Genealogical Data and the
Biodemography of Human Longevity
Leonid A. Gavrilov, Natalia S. Gavrilova,
S. Jay Olshansky, Bruce A. Carnes
Abstract
Biodemography of human longevity is
an emerging interdisciplinary field of sociobiological research with deep
historical roots.Two research questions are examined in this article: (1) What
evidence is there for the familial transmission of human longevity, and (2)
what are the effects of parental age at reproduction on offspring longevity,
and in particular, are there long-term adverse health consequences associated
with the trend toward delayed reproduction? The ability of scientists to
conduct biodemographic studies depends not only on merging theoretical and
methodological elements from the biological and demographic/actuarial sciences,
but unique sources of data and statistical methods must also be
developed. In this article we describe how genealogical data have been
used for over a century to explore basic questions about human longevity, and
how similar kinds of data now being developed are driving the formation of new
testable research hypotheses in the field of biodemography.
Introduction
The biodemography of aging is an
emerging interdisciplinary field of research (Carnes and Olshansky, 1993; Wachter
and Finch, 1997; Gavrilov and Gavrilova, 2001a) with deep historical roots
(reviewed in Olshansky and Carnes, 1997; Olshansky, 1998). The ability of
scientists to conduct research in this field depends not only on merging
theoretical and methodological elements from the biological and
demographic/actuarial sciences, but unique sources of data and statistical
methods must also be developed. In this note we describe how genealogical
data have been used for over a century to explore basic questions about human
longevity, and how similar kinds of data now being developed are driving the
formation of new testable research hypotheses in the field of
biodemography. Two of the many research questions that follow from
developments in this field will be examined in this paper: (1) What
evidence is there for the familial transmission of human longevity, and (2)
what are the effects of parental age at reproduction on offspring longevity,
and in particular, are there long-term adverse health consequences associated
with the trend toward delayed reproduction?
Familial Transmission of Human
Longevity
The last year of the 20th
century marked the 100th anniversary of the first systematic studies
on the familial determinants of human longevity. In 1899 the founder of
biometrics, Karl Pearson (1857-1936) and his student, Mary Beeton analyzed the
correlation of parent/child ages at death based on English genealogies (using
data from the English Peerage and Landed Gentry) dating back to the 17th
century (Beeton and Pearson, 1899). Owing to limitations of their data, Beeton
and Pearson examined only adult males age 20 and over. Their second study was
based on more extensive pedigree records of the members of the English Society
of Friends and of the Friends’ Provident Association – both of which included
data about males and females of all ages (Beeton and Pearson, 1901).
Using such data, Beeton and Pearson (1901) measured the correlation for ages at
death not only for parent/child pairs, but also among siblings. As a result of
their studies, these authors concluded that expectation of life is heavily
influenced by the ages of death of one’s relatives (Beeton and Pearson, 1901,
p. 77).
The familial transmission of human
longevity was also examined by the inventor of the telephone Alexander Graham
Bell (1918) using genealogical data on about 3,000 members of the Hyde family
in
In addition to these traditional studies
on familial longevity, others have explored the genetic and cultural
contributions to inter-individual variation in human life span by evaluating
the relative longevity of twins (Kallman and Sander, 1948; 1949; Kallman,
1957; Jarvik et al., 1960; Harvald and Hauge, 1965; Wyshak, 1978; Hrubec and
Neel, 1981; Carmelli and Andersen, 1981; Carmelli, 1982; Hrubec et al., 1984;
Hayakawa et al., 1992; McGue et al., 1993; Herskind et al., 1996; Yashin and
Iachine, 1997; Ljungquist et al., 1998). A principal finding of this body of
research was that the resemblance in life span among genetically identical
(monozygotic) twins is higher compared to fraternal (dizygotic) twins,
indicating the importance of genetic factors in the determination of human life
span (McGue et al., 1993; Herskind et al., 1996). More recent studies on
the longevity of adopted children have reinforced the importance of
biological parents in predicting the longevity of offspring (Sorensen et al.,
1988; Sorensen, 1991; Nielsen et al., 1992).
