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PubMed2005

A Thomistic understanding of human death.

I investigate Thomas Aquinas's metaphysical account of human death, which is defined in terms of a rational soul separating from its material body. The question at hand concerns what criterion best determines when this separation occurs. Aquinas argues that a body has a rational soul only insofar as it is properly organised to support the soul's vegetative, sensitive, and rational capacities. According the 'higher-brain' concept of death, when a body can no longer provide the biological foundation necessary for the operation of conscious rational thought and volition, a substantial change occurs in which the rational soul departs and the body left behind is a 'humanoid animal' or a mere 'vegetable.' I argue that the separation of soul and body does not occur until the body ceases to function as a unified, integrated organism. A rational soul is not only the seat of a human being's rational capacities; it is also the principle of the body's sensitive and vegetative capacities. Since Aquinas defines a human being as a composite of soul and body, and not with merely the exercise of rational capacities, the determination of death requires incontrovertible evidence that the body has ceased all the operations that correspond to the soul's proper capacities. The evidence of this is the body's loss of its integrative organic unity and the criterion for determining when this loss occurs is the irreversible cessation of whole-brain functioning.

Brain Death↗

PubMed1993

A growth model of a single sugi (Cryptomeria japonica) tree based on the dry matter budget of its aboveground parts.

Growth of a single sugi (Cryptomeria japonica (L.f.) D. Don.) tree was analyzed on the basis of a dry matter budget. The aboveground net production rate and death rate were defined as the anabolic rate and catabolic rate, respectively. Growth rate of aboveground tree weight, v(w) (kg(dw) year(-1)), was defined as follows: v(w) = v(p) - v(d) (1) where v(p) (kg(dw) year(-1)) is the aboveground net production rate and v(d) (kg(dw) year(-1)) is the aboveground death rate. The value of v(d) is obtained by measuring the monthly clippings of new dead leaves and branches attached to a sample tree. The value of v(w) was calculated as the annual difference in the estimated aboveground tree weight, w(T) (kg(dw)). Finally, the value of v(p) was estimated as the sum of the values of v(d) and v(w). The following allometric relationships were found between v(p) and w(T) and between v(d) and w(T): v(p) = aw(T) (alpha), v(d) = bw(T) (beta) (2). Combining Equations 1 and 2 gives a growth equation, Bertalanffy's equation, of the sample tree. dw(T)/dt = v(w) = aw(T) (alpha) - bw(T) (beta) (3). Because the growth curve of w(T) was derived from Equation 3, the analysis of the growth of w(T) is based on direct measurement of the dry matter budget.

Journal Article↗

PubMed2005

Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage.

In glaucoma, harmful intraocular pressure often contributes to retinal ganglion cell death. It is not clear, however, if intraocular pressure directly insults the retinal ganglion cell axon, the soma, or both. The pathways that mediate pressure-induced retinal ganglion cell death are poorly defined, and no molecules are known to be required. DBA/2J mice deficient in the proapoptotic molecule BCL2-associated X protein (BAX) were used to investigate the roles of BAX-mediated cell death pathways in glaucoma. Both Bax+/- and Bax-/- mice were protected from retinal ganglion cell death. In contrast, axonal degeneration was not prevented in either Bax+/- or Bax-/- mice. While BAX deficiency did not prevent axonal degeneration, it did slow axonal loss. Additionally, we compared the effects of BAX deficiency on the glaucoma to its effects on retinal ganglion cell death due to two insults that are proposed to participate in glaucoma. As in the glaucoma, BAX deficiency protected retinal ganglion cells after axon injury by optic nerve crush. However, it did not protect retinal ganglion cells from N-methyl-D-aspartate (NMDA)-induced excitotoxicity. BAX is required for retinal ganglion cell death in an inherited glaucoma; however, it is not required for retinal ganglion cell axon degeneration. This indicates that distinct somal and axonal degeneration pathways are active in this glaucoma. Finally, our data support a role for optic nerve injury but not for NMDA receptor-mediated excitotoxicity in this glaucoma. These findings indicate a need to understand axon-specific degeneration pathways in glaucoma, and they suggest that distinct somal and axonal degeneration pathways may need to be targeted to save vision.

Journal Article↗

PubMed2002

Sex differences in evaluation and outcome after stress testing.

