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At least 19 recordsLinked to original sources
PubMed1978

Coffee consumption and mortality. Total mortality, stroke mortality, and coronary heart disease mortality.

Total mortality showed no association with coffee usage in the four race-sex groups of Evans County, Georgia. Deaths of coronary heart disease (CHD) in white men and women and black men showed no statistically significant difference between high and low coffee consumers. In an area that has been designated as the "Stroke Belt," neither CHD nor cerebrovascular death rates seem related to coffee-drinking habits. However, to refute or confirm the allegations of a detrimental influence of high coffee intake, larger samples are needed. Nevertheless, our finding that mortality from all causes is not increased in the high coffee-consuming group means that a finding of increased CHD mortality with high coffee consumption would have to be compensated by a protective lower rate for other causes of death.

Adult↗
PubMed2005

Relation between trends in late middle age mortality and trends in old age mortality--is there evidence for mortality selection?

STUDY OBJECTIVE: To test whether mortality selection was a dominant factor in determining trends in old age mortality, by empirically studying the existence of a negative correlation between trends in late middle age mortality and trends in old age mortality among the same cohorts. DESIGN AND METHODS: A cohort approach was applied to period data on total and cause specific mortality for Denmark, England and Wales, Finland, France, the Netherlands, Norway, and Sweden, in 1950-1999. The study described and correlated mortality trends for five year centralised cohorts from 1895 to 1910 at ages 55-69, with the trends for the same cohorts at ages 80-89. The research distinguished between circulatory diseases, cancers, and diseases specifically related to old age. MAIN RESULTS: All cause mortality changes at ages 80-89 were strongly positively correlated with all cause mortality changes at ages 55-69, especially among men, and in all countries. Virtually the same correlations were seen between all cause mortality changes at ages 80-89 and changes in circulatory disease mortality at ages 55-69. Trends in mortality at ages 80-89 from infectious diseases, pneumonia, diabetes mellitus, symptoms, or external causes showed no clear negative correlations with all cause mortality trends at ages 55-69. CONCLUSIONS: The consistently positive correlations seen in this study suggest that trends in old age mortality in north western Europe in the late 20th century were determined predominantly by the prolonged effects of exposures carried throughout life, and not by mortality selection.

Age Distribution↗
PubMed2005

Assessment of the Pediatric Index of Mortality (PIM) and the Pediatric Risk of Mortality (PRISM) III score for prediction of mortality in a paediatric intensive care unit in Hong Kong.

OBJECTIVE: To compare two models (The Pediatric Risk of Mortality III score and Pediatric Index of Mortality) for prediction of mortality in a paediatric intensive care unit in Hong Kong. DESIGN: Prospective case series. SETTING: A five-bed paediatric intensive care unit in a general hospital in Hong Kong. PATIENTS: All patients consecutively admitted to the unit between April 2001 and March 2003. MAIN OUTCOME MEASURES: Scores for both models compared with observed mortality. RESULTS: A total of 303 patients were admitted to the paediatric intensive care unit during the study period. The median age was 2 years, with an interquartile range of 7 months to 7 years. The male to female ratio was 169:134 (55.8%:44.2%). The median length of hospital stay was 3 days. The overall predicted number of deaths using The Pediatric Risk of Mortality III score was 10.2 patients whereas that by Pediatric Index of Mortality was 13.2 patients. The observed mortality was eight patients. The area under the receiver operating characteristics curve for the two models was 0.910 and 0.912, respectively. CONCLUSION: The predicted mortality using both prediction models correlated well with the observed mortality.

Child↗
PubMed1990

[Analysis of mortality among the population of productive age in Poland. I. Mortality among men and women and the higher mortality rate among men of productive age in Poland 1951-1985].

