Call for papers

International Seminar on
Lifespan Extension and the Biology of Changing Cause-of-Death Profiles: Evolutionary and Epidemiological Perspectives

Rauischholzhausen, Germany, 13-15 January 2011

Organized by the IUSSP Scientific Panel on Evolutionary Perspectives in Demography.

Deadline for submission of abstract extended to: 30 September 2010.

Online submissions

Background
In all rich societies, the last 100+ years have seen a tremendous extension of the life span.

In the US, for example (Table 1), life expectancy at birth grew by 28 years, to more than 150% of the value in 1900. Clearly there have been considerable changes over this period in the accuracy of the data from which these estimates are derived, but it is instructive to see that the remaining life expectancy at age 100 has proportionally not grown less than life expectancy at birth.

Also interesting – and in fact the classical example of a mortality cross-over – is the higher remaining life expectancy at age 100 among blacks of both sexes, who – despite even larger gains than whites still have a lower life expectancy at birth than whites, although, again, the extent to which this cross-over may reflect differential errors in age reporting, is also the subject of debate.

Table 1. Life Expectancy in the USA at birth and at age 100, 1900–2007.

Race and Sex	2004  - 2007	1989  - 1991	1979  - 1981	1969  - 1971	1959  - 1961	1949  - 1951	1939  - 1941	1929  - 1931	1919  - 1921	1909  - 1911	1900  - 1902
All
0	77.9	75.4	73.9	70.8	69.9	68.1	63.6	59.2	56.4	51.5	49.2
100	2.4	2.5	2.7	2.6	1.9	1.9	2.1	1.5	1.5	1.9	1.6
White male
0	75.8	72.7	70.8	67.9	67.5	66.3	62.8	59.1	56.3	50.2	48.2
100	2.1	2.2	2.4	2.2	1.9	1.9	2.0	1.5	1.6	1.7	1.6
White female
0	80.8	79.5	78.2	75.5	74.2	72.0	67.3	62.7	58.5	53.6	51.1
100	2.4	2.5	2.7	2.5	1.9	1.9	2.0	1.5	1.4	1.7	1.6
Black male
0	69.9	64.5	64.1	60.0	61.5	58.9	52.3	47.6	47.1	34.1	32.5
100	2.8	2.6	3.2	3.6	1.9	1.9	2.3	1.7	1.6	2.1	1.9
Black female
0	76.7	73.7	72.9	68.3	66.5	62.7	55.6	49.5	46.9	37.7	35.0
100	3.0	3.0	3.7	4.2	1.9	1.9	2.7	2.0	2.2	2.4	2.5

Source: National Vital Statistics Reports 56,9 and 58,1 NCHS.

 

The extension of the life span was accompanied by a dramatic change in the cause-of-death profiles (Table 2a-2c for the USA).

Table 2a. Distribution of deaths by cause group, USA (death registration states) 1900.

	1900 (US – death registration states)
Rank	Cause of Death	Codes	Number of Deaths	Death Rate per 100,000
	All Causes		343,217	1,719.1
1	Pneumonia (all forms) and influenza	107-109,33	40,362	202.2
2	Tuberculosis (all forms)	13-22	38,820	194.4
3	Diarrhea, enteritis, and ulceration of the intestines	119,120	28,491	142.7
4	Diseases of the heart	99-95	27,427	137.4
5	Intracranial lesions of vascular origin	83	21,353	106.9
6	Nephritis (all forms)	130-132	17,699	88.6
7	All accidents	169-195	14,429	72.3
8	Cancer and other malignant tumors	45-55	12,769	64.0
9	Senility	162	10,015	50.2
10	Diphtheria	10	8,056	40.3

Cause-of-Death Codes according to Fifth Revision of the International List of Causes of Death, table taken from “Leading Causes of Death 1900-1998,” rates refer to mid-year population – eventually later corrected for census results (see: www.cdc.gov/nchs/data/dvs/lead1900_98.pdf).

Table 2b. Distribution of deaths by cause group, USA 1954.

	1954 (USA)
Rank	Cause of Death	Codes	Number of Deaths	Death Rate per 100,000
	All Causes		1,481,091	919.0
1	Diseases of the heart	410-443	560,077	347.5
2	Malignant neoplasms, including neoplasms of lymphatic and hematopoetic tissues	140-205	234,669	145.6
3	Vascular lesions affecting central nervous system	330-334	167,777	104.1
4	Accidents	E800-E962	90,032	55.9
	Motor vehicle accidents	E810-E835	35,586	22.1
	All other accidents	E800-E802, E840-E962	54,486	33.8
5	Certain diseases of early infancy	760-776	63,486	39.4
6	Influenza and pneumonia, except pneumonia of newborn	480-493	40,991	25.4
7	General arteriosclerosis	450	30,225	18.8
8	Diabetes mellitus	260	25,151	15.6
9	Congenital malformations	750-759	20,081	12.5
10	Chronic and unspecified nephritis and other renal sclerosis	592-594	17,073	10.6

Cause-of-Death Codes according to Sixth Revision of the International List of Causes of Death, table taken from “Leading Causes of Death 1900-1998,” rates refer to mid-year population – eventually later corrected for census results.