OBJECTIVE: To examine sex differences in evaluation and outcome after stress testing for coronary artery disease (CAD) in a geographically defined cohort. SUBJECTS AND METHODS: Subjects were residents of Olmsted County, Minnesota, who underwent an initial stress test between January 1, 1987, and December 31, 1990. End points included referral for coronary angiography, death, and cardiac events, defined as cardiac death, nonfatal myocardial infarction, or congestive heart failure. RESULTS: A total of 2276 men and 1270 women under went stress tests. Women were older and had more risk factors and comorbidities (P < .05). Among persons without documented CAD (86% of the cohort), the median probability of CAD was 11% (interquartile range, 5%-25%) for men and 8% (interquartile range, 2%-31%) for women (P < .001). Within 6 months after stress testing, 9% of men and 7% of women underwent coronary angiography. Among persons without documented CAD, there was no sex difference in referral for angiography when the stress test result was negative. When the test result was positive, men were more likely to be referred for angiography (adjusted odds ratio [OR] for male sex, 2.02; 95% confidence interval [CI], 1.21-3.38; P = .008). After adjusting for the predicted probability of CAD, this association was no longer detected (adjusted OR for male sex, 0.67; 95% CI, 0.26-1.73; P = .41). Among persons with documented CAD, no sex difference was noted. After a mean +/- SD follow-up of 7.6 +/- 2.7 years and among persons without documented CAD, male sex was associated with a higher adjusted risk of death (relative risk for male sex, 1.40; 95% CI, 1.05-1.86; P = .02) and cardiac events (relative risk for male sex, 1.67; 95% CI, 1.24-2.26; P < .001). Among persons with documented CAD, no sex difference in outcome was noted. CONCLUSION: These population-based data indicate that, when the diagnosis of CAD was not established, there was a greater use of angiography among men with positive stress test results, which could be attributed to the increased probability of CAD in men. In the absence of documented CAD, men fared worse than women, with an increase in the risk of death and cardiac events. Among persons with documented CAD, no sex difference in use of angiography and outcome was noted.

Adult↗

PubMed1998

[Evaluation of high amplification ECG and the study of sinus variability in the detection of patients at risk of sudden death].

In order to define the best strategy of prognostic evaluation in relation to patients in heart failure, 415 patients with impaired left ventricular function (ejection fraction < 40%) were prospectively included, between June 1993 and 1996, in a study comparing the respective value of high amplification ECG and Holter analysis of sinus variability, 308 patients in sinus rhythm and narrow QRS complexes were included. The patients were distributed into 4 groups according to the presence or absence of late potentials and altered sinus variability (group I with 2 normal examinations, group II with late potentials and normal variability, group III without late potentials, but with altered variability and group IV with 2 abnormal examinations). The sudden and overall mortality was significantly greater in groups III (28 and 11%) and IV (28 and 9%) than in group I (7 and 3%) and II (11 and 2%). The presence of potential was unable to identify patients at risk of ventricular tachycardia and sudden death. In another 60 patients with complete branch block, the prognosis was also correlated with the alteration of sinus variability. In conclusion, high amplification ECG correctly evaluated the prognosis of subjects in heart failure. However, analysis of sinus variability should be systematically proposed to detect subjects at high risk of mortality, whether the subject has large or narrow QRS complexes.

Adult↗

PubMedDate not supplied

Adults with tetralogy of Fallot: long-term follow-up.

Tetralogy of Fallot is the most common cyanotic heart lesion and one of the most commonly seen by cardiologists caring for adults with congenital heart disease. In the last 50 years, the outlook for these patients has changed dramatically, and most children with tetralogy of Fallot will live well into adulthood. Although most will have undergone a corrective operation, an important minority of patients with tetralogy of Fallot will have had only a previous palliative procedure. Rarely, the clinician may encounter an adult with unoperated tetralogy of Fallot. With surgical correction, the very long-term outcome is excellent, and most patients lead active and productive lives. However, certain issues must be considered for the long-term care of patients with tetralogy of Fallot. These individuals have an important incidence of residual or recurrent lesions as well as an increased risk for late sudden death. The exact mechanisms for late sudden death are incompletely defined but probably include both the residual hemodynamic and electrophysiologic substrates that act in concert.