In spite of a century of research on
familial longevity, there is still no consensus among scientists on many of the
fundamental issues regarding familial longevity. For example, the role of
genetics in familial longevity resemblance was challenged by some authors
(Murphy, 1978; Philippe, 1978; Jacquard, 1982) who not only found that the
familial resemblance is weak, but also emphasized the importance of social
explanations. The mode of longevity inheritance in humans is also not yet
determined (Carnes et al., 1999). For example, are the genes associated
with longevity dominant, recessive, or additive in their action? Are such
genes autosomal or sex-linked? What is the relative importance of the
maternal versus paternal longevity influence on offspring life span? Some
studies suggest that human longevity is inherited more strongly along the
maternal line (Pearl, 1931; Jalavisto, 1951; Abbot et al., 1978; Brand et al.,
1992; Korpelainen, 1999), which is consistent with theories of aging based on
the inheritance of mitochondrial DNA through the cytoplasm of maternal ova
cells (e.g., Sont and Vandenbroucke, 1993; Wallace et al., 1995; Tanaka et al.,
1998; Vandenbroucke, 1998). However, other studies suggest that there is
a predominance of paternal longevity influence on offspring life span (Bell,
1918; Cohen, 1964; Philippe, 1978; Welter, 1978; Bocquet-Appel and Jakobi,
1990).
More recent studies suggest that it
may be reasonable to revise some of the underlying assumptions behind existing
controversies about maternal versus paternal inheritance, and to develop more
refined methods of familial analysis of human longevity (e.g., see Gavrilov and
Gavrilova, 1991). In particular, one testable hypothesis that can now be
evaluated empirically with the use of genealogical data (listed in Gavrilova,
Gavrilov, 1999) is the question of whether there is a linear
relationship between offspring and parental life span (i.e., the observed ages
at death of offspring are shown to rise in equal measure to the observed ages
at death of their parents), as opposed to an accelerating relationship
as suggested by Gavrilova et al., (1998). The assumption of linear dependence
between offspring and parental traits is fundamental in quantitative genetics
because both the theory of quantitative genetics and its applications are based
on this assumption (Falconer, 1989; Falconer and Mackay, 1996).Moreover, the
assumption of linearity is one of the foundations for Path analysis used in
studies of the mechanisms of familial transmission of quantitative traits
(Neale and Cardon, 1989, p.91)1.
[Footnote #1 about here]
The methods of correlation and
linear regression analyses are also based on the assumption of linearity and
were used in previous familial studies of longevity (Holmes, 1928; Yuan, 1931;
Dublin et al., 1949; Jalavisto, 1951; Hawkins et al., 1965; Abbott et al.,
1973; Murphy, 1978; Cohen, 1964; Philippe, 1977; 1978; Welter, 1978; Wyshak,
1978; Desjardins and Charbonneau, 1990; Bocquet-Appel and Jakobi, 1990; 1991).
What are the alternatives to the
linearity assumption and why are they relevant to studies of longevity
inheritance? With large amounts of genealogical data it is possible to test the
linearity assumption against alternative trajectories. The relationship between
offspring and parental longevity may instead be based on a decelerating
function – with a decreasing slope that may even level off (in the case of an
early selection out of the parents who die prematurely, either for genetic or
non-biological reasons). Thus, the population of longer-lived parents may
become more homogeneous because of selection.
