Abstract
For over forty years, demographers have worked intensely to develop methods that assess the gain in life expectancy from a reduction in mortality, either hypothetical or observed. This considerable body of research was motivated by assessing the gains in life expectancy when mortality declined in a particular manner and determining the contribution of a cause of death in observed changes in life expectancy over time. As yet, there has been no framework unifying this important demographic work. In this paper, we provide a unifying framework for assessing the change in life expectancy given a change in age and cause-specific mortality. We consider both conceptualizations of mortality change–counterfactual assessment of a hypothetical change and a retrospective assessment of an observed change. We apply our methodology to violent deaths, the leading cause of death among young adults, and show that realistic targeted reductions could have important impacts on life expectancy.
Keywords: Accidents, Cause-Deleted Life Tables, Decomposition, Entropy, Violent Deaths
1 Introduction
For over forty years, demographers have worked intensely to develop methods that assess the gain in life expectancy from a reduction in mortality, either hypothetical or observed. This considerable body of research was motivated by assessing the gains in life expectancy when mortality declined in a particular manner and determining the contribution of a cause of death in observed changes in life expectancy over time. The first attempt came in the form of single decrement life tables, which estimated the gain in life expectancy at birth under the assumption that one cause of death was completely eliminated (United States Department of Health, Education, and Welfare, 1968). Recognizing the tenuousness of this assumption, Keyfitz (1977) derived the proportional change in life expectancy at birth when either all-cause or cause-specific mortality was reduced by a constant percentage across age. Later developments focused on decomposition approaches. For example, Pollard (1982); Andreev (1982); Arriaga (1982); United Nations (1982); Arriaga (1984); Pressat (1985); Pollard (1988); Andreev et al. (2002) examined absolute gains in life expectancy resulting from absolute reductions in cause and age specific mortality between two discrete times. Subsequently, Vaupel (1986) and Vaupel and Canudas-Romo (2003) further developed decomposition approaches from a continuous-time perspective focusing on continuous progress against mortality. Recently, Beltrán-Sánchez et al. (2008) connected cause-elimination techniques with decomposition methods.l
All of these approaches addressed substantively important research questions. Yet their development was motivated by the very specific type of mortality decline envisioned. Consequently, their development was largely accomplished independently of one another; little opportunity arose to deduce connections. For example, the framework of mortality decline, either hypothetical or retrospective, leads to two seemingly different approaches. Only recently has their equivalence been demonstrated (Beltrán-Sánchez et al., 2008).
In this paper, we provide a systematic review of the literature within the unified functional calculus framework. We use functional calculus to demonstrate that previous approaches for assessing changes in life expectancy may be derived from a common formulation. With this framework, we are now able to concisely study how a change in age and cause-specific mortality contributes to changes in life expectancy. We apply our method to violent deaths, the leading cause of death among young adults. Other methods have been developed to decompose other demographic quantities of interest: the mean, median, mode, and standard deviation of the age of death distribution; healthy life expectancy; and total fertility rate (Das Gupta, 1991, 1999; Andreev et al., 2002; Horiuchi et al., 2008). In contrast, we focus on life expectancy and provide greater mathematical rigor reconciling previous developments related to decomposing changes in life expectancy over time.
2 Theoretical Derivations
2.1 Functionals
We use functional differential calculus to link changes in age and cause-specific mortality with changes in life expectancy. Functional differential calculus was first applied to demography by Arthur (1981, 1984) and by Preston (1982). A function f : 𝒜 → ℬ is a mapping that consists of two sets 𝒜 and ℬ with a rule that assigns to each element a ∈ 𝒜 a specific element of ℬ, which is denoted as f (a). Similarly, a functional F is a mapping from a vector space, ℱ, to the field underlying the vector space (usually the real numbers ℝ), which is denoted as ℱ [f]. Whereas a function is an element-by-element mapping, a functional maps an entire function to an element. For example, the probability of surviving from birth to age a at time t, p(a, t), is equal to exp , where μ(s, t) corresponds to the hazard rate at age s time t. Using a functional approach, p(a, t) is equal to exp (F[μ]), where F[μ] is defined as:
(1) |
F[μ] assigns to every function μ a real number corresponding to the negative of the definite integral of that function μ from 0 to a. Notice that μ could be any function of hazard rates, for example, a Gompertz function. Using the functional F, life expectancy at birth at time t, e(0, t), can be written as .