The paper presents the results of this study on mortality rate during the period of 1951-1985 for men and women aged 20-64. Moreover, the differences between male and female mortalities were analysed with a view of investigating the problem of excessive mortality ratio of men. In the period under study the descending and then ascending tendency of the mortality rate could be observed both in the male and female populations. Up to 1965 male mortality decreased gradually (by 35%) whereas the following years witnessed considerable rise of the level of male mortality (by 30% to 1985), which referred especially to males at the age range between 40 and 49, years. As regards the female population the mortality rate was decreasing till 1975. For the last 10 years increased female mortality has been observed, however, their dynamics is much more lower than that for the female group (by 6.2% less than for 1975). During the whole period examined i.e. 1951-1985 the excessive mortality ratio in men was found to be higher by 60.4%. High dynamics of the ratio concerned male population at lower age ranges.

Adult↗
PubMed1991

Longitudinal Gompertzian analysis of lung cancer mortality in the U.S., 1968-1986. Rising lung cancer mortality is the natural consequence of competitive deterministic mortality dynamics.

Age-adjusted mortality rates for lung cancer (LC) in the United States from 1968 to 1986 were subjected to longitudinal Gompertzian analysis. Age-adjusted LC mortality rate distributions between age 20 and 50 years were determined by a variable environmental factor and a common intersect point. The environmental factor declined (improved) 1.89-fold for men and 3.11-fold for women in 1986 as compared to 1968. The age at the common intersect point was 47.2 years for men and 39.1 years for women. Between 1968 and 1986, the non-age-standardized annual crude LC mortality rate increased 44.8% for men and 217.6% for women. Longitudinal Gompertzian analysis of LC mortality data suggests that the rising LC mortality rates in the United States are the natural consequence of competitive deterministic mortality dynamics and not a reflection of an environment that is directly more conductive to LC mortality. That is, more people are dying of LC because they are not dying from other diseases such as ischemic heart disease and stroke. Longitudinal Gompertzian analysis demonstrates that single disease mortality should not be studied in isolation, but rather examined in relation to other causes of death. When viewed from this perspective, the basis for the more dramatic rise in LC mortality in women becomes immediately evident.

Adult↗
PubMed1990

Longitudinal Gompertzian analysis of Parkinson's disease mortality in the U.S., 1955-1986: the dramatic increase in overall mortality since 1980 is the natural consequence of deterministic mortality dynamics.

Age-adjusted mortality rates for Parkinson's disease (PD) for men and women in the United States, from 1955 to 1986, were calculated and subjected to longitudinal Gompertzian analysis. Annual age-adjusted PD mortality rate distributions were determined by a common intersect point and a variable environmental factor. For men, the death rate at age 73.75 years was 19.15/100,000; for women, the death rate at age 78.99 years was 28.64/100,000 for each year from 1955 to 1986. The environmental factor declined (improved) 360.7-fold for men and 319.6-fold for women in 1986 compared to 1955. Despite this dramatic environmental improvement favoring survival in PD, there has been a 57.6% increase since 1980 in the annual crude PD mortality rate for men compared to the stable annual crude mortality rate from 1955 to 1979. A corresponding 37.9% increase in the annual crude PD mortality rate for women has also occurred since 1980. The increase in overall mortality is due entirely to rapidly increasing age-adjusted mortality rates at ages greater than the intersect points for men and women. The results suggest that overall mortality due to common 'degenerative' diseases may increase dramatically as has occurred in PD.

Age Factors↗
PubMed1990

Longitudinal Gompertzian analysis of stroke mortality in the U.S., 1951-1986: declining stroke mortality is the natural consequence of competitive deterministic mortality dynamics.

Age-adjusted mortality rates for stroke in the United States from 1951 to 1986 were subjected to longitudinal Gompertzian analysis. Age-adjusted stroke mortality rate distributions were determined by a variable environmental factor and a constant Gompertz slope. Compared to 1951 values, the environmental factor in 1986 had declined (improved) 49.8% for men and 59.1% for women. This was associated with a 51.9% and 31.4% decrease in the annual crude mortality rate from stroke for men and women respectively. However, the Gompertz slope remained remarkably constant from 1951 to 1986; 0.050152 for men and 0.048341 for women. The constant Gompertz slope for age-adjusted mortality rate distributions for stroke is in sharp contrast to the increasing Gompertz slope which occurs with an improving environment in 'degenerative' diseases and aging in general. These findings suggest that the recent dramatic decline in overall stroke mortality is the natural consequence of competitive deterministic mortality dynamics. As the overall environment becomes more conducive to human survival, Gompertzian diseases with converging mortality rate distributions must increase as causes of human mortality at the expense of diseases with constant Gompertz slopes.