An alternative prediction is that
dependence should be accelerating (more steep for the offspring of
longer-lived parents) – a hypothesis derived from the evolutionary theory of
aging and mutation accumulation hypothesis in particular (e.g., for a summary
see Gavrilova et al., 1998). According to the evolutionary theory of aging, the
equilibrium gene frequency for deleterious mutations should increase with
age-at-onset of mutation action because of weaker (postponed) selection against
later-acting mutations (Medawar, 1952; Finch, 1990; Rose, 1991; Partridge and
Barton, 1993; Charlesworth, 1994).In accordance with this mutation accumulation
hypothesis, one would expect the observed (e.g. expressed) genetic
variability in survival (additive genetic variance) to increase with age
(Partridge and Barton, 1993; Charlesworth, 1994).2
[Footnote #2 about here]
In general, both the additive
genetic component of variance and dominant component are expected to increase
with age under the mutation accumulation hypothesis because in the case of
traits affected by rare deleterious alleles, both components increase with
increasing mutant allele frequency (Charlesworth, 1987; Falconer 1989; Hughes
and Charlesworth, 1994).As such, the ratio of additive genetic variance to the
observed phenotypic variance (i.e., the heritability of longevity) may be
estimated most reliably as the doubled slope of the regression line for
offspring life span on parental age at death. Therefore, if longevity is indeed
determined by late-acting deleterious mutations, one testable hypothesis is
that this slope will become steeper for longer lived parents (at higher
paternal ages at death) (Gavrilova et al., 1998; Gavrilova and Gavrilov, 2001).
It is this kind of unusual hypothesis that can be tested using data from
genealogical resources (Gavrilova and Gavrilov, 1999)
Thus, biodemographic studies of the
familial transmission of human longevity can be summarized in the form of three
research directions and corresponding hypotheses that are amenable to
evaluation using genealogical resources:
(1) What is the trajectory of the
dependence of offspring longevity on parental longevity – is it linear
(standard assumption in quantitative genetics), decelerating (expected in the
case of early selection out of shorter-lived parents), or accelerating
(predicted by the evolutionary theory of aging and by mutation accumulation
hypothesis in particular)?
(2) Is the familial transmission of
longevity stronger for children born to younger (as compared with older)
parents as would be expected both for genetic reasons (higher genetic diversity
of younger parents) and for cultural reasons (higher overlapping between
parental and offspring life cycles)?
(3) What is the relative importance
of paternal versus maternal longevity on the observed longevity of sons and
daughters?
Biodemographic Studies of Parental
Reproductive Age Effects on Offspring Longevity
Delayed childbearing has become
increasingly common in modern societies because of demographic changes
(population aging), medical progress (e.g., in vitro fertilization (IVF) to
older women) and personal choice. For example, in the United States the number
of births to older mothers (35-39 years and 40+ years) more than doubled since
1980 while the number of births to younger mothers (below age 30) did not
increase (U.S. Bureau of the Census, 1997).
Birth rates for older fathers (ages
45-49 and 50-54) are also increasing (U.S. Monthly Vital Statistics Report,
1997) and this trend may even accelerate in the future due to medical progress
(Viagra, for example). Will the health and longevity of children born to older
parents be adversely influenced by parental age at conception? While the
detrimental effects of late reproduction on infant mortality and genetic
diseases has been well documented (see below), little is known about the
long-term health consequences for offspring born to parents who conceive later
in the reproductive window.
According to existing evidence,
delayed parental age at conception has many detrimental influences on the
longevity of offspring (for a detailed review of this topic see Gavrilov and
Gavrilova, 1997a).The major maternal age-related changes in humans are
increases in fetal aneuploidy later in reproductive life such as Down's
syndrome (trisomy 21), Klinefelter's syndrome (XXY), Edward's syndrome (trisomy
18) and Patau's syndrome (trisomy 13).Advanced maternal age also remains an
important independent risk factor for fetal death.
The detrimental effect of late paternal
reproduction is also well known: advanced paternal age has been associated with
an increase in new dominant mutations in offspring that result in congenital
anomalies (see Gavrilov and Gavrilova, 1997a for review). In particular,
paternal age is responsible for new dominant autosomic mutations that cause
different malformations, including achondroplasia, Apert syndrome, Marfan
syndrome, osteogenesis imperfecta and other inherited diseases (Vogel and
Motulsky, 1997; Gavrilov and Gavrilova, 1997a). Older paternal age was more
common among patients with Costello syndrome, chondrodysplasia punctata,
fibrodysplasia ossificans progressiva, and thanatophoric displasia (Vogel and
Motulsky, 1997, Gavrilov and Gavrilova, 1997a). Advanced paternal age at
reproduction is also associated with an increased risk of preauricular cyst,
nasal aplasia, cleft palate, hydrocephalus, pulmonic stenosis, urethral
stenosis, and hemangioma (seereview by Gavrilov and Gavrilova, 1997a).