2.2 Functional Differentials
The functional differential of F[f], denoted by δF[f; h], approximates the change in F when f changes by a function h (Luenberger, 1968). This functional differential is defined as:
In general, when a model explicitly expresses a variable of interest, say r, in terms of functions fi and parameters xj for i = 1, …, n and j = 1, …, m such that r = F(f1, f2, …, fn, x1, x2, …, xm), we can write the differential change in r as
(2) |
where I and J represent the set of functions and parameters indices, respectively, which may change (Arthur, 1984). In other words, the differential change in the variable r corresponds to the sum of differential changes in functions and parameters. When the variable of interest r is implicitly expressed in the model, we have an implicit functional model of the form: 0 ≡ F(r, f1, f2, …, fn, x1, x2, …, xm). Thus, we have the following functional differential:
(3) |
For example, suppose our variable of interest is the probability of survival from birth to age a at time t, p(a, t). In this case we have an explicit model linking p(a, t) with μ(a, t). Our functional F takes a single argument, a function μ(a, t), as shown in equation 1. Further, suppose we want to find the change on this survivorship when there is a change in μ(a, t). Using equation 2 and the chain rule, the functional change in p(a, t) is defined as1:
(4) |
The quantity δμ(a, t) expresses a change in the force of mortality that may occur along both the age and time dimensions. Thus, from equation 2, we can define δμ(a, t) as
2.3 First Derivations
Let G be a functional defined as:
where F[μ] is defined in equation 1. Using equation 3, the functional differential of G is given by (see A.1):
(5) |
Evaluating each term of the above equation leads to:
(6) |
The relative change in life expectancy at birth, defined as é(0, t), is obtained by diving equation 6 by e(0, t)
(7) |
2.4 Multiple Causes of Death
Let μ1, …, μN be a set of mutually exclusive and exhaustive causes of death. Replacing μ with its sum μ1 + ⋯ + μN in equation 6, the continuous change in life expectancy at birth due to changes in cause-specific mortality equals:
(8) |
Similarly, replacing μ with its sum in equation 7, the relative change in life expectancy at birth due to changes in cause-specific mortality equals:
(9) |
2.5 Particular Cases
The expression δμ(s, t)/δt and in equations 6 and 7 and δμi(s, t)/δt in equations 8 and 9 represent the changes in all cause and cause-specific force of mortality, respectively, for every unit of time. It is precisely these quantities and their evaluation under different contexts that provide a unifying framework linking changes in life expectancy with changes in forces of mortality. For example, we may be interested in estimating how much of the observed change in life expectancy between two time periods is attributed to changes in a particular cause of death (Arriaga, 1982; Pollard, 1982). Similarly, we may also be interested in evaluating the change in life expectancy under two different mortality scenarios (Keyfitz, 1977). In these cases, the functional differential of μ(s, t) and μi(s, t) would be evaluated in the context of a discrete change over time or its equivalent–a discrete change between two different scenarios. Additionally, we may be interested in both of the above questions from a continuous time perspective (Vaupel, 1986; Vaupel and Canudas-Romo, 2003; Beltrán-Sánchez et al., 2008). Then, the functional differential of μ(s, t) and μi(s, t) would be evaluated in the context of a continuous time framework. Equations 6, 7, 8, and 9 precisely represent these approaches in a concise and unifying framework. We fully explore these ideas and their relationship with previous work in the next section.
2.5.1 Discrete Case
There are two general approaches when thinking of discrete changes in mortality. The first case relates to proportional changes in mortality rates, while the second approach is concerned with absolute changes. The first scenario was originally proposed by Keyfitz (1977) and the second approach was derived by several researchers (Pollard, 1982; Andreev, 1982; Arriaga, 1982; United Nations, 1982; Arriaga, 1984; Pressat, 1985; Pollard, 1988; Andreev et al., 2002), but two of the most commonly used formulas are those of Arriaga (1982) and Pollard (1982).
First, we consider a proportional change in mortality. Suppose there is a new scenario in which the force of mortality is proportionally reduced at all ages, i.e. μ*(a, t) = (1 + k) μ (a, t) where k is a small negative number (see Keyfitz, 1977). The functional differential of μ(a, t) is equal to its change between the two scenarios,
Then, substituting the above functional differential into equation 7 leads to a well known result of proportional change in life expectancy by Keyfitz (1977, p.413) (see A.1.1):
The equivalence of the first and second lines in the above equation were shown by Vaupel (1986) and Goldman and Lord (1986).
