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The overall improvement in the health of Americans over the 20th century is best exemplified by dramatic changes in 2 trends: 1) the age-adjusted death rate declined by about 74%, while 2) life expectancy increased 56%. Leading causes of death shifted from infectious to chronic diseases. In 1900, infectious respiratory diseases accounted for nearly a quarter of all deaths. In 1998, the 10 leading causes of death in the United States were, respectively, heart disease and cancer followed by stroke, chronic obstructive pulmonary disease, accidents (unintentional injuries), pneumonia and influenza, diabetes, suicide, kidney diseases, and chronic liver disease and cirrhosis. Together these leading causes accounted for 84% of all deaths. The size and composition of the American population is fundamentally affected by the fertility rate and the number of births. From the beginning of the century there was a steady decline in the fertility rate to a low point in 1936. The postwar baby boom peaked in 1957, when 123 of every 1000 women aged 15 to 44 years gave birth. Thereafter, fertility rates began a steady decline. Trends in the number of births parallel the trends in the fertility rate. Beginning in 1936 and continuing to 1956, there was precipitous decline in maternal mortality from 582 deaths per 100 000 live births in 1935 to 40 in 1956. Since 1950 the maternal mortality ratio dropped by 90% to 7.1 in 1998. The infant mortality rate has shown an exponential decline during the 20th century. In 1915, approximately 100 white infants per 1000 live births died in the first year of life; the rate for black infants was almost twice as high. In 1998, the infant mortality rate was 7.2 overall, 6.0 for white infants, and 14.3 for black infants. For children older than 1 year of age, the overall decline in mortality during the 20th century has been spectacular. In 1900, >3 in 100 children died between their first and 20th birthday; today, <2 in 1000 die. At the beginning of the 20th century, the leading causes of child mortality were infectious diseases, including diarrheal diseases, diphtheria, measles, pneumonia and influenza, scarlet fever, tuberculosis, typhoid and paratyphoid fevers, and whooping cough. Between 1900 and 1998, the percentage of child deaths attributable to infectious diseases declined from 61.6% to 2%. Accidents accounted for 6.3% of child deaths in 1900, but 43.9% in 1998. Between 1900 and 1998, the death rate from accidents, now usually called unintentional injuries, declined two-thirds, from 47. 5 to 15.9 deaths per 100 000. The child dependency ratio far exceeded the elderly dependency ratio during most of the 20th century, particularly during the first 70 years. The elderly ratio has gained incrementally since then and the large increase expected beginning in 2010 indicates that the difference in the 2 ratios will become considerably less by 2030. The challenge for the 21st century is how to balance the needs of children with the growing demands for a large aging population of elderly persons.
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PMID:Annual summary of vital statistics: trends in the health of Americans during the 20th century. 1109 82

This supplement includes a collection of papers that aim at estimating the relationship between per capita alcohol consumption and various forms of mortality, including mortality from liver cirrhosis, accidents, suicide, homicide, ischaemic heart disease, and total mortality. The papers apply a uniform methodological protocol, and they are all based on time series data covering the post-war period in the present EU countries and Norway. In this paper we discuss various methodological and analytical issues that are common to these papers. We argue that analysis of time series data is the most feasible approach for assessing the aggregate health consequences of changes in population drinking. We further discuss how aggregate data may also be useful for judging the plausibility of individual-level relationships, particularly those prone to be confounded by selection effects. The aggregation of linear and curvilinear risk curves is treated as well as various methods for dealing with the time-lag problem. With regard to estimation techniques we find country specific analyses preferable to pooled cross-sectional/time series models since the latter incorporate the dubious element of geographical co-variation, and conceal potentially interesting variations in alcohol effects. The approach taken in the papers at hand is instead to pool the country specific results into three groups of countries that represent different drinking cultures; traditional wine countries of southern Europe, beer countries of central Europe and the British Isles and spirits countries of northern Europe. The findings of the papers reinforce the central tenet of the public health perspective that overall consumption is an important determinant of alcohol-related harm rates. However, there is a variation across country groups in alcohol effects, particularly those on violent deaths, that indicates the potential importance of drinking patterns. There is no support for the notion that increases in per capita consumption have any cardioprotective effects at the population level.
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PMID:Alcohol and mortality: methodological and analytical issues in aggregate analyses. 1122 78