Adult↗

PubMed2005

Analyses of efficacy end points in a controlled trial of interferon-gamma1b for idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a devastating disease, yet validated, reliable criteria for evaluating patient response to therapies in clinical trials are lacking. METHODS: To optimize selection of end point criteria for the study of interferon (IFN)-gamma1b in patients with IPF, we retrospectively analyzed the components of the primary efficacy end point used in a large, controlled study of 330 patients for reliability, validity, and sensitivity to treatment effect. The primary end point components were death, disease progression defined as a > or = 5 mm Hg increase in resting alveolar-arterial oxygen pressure gradient (P[A-a]O2), and disease progression defined as a > or = 10% decrease in percentage of predicted FVC. RESULTS: We found that the P(A-a)O2 criterion was not reliable and was not associated with mortality. In contrast, the FVC criterion was reliable and was associated with a 2.4-fold increase in the risk of death. Of the three measures, only mortality was sensitive to a treatment effect of IFN-gamma1b. Additionally, the tendency for mortality benefit was observed in nearly all patient subgroups defined by baseline physiology. The effect of IFN-gamma1b on mortality was strongest in patients with baseline percentage of predicted FVC > or = 55% (p = 0.004) or percentage of predicted diffusing capacity of the lung for carbon monoxide > or = 30% (p = 0.008). CONCLUSION: We conclude that mortality is the most inclusive end point for future trials of IFN- gamma1b in patients with IPF, and that a > 10% decrement in the percentage of predicted FVC represents a valid measure of disease progression.

Adult↗

PubMed1999

Programmed cell death of an identified motoneuron examined in vivo: electrophysiological and morphological correlates.

A paucity of information exists about the electrophysiological and anatomical correlates of neurons committed to die in vivo. Thus, we examined how an identified neuron, motoneuron MN-12, dies during development in the intact moth Manduca sexta. The developmental programmed cell death of this motoneuron was examined because of its defined commitment point of death. In addition, its ability to be unambiguously identified between animals and its accessibility to recording and dye injection facilitated our examination. MN-12 becomes committed to die approximately 28-30 h after adult emergence. At this time, MN-12 can no longer be saved by manipulations of steroid hormone levels, protein synthesis, or removal of descending inputs. Our initial prediction was that within a few hours after the commitment point, MN-12 would begin showing a gradual loss of central arbors and alterations in membrane properties. Contrary to our expectations, we found the MN-12 motoneuron to exhibit a stable central morphology and electrophysiological profile for approximately 12 h, followed by a rapid dismantling that occurred within a 1- to 2-h period. Several hours prior to the commitment point, the target muscle of MN-12 was no longer viable; yet, this did not affect the death of MN-12 or cause retraction of its motor terminals. We conclude that the delayed (12-h) onset of rapid cell death is not preceded by a slow accumulation of damages to the neuronal membrane (e.g., ion channels or cytoskeletal components) as both the electrical activity and morphology of MN-12 remained measurably unaltered during this 12-h lag.

Action Potentials↗

PubMed2006

Programmed cell death of stressed keratinocytes and its inhibition by vitamin D: the role of death and survival signaling pathways.

The epidermis is confronted with multiple environmental and pathophysiological stresses. This study shows that TNFalpha, oxidative stress, hyperosmotic and heat shock induced both caspase-dependent and independent cell death in human HaCaT keratinocytes. The hormonal form of vitamin D, 1,25(OH)2D3, which is an autocrine hormone in the epidermis, protected the cells from all the examined stresses and pathways leading to cell death. We aimed to define the signaling pathways that determine the life-death balance of stressed keratinocytes and participate in their protection by 1,25(OH)2D3. As assessed by employing specific inhibitors, the survival pathways mediated by the EGF receptor, ERK, PI-3K or Src kinase, or basal transcriptional activity are important for unstressed cell survival. However, only the EGF receptor, PI-3K and the Src kinase pathways mediate the survival of stressed cells in a stimulus-specific manner. Inhibition of the p38 and/or the JNK death pathways reduced caspase activation induced by oxidative stress, hyperosmotic shock and TNFalpha. The protective effect of 1,25(OH)2D3 was not mediated by the examined survival pathways. 1,25(OH)2D3 inhibited the stress-induced activation of p38 and JNK. Since mimicking this effect by pharmacological inhibition resulted in the attenuation of caspase activation, we infer that these pathways are involved in keratinocyte protection by 1,25(OH)2D3.

Apoptosis↗

PubMed2001

Iterated birth and death process as a model of radiation cell survival.