Now suppose there is a new scenario in which the cause-specific force of mortality is proportionally reduced at all ages, i.e. for cause i, where k is a small negative number (see Keyfitz, 1977). In this case, the functional differential of μi(a, t) is equal to k μi(a, t). Following the same approach as in all-cause mortality, one can show that equation 9 reduces to another well known result of proportional change in life expectancy by Keyfitz (1977, p.414):
Second, we consider an absolute change in mortality. Suppose there is an absolute improvement ϕ in the force of mortality μ(a, t) for some a ∈ [x, x + Δx], i.e. μ*(a, t) = μ(a, t) + ϕ, where ϕ is a small negative number (see Pollard, 1982). Substituting this result into equation 6 reduces to the well known result for attributing absolute changes in mortality and the corresponding absolute changes in life expectancy by Pollard (1982) (see A.1.2):
Now suppose there is an absolute improvement for each cause-specific force of mortality such that . Following the same approach as in all-cause mortality, equation 9 reduces to the cause-specific mortality result of Pollard (1982) (see A.1.2):
Pollard (1988) showed the equivalence between his previously developed approach (Pollard, 1982) and that of Arriaga (1982). Similarly, Andreev et al. (2002) showed Pollard (1982) is a special case of the stepwise replacement algorithm.
In addition, we can use our framework to derive a simple formula for the cause-eliminated life table model. This model considers the change in life expectancy when cause-specific mortality rates are set to zero and mortality for all other causes is held constant. Let i represent the cause eliminated. Set k = −1 for cause i; the functional differential of μi(a, t) is equal to −1 μi(a, t). Set k = 1 for all other causes j ≠ i; the functional differential of μj(a, t) is equal to 1 μj(a, t). Substituting these functional differentials into equation 8 leads to the cause-eliminated life table model.
2.5.2 Continuous Case
First, suppose there is continuous progress against all-cause mortality with respect to time such that the rate of progress in μ(a, t) is given by (see Vaupel, 1986). Then, the ratio of the functional differential of μ to that of time, , is equivalent to . Thus, equation 7 reduces to the well known result of Vaupel (1986).
where η(s, t) = μ(s, t) p(s, t) e(s, t)/e(0, t).
Similarly, when there is continuous progress against cause-specific mortality with respect to time, is equivalent to . Thus, equation 9 reduces to:
which is the Vaupel and Canudas-Romo (2003) result for decomposing changes in life expectancy by causes of death.
Second, suppose we are interested in the change with respect to time in the gain in life expectancy at birth when one cause of death is eliminated. This question was recently addressed by Beltrán-Sánchez et al. (2008). The years of life gained at birth at time t if cause of death i is eliminated is computed as Di(0, t) = e−i(0, t)−e(0, t), where e−i(0, t) represents life expectancy at birth at time t when cause of death i is eliminated. Then, the change in Di(0, t) with respect to time is given by
(10) |
Both terms on the right hand side of the above equation are particular cases of equation 6. Thus, evaluating the functional differential of these terms leads to the main result of Beltrán-Sánchez et al. (2008) for linking decomposition approaches and cause-deleted life tables (see A.1.3):
2.6 Varying Proportional Declines By Age and Cause of Death
Revisiting our main substantive research question, suppose we are interested in the change in life expectancy if there had been declines in particular age-specific motor vehicle, homicide, and suicide mortality rates over time. Our quantity of interest is life expectancy at birth. Under this scenario, we suppose there are targeted proportional reductions in the force of mortality for specific ages and causes. Let 𝒜1, …, 𝒜m be the set of targeted age groups for j = 1, …, m. Let cause one be motor vehicle accident mortality, cause two be homicide, cause three be suicide, and cause four be all other causes of death, so that for any given age a at time t. Let ki,𝒜j ≤ 0 be the proportional reduction in mortality for cause i and age group 𝒜j, j = 1, …, m. As discussed in Section 2.5.1, the functional differential of μi(a, t) is equal to:
(11) |
In other words, the change in cause-specific mortality after the targeted reduction is proportional to the original cause-specific mortality for ages within the targeted age range and is zero otherwise. Substituting equation 11 into equation 8, the change in life expectancy at birth between the two scenarios is equal to:
(12) |
The integral in the above equation represents the potential years of life lost (YLL) at time t due to cause i in age group 𝒜j. A similar quantity, aggregated over cause, was previously noted by Vaupel (1986) and further developed by Vaupel and Canudas-Romo (2003); Zhang and Vaupel (2008, 2009). The scalar −ki,𝒜j represents the recovery of potential years of life lost for cause i age group 𝒜j. For example, if −ki,𝒜j = 0.80, we recover 80% of the potential years of life lost at time t due to cause i in age group 𝒜j. Finally, the product represents the realized years of life gained at time t due to cause i in age group 𝒜j.