Serine proteinase inhibitors (Serpins) are irreversible suicide inhibitors of proteases that regulate diverse physiological processes such as coagulation, fibrinolysis, complement activation, angiogenesis, apoptosis, inflammation, neoplasia and viral pathogenesis. The molecular structure and physical properties of serpins permit these proteins to adopt a number of variant conformations under physiological conditions including the native inhibitory form and several inactive, non-inhibitory forms, such as complexes with protease or other ligands, cleaved, polymerised and oxidised. Alterations of a serpin which affect its structure and/or secretion and thus reduce its functional levels may result in pathology. Serpin dysfunction has been implicated in thrombosis, emphysema, liver cirrhosis, immune hypersensitivity and mental disorders. The loss of inhibitory activity of serpins necessarily results in an imbalance between proteases and their inhibitors, but it may also have other physiological effects through the generation of abnormal concentrations of modified, non-inhibitory forms of serpins. Although these forms of inhibitory serpins are detected in tissues and fluids recovered from inflammatory sites, the important questions of which conditions result in generation of different molecular forms of serpins, what biological function these forms have, and which of them are directly linked to pathologies and/or may be useful markers for characterisation of disease states, remain to be answered. Elucidation of the biological activities of non-inhibitory forms of serpins may provide useful insights into the pathogenesis of diseases and suggest new therapeutic strategies.
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PMID:Conformational properties of serine proteinase inhibitors (serpins) confer multiple pathophysiological roles. 1127 63

We evaluated the mortality risk among 306 male alcoholics living in Osaka, Japan, at the time of initial diagnosis between 1972 and 1983, with regard to the cause of death, length of time from diagnosis, and participation in an alcohol abstinence self-help group. By the closing date on 1 March 1992, 110 of the 306 alcoholics had died, yielding an observed-to-expected (O/E) ratio of 4.5 [95% confidence interval (CI) = 3.7-5.4]. The alcoholics had significantly elevated mortality risks from all malignant neoplasms (O/E = 2.1, 95%CI = 1.2-3.3), esophageal cancer (O/E = 8.4, 95%CI = 1.7-24.5), diseases of the circulatory system (O/E = 4.4, 95%CI = 3.0-6.2), liver cirrhosis (O/E = 15.9, 95%CI = 10.2-23.6), diseases of the genitourinary system (O/E = 6.3, 95%CI = 1.3-18.5), and external death (O/E = 10.3, 95%CI = 6.3-15.8). The mortality risk from all causes still remained significantly high beyond the tenth year following initial diagnosis (O/E = 2.6, 95%CI = 1.0-6.2). The mortality risks from liver cirrhosis and external death (such as suicide) were highest within the first year following diagnosis, and were still high beyond the tenth year. A significantly high mortality risk from diseases of the circulatory system was observed between the first and ninth years, and the mortality risk from all malignant neoplasms was significantly elevated beyond 10 years following diagnosis. Alcoholics who did not join a self-help group soon after the initial institutional treatment had different cause-specific and time-specific mortality risks from those who did join a self-help group. These findings show the importance of long-term clinical follow-up of male alcoholics, taking into consideration the cause-specific mortality.
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PMID:Cause-specific mortality risk among male alcoholics residing in the Osaka metropolitan area. 1155 41