Adult↗
PubMed1997

Effect of HLA matching on the relative risk of mortality for kidney recipients: a comparison of the mortality risk after transplant to the mortality risk of remaining on the waiting list.

BACKGROUND: Patients must wait increasingly longer periods on the kidney waiting list (WL) before receiving a transplant. Although patients can be maintained on dialysis, many deaths occur while waiting. To determine whether the risk of mortality on the WL is different from that related to the transplant procedure, data from the Organ Procurement and Transplantation Network and Scientific Registry were used to analyze all adult patients entered on the United Network for Organ Sharing (UNOS) kidney WL for a primary transplant between April 1, 1994, and December 31, 1994 (n=9925). METHODS: To account for the time spent on the WL before transplant, a time dependent, nonproportional hazards model was used to assess the risk of mortality after transplant for both well-matched (zero to two HLA mismatches) and poorly-matched (three to six HLA mismatches) transplants compared with the mortality risk of remaining on the WL. This model incorporated an exponential decay component to account for the transient increased risk after kidney transplantation. Patients were stratified by age, race, creatinine level, panel-reactive antibody at listing, and blood group. RESULTS: Although there was an increased risk of mortality in the initial posttransplant period, the risk of mortality at 1 year for transplanted patients was 59% (three to six mismatches) to 67% (zero to two mismatches) less than that of patients who remained on the waiting list for an additional year. CONCLUSIONS: Kidney transplantation is more beneficial than remaining on the waiting list. Even poorly-matched kidneys provided a significant reduction in the risk of mortality by 6 months as compared with the mortality risk of continuing to wait. Patients receive the maximum benefit when transplanted with well-matched kidneys.

Adult↗
PubMedDate not supplied

[Behavior of mortality indicators in small geographic areas: relative standardized mortality ratio and standardized proportional mortality ratio].

One of the most commonly used indicators in mortality studies is the Standardized Mortality Ratio (SMR) being the Relative Standardized Mortality Ratio (RSMR) an indicator of the relative magnitude of the SMR for a specific cause of death. Along with these indicators, which must be calculated by using the population at risk, there is the Standardized Proportional Mortality Ratio (SPMR), an indicator which measures the excess mortality referring to the proportional mortality established for a standard population. This paper reviews the theoretic conditions described in literature as being necessary to establish a probability interval for the RSMR centered on the SPMR as well as the correlations between both indicators and the use of the SPMR as a predictor of the RSMR. The results obtained clearly show how difficult it is for these theoretic conditions to exist. However, they do suggest that the SPMR be used as a predictor of RSMR.

Cause of Death↗
PubMed1992

Studies of the mortality of A-bomb survivors. 9. Mortality, 1950-1985: Part 3. Noncancer mortality based on the revised doses (DS86).

Deaths in the RERF Life Span Study (LSS) sample have been determined for the years 1950-1985 and an analysis of cancer mortality with the revised DS86 doses has been described separately. In this report, we examine the relationship to dose of deaths from all diseases other than cancer. Although the evidence is still limited, there seems to be an excess risk from noncancer death at high doses (2 or 3 Gy and over). Statistically, a pure quadratic or a linear-threshold model [the estimated threshold dose is 1.4 Gy (0.6-2.8 Gy)] is found to fit better than a simple linear or linear-quadratic model. This increase in noncancer mortality is statistically demonstrable, generally, after 1965 and among the younger survivors (less than 40 at the time of the bombing), suggesting a sensitivity for this age group. For specific causes of death, an excess in relative risk at the high dose level, that is, 2 Gy or more, is seen in circulatory and digestive diseases. The relative risk is, however, much smaller than that for cancer. These findings, based as they are on death certificates, have their limitations. Most significant, perhaps, is the possible erroneous attribution of radiation-related cancer deaths to other causes. At present, the contribution such errors may make to the apparent increase in non-cancer deaths at the higher doses cannot be estimated as rigorously as is obviously desirable. However, even now, this increase does not appear to be fully explicable in terms of errors in classification. Further follow-up of mortality in this LSS cohort as well as disease revealed by the biennial physical examinations of the morbidity subsample (Adult Health Study) of the LSS cohort will be needed to confirm this suggestion of a radiation-related increase in mortality from causes other than cancer, and to determine whether it results in a demonstrable life shortening among the heavily exposed A-bomb survivors.