Although the theoretical derivation of the change in life expectancy at birth is given within the continuous-time framework, data are typically recorded in a discrete form. In this case, equation 12 contains an additional interaction term (see A.1.4):
(13) |
Using life table notation, the above terms can be estimated as:
(14) |
where aj,start and aj,end represent the starting and ending ages of the age group 𝒜j; l0 represents the life table radix, and eajstart and eajstart represent life expectancy at age ajstart and age ajend, respectively, in the life table for all-cause mortality. Terms with subindex i and −i refer to life table quantities where cause of death i and −i, respectively, is the only cause operating in the population. Thus, njdajstart, i represents the number of life table deaths in age group 𝒜j and pi(a) represents the probability of surviving from birth to age a when there is only cause i. The term njLajstart, −i represents the person-years lived in age group 𝒜j when all causes of death except cause i are operating in the population.
3 Applications
3.1 Data
We calculated 1970 and 2005 death counts for the total United States (U.S.) population from the Mortality Detail Files (U.S. Department of Health and Human Services, 2010, 2008), which contain information on all deaths registered on individual U.S. death certificates transmitted to the National Center for Health Statistics. Deaths were disaggregated by age and sex, as well as the following causes: motor vehicle accidents, homicides, suicides, and all other causes. Hereafter, we refer to motor vehicle accident mortality, homicides, and suicides as violent deaths. Comparable codes for these causes of death were derived from the Centers for Disease Control and Prevention (CDC, 2001). We use exposure-to-risk calculated by the Human Mortality Database University of California, Berkeley (USA) and Max Planck Institute for Demographic Research (Germany) (2006). Finally, we combine death counts and exposure-to-risk to calculate mortality rates by age, sex, and cause for 1970 and 2005. The terminal age category begins at age 100.
Considerable progress had been made against violent deaths for most of the ages between 1970 and 2005, as shown in Table 1. For example, improvements in vehicle safety and the introduction of car seats, especially rear-facing car seats, in part led to a more than 60% decline in motor vehicle accident mortality for children under age 10 in this period. Notable exceptions are male and female infanticide and male late adolescent homicide and suicide. For example, infanticides increased by 78% and 59% for males and females between 1970 and 2005, respectively.
Table 1.
Total Deaths | Motor Vehicle Accidents | Homicide | Suicide | ||||||||
---|---|---|---|---|---|---|---|---|---|---|---|
Age Group |
Prop. of Deaths | Prop. of Deaths | Δ Mort. Rate |
Prop. of Deaths | Δ Mort. Rate |
Prop. of Deaths | Δ Mort. Rate |
||||
1970 | 2005 | 1970 | 2005 | 1970 | 2005 | 1970 | 2005 | ||||
Male | |||||||||||