There is, however, one very
important question that has yet to be addressed: does parental age at
conception influence the longevity of the vast majority of the population of
'healthy people', who do not suffer from aneuploidy and other obvious genetic
conditions that tend to appear relatively infrequently early in life?In other
words, are aging-related diseases expressed late in life associated with
paternal and maternal age at conception or birth?It is possible to address this
question by examining the life expectancy of adults (say, at ages 30 and older)
as a function of parental age at reproduction. By adult age a substantial
portion of the subpopulation suffering from lethal genetic disorders has
already died. The information on potential life?shortening effects of late
parental reproduction on adult offspring is notable because it addresses a
possibly important gap in knowledge about the mechanisms of human longevity,
the aging process itself, and of the possible role of accumulated genetic
damage in the germ line on aging and longevity.
The first mention in the historical
literature suggesting a possible life-shortening effect on offspring of delayed
parenting was made by the French naturalist Buffon (1826) who noted that when
older men procreate “they often engender monsters, deformed children, still
more defective than their father” (see Robine and Allard, 1997).In 1950, Eva
Jalavisto analyzed 12,786 published family records of the Finnish and Swedish
middle class and nobility for those born between 1500 and1829. Unfortunately,
in this interesting study the secular changes in human life span during this
long historical period were not taken into account (failure to control for
secular trends can produce biases and artifacts). Also, Jalavisto (1950) did
not attempt to control for the possible effects of other confounding factors
(e.g., parental life span).The author concluded that offspring born to older
mothers live significantly shorter, while the age of the father is of no importance.
This observation is now amenable to verification using our developing database
and related genealogical data resources (Gavrilova and Gavrilov, 1999), and by
controlling for the effects of other confounding factors and historical changes
in the life expectancy of birth cohorts.
In 1980, Pierre Philippe studied
five birth cohorts (1800-29, 1830-49, 1850-69, 1870-79, 1880-99) from a small
rural population of Isle-aux-Coudres, Quebec, Canada.Multiple discriminant
analysis was used to study the effects of familial characteristics (such as
parental consanguinity, maternal and paternal age at time of childbirth, birth
order, time interval since the previous birth, months of birth, viability of
the preceding infant, etc.) on offspring age at death. Surprisingly, possibly
the most evident and important predictors of offspring longevity (paternal and
maternallife spans) were not included in the analysis for unknown
reasons. Also, the authors noted that “taking into consideration the
possibility of differential emigration” from this small rural area
(Isle-aux-Coudres), the results of their analysis “must certainly be regarded
cautiously” (Philippe, 1980, p.215). Indeed, in many cases the results of this
analysis were not statistically significant, perhaps because of the small size
of the birth cohorts (105-298 cases only in each cohort), and also because of
possible overloading of the analysis by too many variables (up to 26 binary
variables were included). In spite of these problems, the authors of this study
made an intriguing observation that increased maternal age at time of
childbirth (35 years and above) is the main factor common to both early (0-5
years) and late (70 years and above) death (Philippe, 1980). By contrast,
increased father’s age was uncommon for long-lived offspring (Philippe, 1980).
These important observations can be
re-evaluated by using larger sample sizes and controlling for parental
longevity.Control for parental longevity is important, because it has been
demonstrated that among long-lived women the proportion of those able to become
mothers after 40 years is 4 times higher compared to women who stop
childbearing at younger ages (Perls et al., 1997). Thus, increased offspring
longevity might not be due to the older age of mother at childbirth per se,
but due to higher longevity of such late reproducing mothers and the
inheritance of longevity-related traits by their offspring. This hypothesis
could be also explored in future studies.
