radon concentration after taking into account the length of time that subjects had lived at each address and adjusting for age, sex, smoking status, county of residence and social class. The relative risk of lung cancer increased by 0.08 (95% CI -0.03, 0.20) per 100 Bq m(-3) increase in the observed time-weighted residential radon concentration. When the analysis was restricted to the 484 subjects with lung cancer and the 1637 control subjects with radon measurements available for the entire 30-year period of interest, the corresponding increase was somewhat higher at 0.14 per 100 Bq m(-3) (95% CI 0.01, 0.29), although the difference between this group and the remaining subjects was not statistically significant. When the analysis was repeated taking into account uncertainties in the assessment of radon exposure, the estimated increases in relative risk per 100 Bq m(-3) were larger, at 0.12 (95% CI -0.05, 0.33) when all subjects were included and 0.24 (95% CI -0.01, 0.56) when limited to subjects with radon measurements available for all 30 years. These results are consistent with those from studies of residential radon carried out in other countries in which data on individual subjects have been collected. The combined evidence suggests that the risk of lung cancer associated with residential radon exposure is about the size that has been postulated on the basis of the studies of miners exposed to radon.

Aged↗
PubMed1998

The benefit of alcohol in moderation.

Small amounts of alcohol were held to be beneficial in the 19th century, but the idea died out. Scientific evidence that moderate amounts prolonged life, published in 1926, was ignored. Further evidence accumulated from the early 1950s but the belief that alcohol was only harmful had become so ingrained that the idea has been taken seriously only since the early 1980s. Now, the evidence that small amounts reduce the risk of vascular disease by about a third and reduce total mortality in middle and old age is massive. Alternative explanations for the observed inverse relationships have been ruled out and beneficial effects have been shown to be biologically plausible. The reduction in mortality is mainly attributable to ischaemic heart disease and cerebral thrombosis, but some other diseases may also contribute to it. The increasing mortality with larger amounts is attributable to many causes that have long been recognized. The optimum level varies with sex and age and may be zero under about age 45 years. The benefit is directly due to ethanol and the extra benefit attributed to wine is due to the pattern of drinking. Public policy needs to take account of medical and social effects other than mortality and will vary in different communities depending on background patterns of injury and disease.

Journal Article↗
PubMed1998

Uncovering the effects of smoking: historical perspective.

Tobacco was introduced into Europe from America at the end of the fifteen century. At first used primarily for medicinal purposes it came to be burnt in pipes for pleasure on a large scale nearly 100 years later, at first in England and subsequently in Europe and throughout the world. Pipe smoking gave way to the use of tobacco as snuff and, in turn, to cigars and cigarettes at different times in different countries until cigarette smoking became the dominant form in most of the developed world between the two world wars. Societies were formed to discourage smoking at the beginning of the century in several countries, but they had little success except in Germany where they were officially supported by the government after the Nazis seized power. In retrospect it can now be seen that medical evidence of the harm done by smoking has been accumulating for 200 years, at first in relation to cancers of the lip and mouth, and then in relation to vascular disease and cancer of the lung. The evidence was generally ignored until five case-control studies relating smoking to the development of lung cancer were published in 1950. These stimulated much research, including the conduct of cohort studies, which, by the late 1950s, were beginning to show that smoking was associated with the development of many other diseases as well. The interpretation that smoking caused these various diseases was vigorously debated for some years but came to be generally accepted in respect of lung cancer by the late 1950s and of many other diseases in the subsequent two decades. Cigarette smoking has now been found to be positively associated with nearly 40 diseases or causes of death and to be negatively associated with eight or nine more. In some instances the positive associations are largely or wholly due to confounding, but the great majority have been shown to be causal in character. The few diseases negatively associated with smoking are for the most part rare or nonfatal and their impact on disease incidence and mortality as a result of smoking is less than 1% of the excess of other diseases that are caused by smoking. The most recent observations show that continued cigarette smoking throughout adult life doubles age-specific mortality rates, nearly trebling them in late middle age. All the diseases related to smoking that cause large numbers of deaths should now have been discovered, but further nonfatal diseases may remain to be revealed by cohort studies that are able to link individuals' morbidity data with their personal characteristics.

Aged↗
PubMed1998

Effects of small doses of ionising radiation.