Age Factors↗
PubMed1990

Studies of the mortality of A-bomb survivors. 9. Mortality, 1950-1985: Part 2. Cancer mortality based on the recently revised doses (DS86).

The present study, the ninth in a series that began in 1961, extends the time of surveillance 3 more years and covers the period 1950-1985. It is based on the recently revised doses, termed the DS86. The impact of the change from the T65D to the DS86 on the dose-response relationships for cancer mortality was described in the first of this series of reports. Here, the focus is on cancer mortality among the 76,000 A-bomb survivors within the LSS sample for whom DS86 doses have been estimated, with the emphasis on biological issues associated with radiation carcinogenesis. Briefly, the following is found: The excess in leukemia mortality has continued to decline with time, but remains slightly but significantly elevated in 1981-1985 in Hiroshima. For cancers other than leukemia, as a group, excess deaths continue to increase over time in direct proportion to the normal increase in natural cancer mortality with increasing age, and the relative risk seems unchanged over time within age ATB cohorts. The single exception is the cohort under 10 years of age ATB. Within this group of survivors, where the relative risk, although based on relatively few deaths, has been quite high at the higher doses, as judged by deaths before the age of 30, the risk has fallen and has remained fairly constant at a lower level thereafter. Thus the present analysis still supports, in the main, estimation of lifetime risk based on the assumption of a constant relative risk. For the same age ATD, both the relative and absolute risks are higher for younger age ATB cohorts than older ones for cancers other than leukemia. There is no statistically significant difference in excess deaths between males and females except for leukemia, though the relative risk is higher for females than for males, significantly so for cancers of the esophagus and lung, reflecting the higher background cancer rate for males. Significant dose responses are observed for leukemia, cancers of the esophagus, stomach, colon, lung, breast, ovary, and urinary bladder and multiple myeloma, as previously observed. No significant increase is demonstrable as yet for cancers of the rectum, gallbladder, pancreas, uterus, and prostate and malignant lymphoma. In the present report, cancers of the bone, pharynx, nose, and larynx, and skin except melanoma are also examined, but none of these sites show a significant increase with dose.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1995

Subgroup analyses of the major clinical endpoints in the Program on the Surgical Control of the Hyperlipidemias (POSCH): overall mortality, atherosclerotic coronary heart disease (ACHD) mortality, and ACHD mortality or myocardial infarction.

The Program on the Surgical Control of the Hyperlipidemias (POSCH) was a secondary atherosclerosis intervention trial employing partial ileal bypass surgery as the intervention modality. For this report, we analyzed 105 subgroups in 35 variables in POSCH, chosen predominantly for their potential relationship to the risk of atherosclerotic coronary heart disease (ACHD). We defined potential differential effects as those with: (1) an absolute z-value > or = 2.0 for the subgroup, if the absolute z-value for the overall effect was < 2.0; and (2) an absolute z-value > or = 3.0 for the subgroup and a relative risk < or = 0.5, if the absolute z-value for the overall effect was > or = 2.0. For each of three major POSCH endpoints of overall mortality, ACHD mortality and ACHD mortality or confirmed nonfatal myocardial infarction, we found seven subgroups with a differential risk reduction in the surgery group as compared to the control group. Allowing for identical subgroups for more than one endpoint, there were 13 individual subgroups with differential effects. Of these, seven demonstrated internal consistency across endpoints, and five of these seven displaced external consistency with known ACHD risk factors and for biological plausibility: triglyceride concentration > or = 200 mg/dl; cigarette smoking; overt or borderline diabetes mellitus; a Minnesota ECG Q-QS code of 1-1; and obesity. A greater risk reduction, in comparison to the overall treatment effect, by the reduction of a single risk factor, hypercholesterolemia, in patients with at least two major ACHD risk factors was a provocative and an hypothesis-generating outcome of this analysis. The clinical implications of this finding may lead to more aggressive cholesterol intervention in patients with multiple ACHD risk factors.