Biodemographic studies of parental
age effects on offspring longevity can be summarized in the form of 4 research
objectives driven by corresponding hypotheses (see below):
(1) Do persons born to older fathers
live shorter lives (as predicted by the hypothesis of age-related accumulation
of spontaneous mutations in paternal germ cells) – a research question that can
be tested more appropriately using a larger sample size (Gavrilov and
Gavrilova, 1997a; 1997b; 2000; Gavrilov et al., 1997), and that only daughters
born to older fathers have a shorter life expectancy relative to daughters born
to younger fathers (consistent with hypothesis of the critical importance of
mutation load on paternal X chromosome inherited by daughters only)?
(2) What is the effect, if any, of
mother's age at conception on offspring longevity in relation to the hypothesis
that there is an age-related accumulation of oxidative damage to mitochondrial
DNA in maternal ova cells?
(3) It would be interesting to
examine the prediction of the X-chromosome hypothesis that there should be a specific
life-shortening effect among grandchildren (grandsons in particular) if their
mother was born to an older grandfather. Preliminary studies have demonstrated
the sex-specific decrease of daughters’ longevity born to older fathers: a
finding consistent with the mutation load hypothesis and the critical role of
the X-chromosome transmitted from father to daughter only (Gavrilov and
Gavrilova, 1997a; 1997b; 2000). This X-chromosome hypothesis provides a
specific prediction that we propose to test in future studies. Since the
grandfather's X-chromosome is inherited through the mother's side only, one
might expect a specific effect of the reproductive age of the maternal
grandfather. Specifically, this hypothesis predicts that grandchildren
(grandsons in particular) should live shorter lives if their mother was born to
an older grandfather.
(4) The parental support hypothesis
is that among the offspring of longer-lived parents, the parental age effects
will be less expressed. According to this hypothesis, children born to older
parents may live shorter lives because they lose their parents too early, in
the formative years of their life.
Genealogical Data and their use in
Biodemographic Studies
There are some genealogical datasets
already in use in biodemographic studies, some of which have already been
mentioned. We are in the process of creating a comprehensive computerized
genealogical database for biodemographic studies based on the NIH/NIA-sponsored
review of the feasibility of this kind of research (Gavrilov and Gavrilova,
1998).Several factors support the continued development of this source of data.
There are two mutually exclusive constraints on data sources that should be
taken into account in biodemographic studies:On the one hand, in order to have
complete data on parental life span (for heritability studies or for their use
as control variables), it is necessary to go back in history for about a
century in order to have extinct parental birth cohorts. On the other hand, the
historical genealogical databases are often criticized because the genealogical
longevity data collected in the pre-antibiotic era and particularly in the
pre-public health era are often considered to be irrelevant to current low
mortality populations (Cohen, 1964; Smith, 1993). This is thought to be the
case because living conditions were quite different in the past. For example,
there used to be extremely high mortality from infectious diseases
(tuberculosis and pneumonia, in particular), under-nutrition and sometimes even
starvation were common (see Carnes et al., 1996; Fogel and Costa, 1997), the
poverty rate was high and poor sanitary conditions prevailed, and high seasonal
mortality was common (especially in winter).
There is, however, one fortunate
exception that perfectly fits the purpose of biodemographic studies – socially
elite aristocratic families, which are reasonably homogeneous and in which
social deprivation has not interfered unduly with the chances of survival.
Based on pilot studies already conducted using data of this sort (Gavrilova et
al., 1998), it has been determined that the modal age at death for parents in
these socially elite families in the 19th century is remarkably high
(70-75 years for fathers and 75-80 years for mothers) – which is comparable with
modern low mortality populations.
Another important advantage of this
kind of data is their high reliability, accuracy, and completeness, since data
for aristocratic families were recorded in great detail for many centuries.
Moreover, these data are widely published by numerous independent publishers,
thus creating a unique opportunity to cross check the information with other
data sources to ensure the highest possible data quality and completeness (see
Gavrilov and Gavrilova, 1998; Gavrilova and Gavrilov, 1999).