The updated cohort consisted of 3328 workers who were employed at the Mobil (now ExxonMobil) Torrance, California, refinery for at least 1 year between 1959 and 1997. The vital status of the cohort was determined through a variety of sources, including company employment or retirement records, the Social Security Administration's Death Master File, and the National Death Index. The updated study covered an observation period of 38 years from 1960 to 1997, with a total of 60,612 person-years of observation. A total of 705 (21.2%) cohort members were identified as having died. Mortality data were analyzed in terms of cause-specific standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs), with expected deaths based on US national cause-, gender-, race-, year-, and age-specific mortality rates. The overall mortality of the cohort was significantly lower than expected when compared with the US general population (SMR, 81.9; 95% CI, 76.0 to 88.2). Overall cancer mortality was also lower than expected (SMR, 79.8; 95% CI, 67.9 to 93.1). For specific cancer sites, significant mortality deficits were observed for cancer of the digestive system (SMR, 70.9; 95% CI, 49.4 to 98.6) and cancer of the respiratory system (SMR, 74.1; 95% CI, 55.5 to 97.0). No significant increase was reported for any site-specific cancer. For nonmalignant diseases, no significant increase was observed for any cause. In particular, significant mortality deficits were reported for ischemic heart disease (SMR, 87.7; 95% CI, 77.2 to 99.3), chronic endocardial disease and other myocardial insufficiencies (SMR, 8.3; 95% CI, 0.2 to 46.0), all other heart disease (SMR, 64.2; 95% CI, 43.0 to 92.2), and influenza and pneumonia (SMR, 59.2; 95% CI, 33.1 to 97.6). Detailed analysis by length of employment did not reveal any significant mortality excess or upward trend. Analyses of male employees by job classification (process and maintenance) were conducted. Among maintenance workers, mortality from cirrhosis of the liver (SMR, 190.1; 95% CI, 101.2 to 325.1) and suicide (SMR, 208.6; 95% CI, 111.1 to 356.7) were significantly elevated. However, these mortality excesses did not seem to be related to employment at the refinery. No other causes of death showed significant increase among maintenance workers. A similar separate analysis was conducted for process workers, and no significant excess was detected for any cause. The findings from the present study are discussed in conjunction with results from previous investigations of employees at the Torrance refinery and with results from other refinery studies. Potential limitations of the study are also discussed.
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PMID:Updated mortality study of workers at a petroleum refinery in Torrance, California, 1959 to 1997. 1176 80

The shortage of organ donors has impeded the development of human hepatocyte transplantation. Immortalized hepatocytes could provide an unlimited supply of transplantable cells. To determine whether immortalized hepatocytes could provide global metabolic support in end-stage liver disease, 35 immortalized rat hepatocyte clones were developed by transduction with the gene encoding the simian virus 40 T antigen (SV40Tag). The SV40Tag sequence and a suicide gene, herpes simplex virus thymidine kinase (HSV-tk), were flanked by loxP sequences so that they could be excised by Cre/lox recombination. When transplanted into the spleens of portacaval-shunted rats, 3 of the 35 immortalized hepatocyte clones prevented the development of hyperammonemia-induced hepatic encephalopathy. The protection was reversed by treatment with ganciclovir, which kills HSV-tk-expressing cells. Transplantation of alginate-encapsulated, immortalized hepatocytes into the spleens of cirrhotic rats resulted in significant improvement in prothrombin time, serum albumin and bilirubin levels, hepatic encephalopathy score, and duration of survival. The metabolic support provided by the immortalized cells equaled that observed after transplantation of primary rat hepatocytes. In conclusion, immortalized hepatocytes can function as well as primary hepatocytes following transplantation and can be engineered to contain safeguards that could make them clinically useful. Further investigation is warranted regarding the mechanisms of loss of mass or function of the transplanted hepatocytes over time and how the relatively few engrafted hepatocytes can ameliorate liver decompensation in cirrhosis.
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PMID:Treatment of liver failure in rats with end-stage cirrhosis by transplantation of immortalized hepatocytes. 1214 47