Table 2c. Distribution of deaths by cause group, USA 2007.

	2007 (USA)
Rank	Cause of Death	Codes	Number of Deaths	Death Rate per 100,000
	All Causes		2,424,059	803.7
1	Diseases of heart	(I00-I09,I11,I13,I20-I51	615,651	204.1
2	Malignant Neoplasms	(C00-C97)	560,167	185.7
3	Cerebrovascular Diseases	(I60-I69)	133,990	44.4
4	Chronic lower respiratory diseases	(J40-J47)	129,311	42.9
5	Accidents (unintentional injuries)	(V01-X59,Y85-Y86)	117,075	38.8
6	Alzheimer’s disease	(G30)	74,944	24.8
7	Diabetes mellitus	(E10-E14)	70,905	23.5
8	Influenza and pneumonia	(J09-J18)	52,847	17.5
9	Nephritis, nephritic syndrome and nephrosis	(N00-N07, N17-N19, N25-N27)	46,095	15.3
10	Septicemia	(A40-A41)	34,851	11.6
11	Intentional self-harm (suicide)	(U03, X60-X84, Y87.0)	33,185	11.0
12	Chronic liver disease and cirrhosis	(K70-K73-K74)	28,504	9.5
13	Essential hypertension and hypertensive renal disease	(I10-I12,I15)	23,769	7.9
14	Parkinson’s disease	(G20-G21)	20,136	6.7
15	Assault (homicide)	(U01-U02, X85-Y09,Y87.1)	17,520	5.8

Cause-of-Death Codes according to Tenth Revision of the International Classification of Diseases, Source National Vital Statistics Reports 58,19 NCHS, Rates age-adjusted US standard population of the year 2000.

Associations between changes in cause-of-death distributions and overall level of mortality have long attracted attention (Preston 1976) and various explanations proposed for the interaction between life span extension and cause-of-death profile change:

1. The cause-of-death profile change may be the effect of life span extension: for example Alzheimer’s Disease. The incidence of the disease increases with age, and the more people survive into old age the more cases of the disease will be seen.
    
2. Life span extension plus cause-of-death profile change may be both the effects of the partial or almost total elimination of certain causes-of-death:

• For example fatal cases of measles or diphtheria tend to be children or adolescents. Consequently, elimination of these diseases by high vaccination quotas increases the life span in those populations and – all other things being equal – at the same time increases mortality from other, mostly non communicable diseases later in life.
   
• Similarly, differential advances of medical technology: for example pneumonia and tuberculosis can be prevented and treated with much better results than cancer, therefore mortality from pneumonia and tuberculosis has gone down and, since people have to die from some disease, cancer mortality has gone up.
   
• Improved sanitation, food processing and storage technology prevent many cases of diarrhea, a major cause-of-death especially of children after weaning.
   
• Genetics I: in natural fertility societies, with an adequate food supply, infant mortality tends to be around 15%. In more developed societies, there are greater internal differences. For example, in Berlin, in the poorest of 20city districts (Wedding) in the year 1905, infant mortality was approximately 40%, but only 5% in the richest (Tiergarten), with a social gradient of 12.5%. In the late 1990s infant mortality in deprived city districts in rich countries with high levels of inequality was around 2%, with a social gradient of 40%; in countries with less inequality even less (Figure 1). Since child and adolescent mortality is very low in developed countries, the vast majority of all infants will survive to reproductive age. These unprecedented survival rates could rapidly change the genetic composition of all rich societies.

Figure 1. Box plots of neighbourhood infant mortality rate distributions for London, Manhattan, Paris, and Tokyo for 1993–1997, showing differences in spread and symmetry in the distribution of neighbourhood infant mortality rates for the 4 cities. (Source: Neuberg LG, Rodwin VG (2002): Neighbourhood Matters. Infant Mortality Rates in Four Cities: London, Manhattan, Paris, and Tokyo. NYU Indicators/Winter 2002–3, 15-38).
 

3. Genetics II: In historical perspective, a larger share of all young adults entering reproductive age actually reproduce in adulthood. At the same time, the average number of children has decreased dramatically. Reproductive success is always in relation to the reproductive output of others in the population. Thus, since, normally, larger families are achieved by starting childbearing early and/or stopping late, now reproductive success of those who for genetic reasons start late and/or stop early is dramatically improving, when average number of children as well as infant mortality is going down. That effect also may be rapidly changing the genetic composition of all rich societies.
    