One unique feature of
this data set is that it contains a significant sample of males who achieved
fatherhood later in life – a product of the fact that older kings and princes
often married much younger women. For example, Queen Victoria of
Since this privileged
social group lived in rather favorable conditions for many centuries, one could
expect less influence of adverse social factors (poverty, for example) on life
span and hence reduced environmental variation in longevity caused by these
factors. This kind of data allows the researchers to minimize the social
heterogeneity of the population under study and to limit socioeconomic
diversity, compared to other data sets where a mixture of families with
different social status is analyzed. Thus, although this data set does not
represent the whole human population (as laboratory animals do not represent
species in the wild), it is an ideal source of data to test biodemographic
hypotheses about the familial transmission of human longevity because the
effects of population heterogeneity are minimized with regard to social status
(which can be also controlled for by indicator socioeconomic variables such as
nobility rank and the lifespan of spouses who share the same familial
environment). This is particularly important for testing biological theories of
aging using data on humans.
While discussing the
generalizability concerns, it is also important to understand the difference
between the analytical and the descriptive studies (Levy and Lemeshow,
1999).Analytical studies that intend to test specific hypotheses (for example,
biodemographic hypotheses described in this article) are less dependent on data
representativeness than the descriptive studies, which intend to describe “a
whole population” (Levy and Lemeshow, 1999).
Also, all the cases of familial
inbreeding (consanguinity) are well documented for noble families, so the data
can be used to study the effects of consanguinity too (Gavrilov and Gavrilova,
2001b). It is interesting to note that in one study of inbred families there
was no significant effect of inbreeding on survival curves and heritability of
human longevity (Mayer, 1991).Mayer (p.56) concluded that his study
"indicates negligible "inbreeding depression" with respect to
longevity.”
Recently, arguments in
favor of historical genealogical databases for aristocratic families have
received increasing recognition in the scientific community. In
particular, Nature has published an article based on
biodemographic analysis of the life span and fertility data for British
aristocratic families (Westendorp and Kirkwood 1998).Specific reference was
made in the Westendorp and Kirkwood (1998, p.746) paper to our identification
of the database used in the study.For further discussion of this Nature
article, see (Gavrilov and Gavrilova, 1999a; 2002; Gavrilova and Gavrilov,
1999).By now, we have computerized more than 15,000 complete genealogical
records ("European Aristocratic Families" database for 1800-1880
birth cohorts) in collaboration with Russian colleagues (Victoria Semyonova,
Ph.D. and Galina Evdokushkina, M.Sc.) that are already used in biodemographic
studies (Gavrilov and Gavrilova 1997a; 1997b; 1999b; 2001a; Gavrilov et al.
1997; Gavrilova et al. 1998; Gavrilova, Gavrilov, 2001).The main difficulties
with developing this type of dataset are related to the need of extensive data
cross-checking with many different sources, which is very laborious and time
consuming (but produce high quality data).Some of the new preliminary results
obtained with this database are described in the Appendix.
The
studies on biodemography of human longevity are progressing rapidly and such
progress can be enhanced by the identification and use of new and novel
databases that permit investigators to test research hypotheses that were
difficult to test in the past. We have been developing a new database just for
this purpose with the initial funding from the NIH/NIA - a database that will
be made available to the research community once complete (publicly available
data resources are reviewed in Gavrilova and Gavrilov, 1999).For now,
preliminary results are interesting enough to warrant the expansion and
continued use of such databases.
APPENDIX
Preliminary Findings
Preliminary research
already conducted with the use of data on European aristocratic families has
produced some interesting results (see Table 1).
Table 1 about here
First, we have tested the validity
of the general assumption of the linear dependence between offspring life span
and parental life span. For this purpose, the sample was split into two parts
with approximately equal number of cases: one subset with longer lived parent
(above 70 years) and another subset with shorter lived parent (below 70 years).
The regression slopes for linear regression of offspring life span
(pre-adjusted for secular effects) on parental life span were calculated and compared.