The iterated birth and death process is defined as an n-fold iteration of a stochastic process consisting of the combination of instantaneous random killing of individuals in a certain population with a given survival probability s with a Markov birth and death process describing subsequent population dynamics. A long standing problem of computing the distribution of the number of clonogenic tumor cells surviving a fractionated radiation schedule consisting of n equal doses separated by equal time intervals tau is solved within the framework of iterated birth and death processes. For any initial tumor size i, an explicit formula for the distribution of the number M of surviving clonogens at moment tau after the end of treatment is found. It is shown that if i-->infinity and s-->0 so that is(n) tends to a finite positive limit, the distribution of random variable M converges to a probability distribution, and a formula for the latter is obtained. This result generalizes the classical theorem about the Poisson limit of a sequence of binomial distributions. The exact and limiting distributions are also found for the number of surviving clonogens immediately after the nth exposure. In this case, the limiting distribution turns out to be a Poisson distribution.

Cell Survival↗

PubMed2002

Mitochondrial aconitase modification, functional inhibition, and evidence for a supramolecular complex of the TCA cycle by the renal toxicant S-(1,1,2,2-tetrafluoroethyl)-L-cysteine.

Metabolism of the common industrial gas tetrafluoroethylene in mammals results in the formation of S-(1,1,2,2)-tetrafluoroethyl-L-cysteine (TFEC), which can be bioactivated by a mitochondrial C-S lyase commonly referred to as beta-lyase. The resultant "reactive intermediate", difluorothioacetyl fluoride (DFTAF), is a potent thioalkylating and protein-modifying species. Previously, we have identified mitochondrial HSP70, HSP60, aspartate aminotransferase, and the E2 and E3 subunits of the alpha-ketoglutarate dehydrogenase (alphaKGDH) complex as specific proteins structurally modified during this process. Moreover, functional alterations to the alphaKGDH complex were also detected and implicated in the progression of injury. We report here the identification, by tandem mass spectrometry, and functional characterization of the final remaining major protein species modified by DFTAF, previously designated as P99(unk), as mitochondrial aconitase. Aconitase activity was maximally inhibited by 56.5% in renal homogenates after a 6 h exposure to TFEC. In comparison to alphaKGDH, aconitase inhibition (up to 79%) in a cell culture model for TFEC-mediated cytotoxicity was greater and preceded alphaKGDH inhibition, indicating that aconitase modification may constitute an early event in TFEC-mediated mitochondrial damage and cell death. These findings largely define the initial lesion of TFEC-mediated cell death and also have implications for the modeling of mitochondrial enzymatic architecture and the localization and identity of renal mitochondrial cysteine S-conjugate beta-lyase.

Aconitate Hydratase↗

PubMed2006

Chronic diseases now a leading cause of death in rural India--mortality data from the Andhra Pradesh Rural Health Initiative.

INTRODUCTION: India is undergoing rapid epidemiological transition as a consequence of economic and social change. The pattern of mortality is a key indicator of the consequent health effects but up-to-date, precise, and reliable statistics are few, particularly in rural areas. METHODS: Deaths occurring in 45 villages (population 180 162) were documented during a 12-month period in 2003-04 by multipurpose primary healthcare workers trained in the use of a verbal autopsy tool. Algorithms were used to define causes of death according to a limited list derived from the international classification of disease version 10. Causes were assigned by two independent physicians with disagreements resolved by a third. RESULTS: A total of 1354 deaths were recorded with verbal autopsies completed for 98%. A specific underlying cause of death was assigned for 82% of all verbal autopsies done. The crude death rate was 7.5/1000 (95% confidence interval, 7.1-7.9). Diseases of the circulatory system were the leading causes of mortality (32%), with similar proportions of deaths attributable to ischaemic heart disease and stroke. Second was injury and external causes of mortality (13%) with one-third of these deaths attributable to deliberate self harm. Third were infectious and parasitic diseases (12%). Tuberculosis and intestinal conditions each caused one-third of deaths within this category. HIV was assigned as the cause for 2% of all deaths. The fourth and fifth leading causes of death were neoplasms (7%) and diseases of the respiratory system (5%). CONCLUSION: Non-communicable and chronic diseases are the leading causes of death in this part of rural India. The observed pattern of death is unlikely to be unique to these villages and provides new insight into the rapid progression of epidemiological transition in rural India.

Adolescent↗

PubMed2002

Characterization of methadone overdose: clinical considerations and the scientific evidence.