0–1 | 3.9 | 0.9 | 0.4 | 0.6 | −63.1 | 0.2 | 1.4 | 78.7 | 0 | 0 | – |
1–4 | 0.6 | 0.2 | 13.8 | 13.7 | −68.7 | 2 | 8.7 | 35.2 | 0 | 0 | – |
5–9 | 0.5 | 0.1 | 27.3 | 22.9 | −75.4 | 1.2 | 4.5 | 11.3 | 0 | 0.1 | 1.1 |
10–14 | 0.5 | 0.2 | 24.4 | 21.5 | −63.5 | 2.8 | 5.8 | −15.1 | 1.8 | 8.3 | 85.7 |
15–19 | 1.4 | 0.9 | 40.6 | 27.4 | −52.9 | 8.1 | 15.3 | 32 | 5.6 | 10.7 | 33.9 |
20–24 | 1.6 | 1.4 | 37.3 | 23.7 | −49.7 | 11.8 | 15.5 | 4 | 8.5 | 11.1 | 3.5 |
25–29 | 1.2 | 1.3 | 27.3 | 17.7 | −47.6 | 13.9 | 14.1 | −18 | 9.7 | 11.3 | −5.6 |
30–34 | 1.2 | 1.3 | 18.4 | 14.4 | −43.3 | 11.8 | 10.2 | −37 | 8.6 | 12 | 1.6 |
35–39 | 1.6 | 1.5 | 12.1 | 11.3 | −44 | 7.7 | 6.1 | −51.8 | 6.7 | 11.1 | −0.4 |
40–44 | 2.6 | 2.2 | 7.7 | 8.5 | −40.3 | 4.3 | 3.9 | −51.2 | 4.8 | 9.3 | 4.4 |
45–49 | 4.1 | 3 | 4.9 | 6.2 | −41.6 | 2.4 | 2.4 | −53.4 | 3.6 | 7.1 | −7.2 |
50–54 | 5.9 | 3.5 | 3.1 | 4.6 | −40.3 | 1.3 | 1.4 | −57.6 | 2.5 | 5.2 | −15.1 |
55–59 | 8.2 | 4.1 | 2.2 | 3.2 | −48.8 | 0.7 | 0.7 | −64.7 | 1.8 | 3.4 | −32.7 |
60–64 | 10.4 | 4.8 | 1.5 | 2 | −50.8 | 0.4 | 0.4 | −62.9 | 1.2 | 2.1 | −32.8 |
65–69 | 11.9 | 5.7 | 1.1 | 1.3 | −51.1 | 0.2 | 0.2 | −66.5 | 0.8 | 1.3 | −41.1 |
70–74 | 12.7 | 7.8 | 0.9 | 0.9 | −52.1 | 0.1 | 0.1 | −54.5 | 0.6 | 0.9 | −32.7 |
75–79 | 12.6 | 11.3 | 0.7 | 0.6 | −54 | 0.1 | 0.1 | −46.2 | 0.5 | 0.7 | −18.5 |
80–84 | 10.1 | 15.3 | 0.6 | 0.4 | −52 | 0.1 | 0 | −66.7 | 0.4 | 0.4 | −15.6 |
85–89 | 6.1 | 15.9 | 0.4 | 0.2 | −36.1 | 0 | 0 | −68.2 | 0.3 | 0.2 | −14.6 |
90–94 | 2.3 | 12.3 | 0.3 | 0.1 | −47.1 | 0 | 0 | −71.2 | 0.1 | 0.1 | 30.4 |
95–99 | 0.5 | 5.3 | 0.1 | 0 | −20.5 | 0 | 0 | – | 0.1 | 0 | 24.9 |
Female | |||||||||||
100+ | 0.1 | 1.2 | 0.3 | 0 | −67.7 | 0 | 0 | – | 0 | 0 | – |
0–1 | 3.7 | 1.4 | 0.6 | 0.4 | −67.2 | 0.2 | 0.8 | 58.8 | 0 | 0 | – |
1–4 | 0.6 | 0.2 | 13.3 | 11.5 | −66.6 | 2.5 | 6.7 | 1.3 | 0 | 0 | – |
5–9 | 0.4 | 0.1 | 23 | 19.9 | −64.4 | 1.6 | 3.4 | −13.3 | 0 | 0 | – |
10–14 | 0.4 | 0.2 | 22.2 | 17.2 | −53.3 | 3 | 4.5 | −8.7 | 1 | 3.5 | 110.9 |
15–19 | 0.7 | 0.4 | 36.8 | 32.2 | −30 | 5.2 | 5 | −22.6 | 4.7 | 5.5 | −5.2 |
20–24 | 0.7 | 0.6 | 27 | 19.5 | −35.7 | 8.3 | 6.3 | −32.3 | 7.4 | 5.7 | −31.7 |
25–29 | 0.7 | 0.6 | 15 | 11.8 | −33.7 | 7.2 | 5.3 | −37.8 | 9.5 | 5.2 | −53.6 |
30–34 | 0.8 | 0.8 | 10.6 | 8.7 | −32.9 | 4.7 | 3.6 | −37.3 | 7.7 | 5.4 | −42.4 |
35–39 | 1.2 | 1.3 | 7.1 | 5.7 | −36.7 | 3.3 | 2.7 | −36.4 | 6.1 | 4.1 | −47.6 |
40–44 | 2 | 2.4 | 4.6 | 3.5 | −33.1 | 2 | 1.4 | −39.1 | 4.6 | 3 | −42.8 |
45–49 | 3.1 | 3.8 | 3.2 | 2.2 | −38.9 | 1 | 0.7 | −36.1 | 3 | 2.1 | −35.4 |
50–54 | 4.2 | 5.2 | 2.5 | 1.3 | −51.1 | 0.5 | 0.3 | −44 | 2 | 1.3 | −39.8 |
55–59 | 5.6 | 6.5 | 1.7 | 1 | −47.3 | 0.3 | 0.2 | −45.5 | 1.3 | 0.8 | −46.2 |
60–64 | 7.2 | 7.4 | 1.3 | 0.7 | −46.8 | 0.2 | 0.1 | −43.2 | 0.8 | 0.4 | −49.7 |
65–69 | 9.4 | 8.4 | 1 | 0.6 | −46 | 0.1 | 0.1 | −34 | 0.4 | 0.2 | −54.5 |
70–74 | 12.1 | 10.7 | 0.7 | 0.4 | −52.6 | 0.1 | 0.1 | −24.7 | 0.3 | 0.1 | −60.5 |
75–79 | 14.6 | 13.7 | 0.5 | 0.4 | −44.9 | 0 | 0 | −23.2 | 0.1 | 0.1 | −50.3 |