In the case of strictly linear
dependence for the whole range of parental longevity, the regression slopes for
the subsets of longer and shorter lived parents should be essentially the same.
This is obviously not the case - for all 4 offspring-parent pairs the
heritability of longevity was much higher for longer lived parents,
particularly fathers.
In fact, human life span seems to be
not heritable (in the narrow sense of familial resemblance) if parents live
shorter lives - all the regression slopes are close to zero and are
statistically insignificant (Table 1). This may explain why some of the
previous investigators (Philippe, 1978) were frustrated by low heritability
estimates for human life span - they simply did not have enough cases of longer
lived parents in their data sets. On the contrary, the regression slopes for
the longer lived parents are quite high, keeping in mind that the theoretical
upper limit for this slope is equal to 0.5, corresponding to 100% heritability
of the trait (Falconer, 1989; Falconer and Mackay, 1996). For example, the
daughters gain 2.65 years of additional life span per each 10 years of
additional life span of longer lived fathers (Table 1) which formally
corresponds to 53% of the narrow sense heritability (Falconer, 1989).
These results are consistent with
the prediction of the evolutionary theory of aging (see section 2.1.) and
indicate that there may be an increasing genetic limitation for the further
increase of human life expectancy in low mortality populations.
Another
interesting observation using available data is that the paternal longevity
effects on offspring lifespan are more than double that of maternal effects
(Table 1). Since the frequency of chromosomal crossing over is much less in
fathers compared to mothers (Strickberger, 1976; Vogel and Motulsky, 1997), the
fortunate gene combinations predisposing to longevity are more likely to be
transmitted intact (not destroyed by genetic recombination) from fathers rather
than from mothers. Other explanations are also possible, so larger
biodemographic studies are planned to cast more light on the familial
determinants of human longevity.
____________________________________________________________________
Acknowledgments
This work was supported in part by
the National Institute on Aging grants P20 AG12857, AG13698-01, AG16138-01A1,
K02AG13698-01, K02AG00894-01, and K02AG00976-01A2. Contact Leonid A. Gavrilov,
Center on Aging, NORC/University of
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Footnote #1:
The methods of path analysis (also
known as the structural equation models) and their applications in quantitative
genetics are reviewed comprehensively in (Neale and Cardon, 1989; Lynch and
Walsh, 1998), and, therefore, will not be discussed in this article focused on
another topic (the importance of genealogical data for biodemographic studies).
Footnote #2:
It may be difficult to observe
directly this theoretically predicted age-related increase in population
heterogeneity for survival probabilities.Direct testing of this theory would
require identification of reliable biomarkers for individual survival
probabilities (individual frailty predictors).Fortunately, it is also possible
to test a related prediction of this theory regarding heritability of lifespan,
as discussed later.
TABLE 1 Heritability of human longevity for
different sex combinations in offspring/parent pairs and for different parental
longevity ranges
|
Type of the child/parent pair |
Regression slope of offspring life span
(adults, 30+ years) on parental life span ± standard error |
|
|
|
(1) Longer lived parent, 70-100 years (sample size) |
(2) Shorter lived parent, 30-70 years (sample size) |
Difference
between (1) and (2) |
|
|
Son-Father |
0.189 ± 0.035*** (5,120) |
0.037 ± 0.020 (6,211) |
0.152 ± 0.040*** |
|
Son-Mother |
0.054 ± 0.031 (5,783) |
-0.014 ± 0.017 (5,218) |
0.067 ± 0.035 |
|
Daughter-Father |
0.265 ± 0.055*** (2,213) |
0.022 ± 0.031 (2,616) |
0.243 ± 0.063*** |
|
Daughter-Mother |
0.114 ± 0.048* (2,534) |
0.024 ± 0.028 (2,156) |
0.091 ± 0.056 |
* Significant at p < 0.05;** p
< 0.01;*** p < 0.001
NOTE: The data for analysis are
taken from our "European Aristocratic Families" database for extinct
birth cohorts (1800-1880). Data for offspring life span were pre-adjusted for
secular changes before their use in the linear regression analysis.
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