"The death rates at ages over 40 in Japan were analyzed using Japanese Vital Statistics for 1947-1988. Secular changes in the death rate and the age-specific death rate were analyzed according to sex and major causes of death. Twelve major causes of death were as follows: (1) malignant neoplasms, (2) heart disease, (3) cerebrovascular disease, (4) pneumonia and bronchitis, (5) accidents and adverse effects, (6) senility without mention of psychosis, (7) suicide, (8) chronic liver disease and cirrhosis, (9) nephritis, nephrotic syndrome and nephrosis, (10) hypertensive disease, (11) diabetes mellitus and (12) mental disorders.... The mean age at death increased 50 years [over] the last 38 years." (SUMMARY IN ENG)
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PMID:[[Mortality in the elderly population aged over 40 in Japan, 1947-1988]]. 1228 12

"Mortality data of the Federal Republic of Germany and the GDR [German Democratic Republic] are compared by age, sex and cause of death....Within the period from 1976 to 1986 life expectancy has risen in the Federal Republic of Germany, whereas in the GDR it increased to a minor extent only, so that the gap between the two parts of Germany has clearly enlarged. This enlarged gap in life expectancy largely depends on a higher mortality in the GDR due to diseases of the circular system and the respiratory organs, external influences and 'other' causes of death. The last-mentioned two groups also 'contain' the normally [separately] reported causes of death 'cirrhosis of the liver', 'suicide', 'accidents', and some diseases of the digestive system." (SUMMARY IN FRE)
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PMID:Mortality in the two Germanies in 1986 and trends 1976-1986. 1228 62

Information was gathered on the smoking habits of 187,783 white men between the ages of 50 and 69 between January 1 and May 31, 1952. The men were subsequently traced through October 31, 1955. 11,870 men died during this period. The total experience covered 667,753 man years. For microscopically proved cases of cancer and for the total cases reported as cancer it was found that the death rates were higher among regular cigarette smokers than among men who never smoked, that the mortality ratio increased with the number of cigarettes smoked each day, and that the death rates were higher among pipe and cigar smokers than among men who never smoked. 7316 deaths occurred among regular cigarette smokers; this was an excess of 2665 over the 4651 deaths that would have occurred had the age-specific death rates for smokers been equal to that for nonsmokers. Coronary disease accounted for 52.1% of the excess; lung cancer accounted for 13.5% of the excess; and cancer of other sites accounted for 13.5% of the excess. An extremely high association between cigarette smoking and death rates for men with lung cancer was found in both rural areas and large cities. Only 338 deaths were ascribed to pulmonary diseases other than lung cancer. Only 1120 (9.4%) of the 11,870 deaths were attributed to diseases other than cancer, cardiac, circulatory, and pulmonary diseases and accidents, violence, and suicide. Only 3 of the specific disease entities - gastric and duodenal ulcers and cirrhosis of the liver - showed a statistically significant degree of association with smoking habits. The most important finding of this study was the high degree of association between cigarette smoking and the total death rate.
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PMID:Smoking and death rates: report on forty-four months of follow-up of 187,783 men. 2. Death rates by cause. 1230 37

Alcohol abuse ranks among the most common and severe environmental hazards to human health. Alcohol is a dependence producing drug and this dependence is associated with an increased risk of morbidity and mortality. While the social and behavioural consequences of alcoholism including psychiatric disorders are staggering, the manifestation of alcohol-related diseases is the most widespread somatic effect. In research conducted both at the social and individual level, alcohol was found to increase the risk of death from a number of specific causes, including injury from traffic accidents and other trauma, violence, suicide, liver cirrhosis, cancer of the liver, breast cancer, haemorrhagic stroke, alcoholic psychosis, alcohol dependence and chronic pancreatitis. The apparent beneficial effect of modest alcohol consumption (one to three drinks per day) on mortality and morbidity rates particularly relating to cardiovascular disease on the other side are of recent interest. Public health policy should aim at reducing the harm done by alcohol use, whilst recognizing its perceived and possible real benefits. The aim of this review is to introduce the reader to the definition of alcohol dependence and alcoholism, and summarize our knowledge about the effects of alcohol consumption on the gastrointestinal tract.
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PMID:Effect of ethanol and alcoholic beverages on the gastrointestinal tract in humans. 1236 39


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