4. Epigenetics I: Various mechanisms have been described which identify how a trait can be transferred from parents to future generations without modifying the DNA. Exemplary would be effects of the nutritional experiences of parents on children or grandchildren, as various famine studies in Dutch, Chinese, Russian, Ukrainian, Nordic populations have demonstrated for breast and other cancer, schizophrenia, growth retardation or all-cause-mortality (see: Lorentz Center Leiden University Workshop - “Long Term consequences of exposure to famine” 3 – 6 Nov 2008. References: http://www.lc.leidenuniv.nl/lc/web/2008/319/extra.php3?wsid=319). Of particular interest are examples of sex-specific transgenerational responses, where genes are differently expressed depending on whether they come from the father of the mother.
    
5. Epignetics II: In both sexes, in rich societies there is a tendency towards late reproduction. It is known (Aviv and colleagues 2008) that older men have more sperm with elongated telomeres, to the effect that having an old father may slow down the annual attrition in sons’ and daughters’ own leukocyte telomere length, known to be a powerful indicator of ageing. In males, within the population of germ-line stem cells, with advancing age-cell lineages with even slower rates of replication may outgrow the rest and, therefore, increase the median telomere length. Analogous changes over the female reproductive lifespan in the population of primary follicles from which fertile egg cells develop may be possible. Since leukocyte telomere length predicts lifespan as well as age-related diseases including hypertension, atherosclerosis, myocardial infarction, stroke and dementia, late reproduction itself, to a certain extent, may contribute to lifespan expansion.

There is a general consensus in biodemography that not only the timing of reproduction within the life course, but the entire life course including lifespan itself is the result of directed evolution. Within the grand framework of improving standards of living, better work conditions and better medical technology, many selective as well as adaptative processes may be occurring.

Therefore, changing disease profiles, and, consequently, changing cause-of-death profiles over the life course in varying environments is a genuine subject of evolutionary demography, and so is the changing genetic composition of populations due to decreasing infant and child mortality and decreasing family size. In addition, inter-generational wealth transfers and investment in children depends on health and survivorship over the lifespan.

There is, however, little research undertaken in these subjects and little integration of evolutionary biodemography and population-based epidemiology.

Aim of the Seminar
The goal of this seminar is to improve cross-disciplinary work by bringing together innovative researchers from related and complementary areas. The changing morbidity spectrum and changing cause-of-death profile over the life course, in stable or in changing environments, will be analyzed as direct or side effects of evolutionary adaptation. The usefulness of this approach for basic research and for clinical health care research will be assessed.

The Seminar will be focussed on the following sessions:

1. changes in lifestyle including but not limited to dietary, exercise and work conditions;
2. innovations in medical technology – prevention and therapy;
3. innovations in sanitation and food technology;
4. changes in genetic composition of contemporary societies;
5. epigenetics effects – nutrition and other factors, including telomere length;
6. methodological aspects of measuring evolutionary effects.

Submissions
The IUSSP Scientific Panel on Evolutionary Perspectives in Demography invites researchers in the field to submit online by 30 September 2010 a short 200-word abstract AND to upload either an extended abstract (2 to 4 pages, including tables) or a full paper, which must be unpublished. To submit and fill out the online submission form, please click here: Online submission form.

Applicants will be notified whether their paper has been accepted by 15 October 2010. In the case of acceptance on the basis of an abstract, the completed paper must be uploaded on the IUSSP website by 15 December 2010.

The seminar will be limited to a maximum of 20 contributed papers and to one author per paper. If the paper is co-authored, please indicate the names of co-authors at the end of the abstract. Submission should be made by the author who will attend the seminar.

Abstracts and final papers must be submitted in English and presentations at the seminar will be English.

Seminar Organizers will explore possibilities for publishing the papers. Preference will be given to publication in a special issue of an international journal. Papers submitted should be unpublished and remain the property of the IUSSP until the committee makes a decision with regard to their possible publication.

Current funding for the seminar is limited and efforts are under way to raise additional funds. At present, seminar organizers can cover accommodation expenses for all participants but there is no funding for air travel. Applicants are therefore encouraged to seek their own travel funding; if they require travel assistance, they should indicate that need by ticking the appropriate box on the on-line submission form when submitting their paper or abstract. Travel funding provided by the IUSSP is for IUSSP members only.

For further information, please contact Martina Schmidt-Stolte (schmidtstolte@staff.uni-marburg.de).

Scientific Committee:
Gillian Bentley (Durham University, United Kingdom)
Viviana Egidi (University La Sapienza, Rome, Italy)
Emily Grundy (London School of Health and Tropical Medicine, United Kingdom)
Ulrich Mueller (Medical School, Philipp’s University Marburg, Germany)
Andrew Noymer (University of California, Irvine CA, USA)
Anatoli Yashin (Duke University, NC, USA)

Local and Principal Organizer: Ulrich Mueller (Medical School, Philipp’s University Marburg, Germany)

 

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