Overdosing with methadone is a growing phenomenon in Britain and other countries due to the increase in prescription and the availability of this compound. Little is known of the circumstances surrounding methadone death due to some extent to the difficulty of defining drug-related death and also the difficulty of collecting clinical and biographical data in a predominantly illegal and marginal milieu. However, the evidence points to highest risk at night (to this end manifestations of its toxicity often go unrecognized) in those whose usual tolerance has been reduced and occurring some considerable time after ingestion. Further investigations are needed to elucidate fully the mechanism and spectrum of methadone overdose. Death from methadone is eminently preventable more so because of the long-term nature of the clinical sequelae. Indeed the key issue with methadone that sets it apart from other opioids is its potential for delayed toxicity. Consequently steps should be taken to disseminate the salient facts to all those who come into contact with the drug.

Depression↗

PubMed1996

Long-term outcome in single-vessel coronary artery disease in Japanese patients.

We assessed the long-term outcome of medical therapy in 453 patients who underwent coronary angiography in the period from September 1973 to February 1984, and who had a significant stenotic lesion (75% or more stenosis) in a single coronary artery. The mean follow-up period was 9.8 years. The 5- and 10-year survival rates were, respectively, 96.0% and 91.3% in these patients, and these survival rates were comparable to the cumulative survival rates in the age-matched healthy male controls determined on the basis of overall death. Cardiac death occurred in 35/453 patients (7.7%) with single-vessel disease (SVD), and non-fatal myocardial infarction occurred in 17 patients (3.8%) during the follow-up period. The incidence of cardiac events, which was defined as cardiac death and nonfatal myocardial infarction, was as low as 1.2% per year. The survival rates were compared in terms of the presence or absence of myocardial infarction, the type of the coronary artery with stenosis, and proximal versus distal location of the stenotic lesion in the left anterior descending artery (LAD). The survival rates were similarly high in both assessed groups, with no significant differences. Patients with SVD treated medically had a good prognosis, except for those patients with decreased left ventricular function (ejection fraction < or = 40%). These factors should be taken into consideration when selecting therapies for patients with SVD.

Case-Control Studies↗

PubMed1989

Causes of death at Tshepong, a rural hospital, 1986-1987.

A prospective study was undertaken to determine causes of death at Tshepong Hospital in the western Transvaal over 1 year. Specific attention was paid to the accurate coding of causes of death; this entailed discussions with the attending doctor as well as 38 autopsies. Only 2.4% of deaths were coded under 'symptoms, signs and ill-defined conditions'. The 1046 deaths followed a typical Third-World pattern when classified according to the International Classification of Diseases (1979). Deaths during the perinatal period were additionally classified according to the recommendations of the Third Conference on Priorities in Perinatal Care in South Africa. The commonest cause of death was conditions originating in the perinatal period (19.2%), followed by infections and parasitic diseases (15.9%), diseases of the circulatory system (14.8%), endocrine, nutritional and metabolic diseases and immune-disorders (12.1%), and neoplasms (8.8%). The other main groups accounted for under 8% each. The commonest cause of death in all age groups above 35 years was diseases of the cardiovascular system, and the commonest cause of death among females aged 15 - 35 years was complications of pregnancy, childbirth and the puerperium. The hospital maternal mortality rate was 4.7/1,000 deliveries and the hospital perinatal mortality rate was 53/1,000 deliveries.

Adolescent↗

PubMed2003

The problematic role of 'irreversibility' in the definition of death.

Most definitions of death--whether cardiopulmonary, whole brain and brain stem, or just upper brain--include an irreversibility condition. Cessation of function is not enough to declare death. Irreversibility should be limited to an organism's ability to 'restart' itself after vital organs have ceased to function. However, this would mean that every hour people who cannot be revived without the intervention of medical personnel and their technology are coming back from the dead. However, the alternative of irreversibility being dependent upon technology will lead to even more counterintuitive results such as: some people are dead at a particular time and place, but others in more technologically advanced eras and locations are alive despite their being in identical physical states; in the future, millions of cryogeneically frozen human beings could spend centuries in a non-dead state because of the future technological breakthroughs; or large numbers of 'frozen' people are dead for aeons but coroners are not able to declare them so because they are unaware of what biological conditions science will never be able to reverse. So death should be defined only in non-relational biological terms, with a self-starting condition similar to that once advocated by Lawrence Becker.

Brain Death↗

PubMed2004

Suicide risk in cancer patients from 1960 to 1999.