Uncertainty remains about the quantitative effects of doses of ionising radiation less than 0.2 Sv. Estimates of hereditary effects, based on the atomic bomb survivors, suggest that the mutation doubling dose is about 2 Sv for acute low LET radiation, but the confidence limits are wide. The idea that paternal gonadal irradiation might explain the Seascale cluster of childhood leukaemia has been disproved. Fetal irradiation may lead to a reduction in IQ and an increase in seizures in childhood proportional to dose. Estimates that doses to a whole population cause a risk of cancer proportional to dose, with 0.1 Sv given acutely causing a risk of 1%, will need to be modified as more information is obtained, but the idea that there is a threshold for risk above this level is not supported by observations on the irradiated fetus or the effect of fallout. The idea, based on ecological observations, that small doses protect against the development of cancer is refuted by the effect of radon in houses. New observations on the atomic bomb survivors have raised afresh the possibility that small doses may also have other somatic effects.

Dose-Response Relationship, Radiation↗
PubMed1997

Alcohol consumption and mortality among middle-aged and elderly U.S. adults.

BACKGROUND: Alcohol consumption has both adverse and beneficial effects on survival. We examined the balance of these in a large prospective study of mortality among U.S. adults. METHODS: Of 490,000 men and women (mean age, 56 years; range, 30 to 104) who reported their alcohol and tobacco use in 1982, 46,000 died during nine years of follow-up. We compared cause-specific and rates of death from all causes across categories of base-line alcohol consumption, adjusting for other risk factors, and related drinking and smoking habits to the cumulative probability of dying between the ages of 35 and 69 years. RESULTS: Causes of death associated with drinking were cirrhosis and alcoholism; cancers of the mouth, esophagus, pharynx, larynx, and liver combined; breast cancer in women; and injuries and other external causes in men. The mortality from breast cancer was 30 percent higher among women reporting at least one drink daily than among nondrinkers (relative risk, 1.3; 95 percent confidence interval, 1.1 to 1.6). The rates of death from all cardiovascular diseases were 30 to 40 percent lower among men (relative risk, 0.7; 95 percent confidence interval, 0.7 to 0.8) and women (relative risk, 0.6; 95 percent confidence interval, 0.6 to 0.7) reporting at least one drink daily than among nondrinkers, with little relation to the level of consumption. The overall death rates were lowest among men and women reporting about one drink daily. Mortality from all causes increased with heavier drinking, particularly among adults under age 60 with lower risk of cardiovascular disease. Alcohol consumption was associated with a small reduction in the overall risk of death in middle age (ages 35 to 69), whereas smoking approximately doubled this risk. CONCLUSIONS: In this middle-aged and elderly population, moderate alcohol consumption slightly reduced overall mortality. The benefit depended in part on age and background cardiovascular risk and was far smaller than the large increase in risk produced by tobacco.

Adult↗
PubMed1997

Accumulation of lovastatin, but not pravastatin, in the blood of cyclosporine-treated kidney graft patients after multiple doses.

OBJECTIVES: To study pravastatin and lovastatin pharmacokinetic and pharmacodynamic effects and their interactions with cydosporine (INN, ciclosporin) in kidney transplant patients after single and multiple doses. SUBJECTS AND METHODS: The pharmacokinetic and pharmacodynamic effects of administration of 20 mg/day oral pravastatin and lovastatin for 28 days and their interactions with cyclosporine (2 to 6 mg/kg/day) were studied in a double-blind, double-dummy, randomized, parallel-group multicenter trial in 44 stable kidney graft recipients. RESULTS: The median area under the curve [AUC(0-24)] of pravastatin was 249 microg x hr/L (range, 104 to 1026 microg x hr/L) after a single dose (day 1) and 241 microg x hr/L (114 to 969 microg x hr/L) after multiple doses (day 28) and was fivefold higher than values reported in the absence of cyclosporine. The median AUC(0-24) of lovastatin was 243 microg x hr/L (105 to 858 microg x hr/L) on day 1 and 459 microg x hr/L (140 to 1508 microg x hr/L) on day 28. Besides a significant accumulation during the study period (p < 0.001), the lovastatin AUC(0-24) values were twentyfold higher than values reported without cyclosporine. Coadministration of pravastatin or lovastatin did not alter cyclosporine pharmacokinetics. In this study, 20 mg/day doses of both drugs resulted in a significant improvement of the lipid profile and were well tolerated. CONCLUSIONS: In contrast to lovastatin, pravastatin did not accumulate over the study period, which is probably one of the reasons rhabdomyolysis has been reported in lovastatin-treated but not pravastatin-treated transplant patients receiving cyclosporine immunosuppression.

Adult↗