Adult↗
PubMed1988

Perinatal mortality in twin pregnancy: an analysis of birth weight-specific mortality rates and adjusted mortality rates for birth weight distributions.

The objective of this study is to compare the fetal mortality rate (FMR), early neonatal mortality rate (ENMR) and perinatal mortality rate (PMR) of twin and single births. It is based on a survey which was carried out in 22 Hospital Centers in Spain in 1980, and covered 1,956 twins born and 110,734 singletons born. The FMR in twins was 36.3/1000 and 8.8/1000 for singletons. The ENMR in twins was 36.1/1000 and 5.7/1000 for singletons. The PMR in twins was 71.1/1000 and 14.4/1000 for singletons. When birthweight-specific PMR in twin and singletons births are compared, there were no differences between the rates for groups 500-999 g and 1000-1499 g. For birthweight groups of 1500-1999 g (124.4 vs 283.8/1000) and 2000-2999 g (29.6 vs 73.2/1000) the rates for twins were about twice lower than those for single births. The PMR for 2500 g and over birthweight was about twice higher in twins than in singletons (12.5 vs 5.5/1000). After we adjusted for birthweight there was a difference in the FMR (12.6 vs 9.8/1000) and the PMR (19.1 vs 16.0/1000, and no difference in the ENMR between twins and singletons (5.9 vs 6.4/1000), indicating that most of the differences among crude rates are due to differences in distribution of birthweight.

Birth Weight↗
PubMed1990

[A statistical study of the countermeasures to reduce the maternal mortality based on the relationship between the maternal mortality rate and perinatal mortality rate].

Although both the Japanese maternal mortality rate (MMR) and the perinatal mortality rate (PMR) have decreased remarkably in recent decades, the former is still high compared with other advanced countries. A statistical analysis on the relationship between the MMR and the PMR was performed to investigate this discrepancy. During the period of study, both rates fell by over 50 percent. There were definite statistical differences among the PMR for each prefecture but almost none among the MMR. The prefectures with high PMR remained generally high in the PMR and the prefectures with low PMR also remained low in the MMR. There was no significant correlation between the PMR and the MMR. Both maternal and perinatal deaths due to common causes decreased in number, and there were few regional differences concerning effective measures against them. The leading causes of maternal death which are irrelevant to perinatal death are emboli, bleeding, and some other rare medical complications. Emphasis should therefore be laid upon the early diagnosis and treatment of amniotic fluid embolism apart from measures against haemorrhage. Countermeasures for rare complications are also of great importance.

Embolism, Amniotic Fluid↗
PubMedDate not supplied

[Analysis of survival and mortality curves with the model of vital receptors. The maximal life span. Effect of temperature on the life span. The mortality probability density function (mortality curve) and its parameters].

We have continued an analysis of survival curves by the model of the vital receptors (MVR). The main types survival function (E-, TW- and GM-distributions) have been considered. It was found that the maximal life span depends on the threshold concentration of vital receptors. Equations are obtained for the dependence of the maximal life span on the kinetic parameters in the reactions of inactivation, destruction and inactivation. Dependence of maximal time life on initial size of the population have been considered. The influence of temperature on the survival curves is analysed by E-distribution. Equations are founded for the description of thermosurvival and thermoinactivation curves. Equation are obtained for the dependence of density function and it characteristics (modal and antimodal age, coefficient of asymmetry) on the MVR parameters. It was shown that E-, TW- and GM-distribution has different types of asymmetry. The coefficient of asymmetry of GM-distribution is associated on the MVR parameters. It is assumed that symmetry of the curves of mortality and birth-rate is coordinated by the mechanisms of MVR.