PURPOSE: Suicide risk is reportedly higher for cancer patients than for the general population, but estimates vary and analyses of trends are few. The aim of the present study was to determine whether cancer patients had a higher suicide risk between 1960 and 1999. PATIENTS AND METHODS: A cohort comprising patients from the Cancer Registry of Norway 1960 to 1997 was linked to suicide diagnosis in the Register of Deaths at Statistics Norway and observed during 1960 to 1999. The cohort consisted of all cancer patients registered in the Cancer Registry of Norway 1960 to 1997 (N = 490,245 patients with 520,823 cancer diagnoses). Suicide was defined according to death certificates based on the International Classification of Diseases (versions 7, 8, 9, and 10). RESULTS: During the period, 589 cancer patients (407 males and 182 females) committed suicide. The relative risk was elevated for males and females, with standardized mortality ratios (SMRs) of 1.55 (95% CI, 1.41 to 1.71) and 1.35 (95% CI, 1.17 to 1.56), respectively. Risk was highest in the first months after diagnosis. For both sexes, there was a significant decrease in the relative suicide risk over decades. The risk was markedly increased among male patients with cancer of respiratory organs (SMR, 4.08; 95% CI, 2.96 to 5.47). Otherwise, the SMRs varied from 0.76 to 3.67 across cancer types. CONCLUSION: Cancer may be a risk factor for suicide, particularly shortly after diagnosis. However, the relative risk gradually decreased during the period 1960 to 1999.

Adolescent↗

PubMedDate not supplied

[Analysis of mortality in cancer of the large intestine in a cohort group in Serbia from 1971 to 1996].

Colorectal cancer is one of the most frequent malignant neoplasms in both sexes within developed countries. In the Republic of Serbia(Serbia), colorectal cancer mortality in 1971 range 5 in females, and 4 in males; it became the second leading malignancy in 1982 in females (after breast cancer), and in 1992 in males (after lung cancer). The objective of this descriptive-epidemiological study was to examine colorectal cancer mortality in Serbian population, particularly the effect of cohort variations on death rates in defined age groups over the period 1971-1996. Mortality rates were calculated from unpublished national vital statistics data of the Institute of Statistics of the Republic of Serbia. To estimate the age effect on colorectal cancer mortality, specific death rates were computed for cohorts born between 1992-96 and 1972-76, and died at subsequent time periods. The mortality rates were adjusted by direct method, using the world standard population. Confidence intervals (CI) for death rates were assessed with 95% level of probability. In time trend analysis of mortality, Fisher's test was used as a significance test for linear regression coefficient. In the study period (1971-1996), a share of all digestive tumours in cancer mortality has decreased from 42.0% to 32.3%. However, the mortality risk of colorectal cancer and its share in cancer mortality have increased. For example, in men, the share of colorectal cancer in digestive cancer mortality increased from 20.7% (1971) to 32.8% (1996) and in overall cancer mortality from 7.5% to 10.5%. In women, the share of colorectal cancer in digestive cancer mortality increased from 23.0% (1971) to 35.6% (1996), and in overall cancer mortality from 8.5% to 11.6%. The average colorectal cancer age-adjusted death rates (1971-1996) were 11.2 per 100,000 men (95% CI: 10.1-12.3), and 8.3 per 100,000 women (95% CI: 7.7-8.9). The secular linear mortality trends showed significant increase both in males (y = 11.2 + 0.2x; p = 0.000), and females (y = 8.3 + 0.1x; p = 0.000). The highest rise in age-specific death rates, according to linear mortality trends, was observed in males over 65 years (7.8% annually), and females between 60 and 69 years (5.9% annually). In cohort analysis of age-specific rates in males, younger birth cohorts were compared with older ones. The increasing colorectal cancer mortality risk has been observed for ages over 40, with statistical significance in age groups over 45. In ages between 45 and 59, and over 60, the youngest birth cohorts were at 2 and 2.5-fold higher cancer mortality risk than birth cohorts of the oldest generations. For example, the age specific colorectal cancer death rates in a 70-74 year group were 2.5-fold higher in men born between 1922 and 1926 (139.3/100,000) than in cohorts born 25 years earlier (58.7/100,000). In cohort analysis of age-specific rates in females, changes in the age under 50 were not so expressive. In all age groups over 50, women of younger generations were at 2-fold higher cancer mortality risk than the oldest ones. The age specific colorectal cancer death rates in a 65-69 year group were doubled in women born between 1927 and 1931 (61.0/100,000), than in cohorts born 25 years earlier (30.5/100,000). According to the present mortality trends, the further increase in colorectal cancer death rates, especially in the ages over 40, should be expected in future generations. Consistent increase in mortality risk in all younger birth cohorts of older ages, as well as in successive five-year age groups of the observed generations, could reflect the continuous increase in colorectal cancer incidence attributed to predominantly environmental exposures.

Adult↗