Algorithms↗
PubMed2005

Shifting dollars, saving lives: what might happen to mortality rates, and socio-economic inequalities in mortality rates, if income was redistributed?

Personal or household income predicts mortality risk, with each additional dollar of income conferring a slightly smaller decrease in the mortality risk. Regardless of whether levels of income inequality in a society impact on mortality rates over and above this individual-level association (i.e., the 'income inequality hypothesis'), the current consensus is that narrowing income distributions will probably improve overall health status and reduce socio-economic inequalities in health. Our objective was to quantify this impact in a national population using 1.3 million 25-59-year-old respondents to the New Zealand 1996 census followed-up for mortality over 3 years. We modelled 10-40% shifts of everyone's income to the mean income (equivalent to 10-40% reductions in the Gini coefficient). The strength of the income-mortality association was modelled using rate ratios from Poisson regression of mortality on the logarithm of equivalised household income, adjusted for confounders of age, marital status, education, car access, and neighbourhood socio-economic deprivation. Overall mortality reduced by 4-13% following 10-40% shifts in everyone's income, respectively. Inequalities in mortality reduced by 12-38% following 10-40% shifts in everyone's income. Sensitivity analyses suggested that halving the strength of the income-mortality association (i.e., assuming our multivariable estimate still overestimated the causal income-mortality association) would result in 2-6% reductions in overall mortality and 6-19% reductions in inequalities in mortality in this New Zealand setting. Many commentators have noted the non-linear association of income with mortality predicts that narrowing the income distribution will both reduce overall mortality rates and reduce inequalities in mortality. Quantifying such reductions can only be done with considerable uncertainty. Nevertheless, we tentatively suggest that the gains in overall mortality will be modest (although still potentially worthwhile from a policy perspective) and the reductions in inequalities in mortality will be more substantial.

Adult↗
PubMed2004

Birth dimensions, parental mortality, and mortality in early adult age: a cohort study of Danish men born in 1953.

BACKGROUND: Birthweight has, in several studies, been associated with mortality in adult age, even after adjustment for available socioeconomic factors. This association has been explained as a biological result of fetal undernutrition (fetal programming), by genetic predisposition, as a result of confounding by factors related to social position and lifestyle, or by a combination of these mechanisms. This study examines the relationship between birth dimensions and all-cause and cause-specific mortality in early adulthood, taking parental lifespan and social position at time of birth into account. Furthermore, the relationship between offspring birth dimensions and parental mortality is addressed. METHODS: In all 10 753 male singletons born in the metropolitan area of Copenhagen, Denmark in 1953 whose birth certificates had been traced manually in 1965 were followed from 1968 to 2002 for information on parents' and own vital status by linkage with the Civil Registration System. Causes of death for the cohort members were identified by record linkage with the Cause-of-Death Registry. Hazard ratios and 95% CI were calculated using Cox regression models. RESULTS: Low birthweight and especially short birth length were strongly associated with adult mortality risk, but no relationship between low ponderal index at birth and mortality was found. The relationship between birth size and early adult mortality was only slightly attenuated after adjustment for early-life social position and/or maternal and paternal lifespan. The associations between birthweight/birth length and mortality were stronger for the age group 35-49 years compared with the age group 15-34 years. Cause-specific mortality was inversely related to small birth dimensions for all causes of death, but strongest and graded for death from liver cirrhosis. Offspring birth dimensions showed an inverse association with parental mortality, which was most pronounced for maternal mortality. CONCLUSIONS: The strong inverse association between birth dimensions and adult mortality, but lack of association between ponderal index and mortality, indicates that more complicated mechanisms than a general long-term detrimental effect of intrauterine growth retardation explain the association between birth size and adult mortality. The heterogeneous associations between birth dimensions and mortality in young and later adulthood, the minor differences in relative risk of cause-specific mortality, and the heterogeneity in the association between birth dimensions and maternal and paternal mortality, respectively, indicate that several mechanisms (factors related to social position, common genetic factors, and specific organ programming) may account for the relation between birth measures and later mortality.

Adult↗