80–84 | 14.7 | 15.3 | 0.3 | 0.3 | −35.1 | 0 | 0 | −37 | 0.1 | 0.1 | −33.7 |
85–89 | 10.9 | 12.2 | 0.1 | 0.3 | −8.7 | 0 | 0 | −14.7 | 0 | 0.1 | −28.5 |
90–94 | 5.3 | 6.6 | 0.1 | 0.2 | −1.1 | 0 | 0 | −52 | 0 | 0 | −59 |
95–99 | 1.5 | 1.9 | 0.1 | 0.1 | −75.1 | 0 | 0 | – | 0 | 0 | −40.2 |
100+ | 0.2 | 0.3 | 0 | 0.2 | – | 0.1 | 0 | −100 | 0 | 0 | – |
Note: Prop. is proportion, Mort. is mortality, and Δ represents change For age groups and causes in which no deaths occurred in 1970 and 2005, the change is not applicable (–). Source: Mortality Detail Files, 1970 and 2005, and Human Mortality Database.
3.2 Case 1
Suppose we are interested in the change in life expectancy at birth if the same proportional reductions as historically observed in Table 1 are again applied to 2005 mortality rates. For example, there was a 75.4% decline in male age 5–9 motor vehicle accident mortality between 1970 and 2005; in this new scenario, the 2005 male motor vehicle accident mortality rate for this age group is reduced by another 75.4%. If the mortality rate increased between 1970 and 2005, it remains at the 2005 level in the new scenario. The matrix of ki,𝒜j values for this scenario is identical to columns 6, 9, and 12 of Table 1 (“Δ Mort. Rate”) except that positive values are replaced with 0. We present the mortality rates of this new scenario in Figure 1, along with historically observed 1970 and 2005 rates. We also calculate period life expectancy in 2005, as well as under this new mortality scenario in Table 2.
Table 2.
Case 1 | Case 2 | ||||
---|---|---|---|---|---|
e0 | New Scenario e0 | Difference | New Scenario e0 | Difference | |
Male | 74.91 | 75.28 | 0.37 | 75.36 | 0.45 |
Female | 80.49 | 80.66 | 0.17 | 80.63 | 0.14 |
Note: Change in Male and Female Life Expectancy at Birth: Case 1 and Case 2 Compared to Year 2005. Source: Authors’ calculations based on data from Mortality Detail Files and Human Mortality Database.
We estimate the gain in life expectancy at birth under this scenario using equation 14 and present results in Table 3. The estimated potential years of life lost by age and cause are shown in columns (2), (5), and (8). The age and cause-specific reductions, which form the −ki,𝒜j matrix, are shown in columns (1), (4), and (7). The pairwise product that represents the estimated years of life gained under this scenario is shown in columns (3), (6), and (9). Finally, column (10) represents the contribution of each age group to the total gain in life expectancy.
Table 3.
Age Group |
Motor Vehicle Accidents | Homicide | Suicide | Total | ||||||
---|---|---|---|---|---|---|---|---|---|---|
−k𝒜j (1) |
(2) |
(3)= (1)×(2) |
− k𝒜j (4) |
(5) |
(6)= (4)×(5) |
− k𝒜j (7) |
(8) |
(9)= (7)×(8) |
(10)= (3)+(6)+(9) |
|
Male | ||||||||||
0–1 | 0.631 | 0.002 | 0.002 | 0.000 | 0.006 | 0.000 | 0.000 | 0.000 | 0.000 | 0.002 |
1–4 | 0.687 | 0.011 | 0.008 | 0.000 | 0.007 | 0.000 | 0.000 | 0.000 | 0.000 | 0.008 |
5–9 | 0.754 | 0.011 | 0.008 | 0.000 | 0.002 | 0.000 | 0.000 | 0.000 | 0.000 | 0.008 |
10–14 | 0.635 | 0.014 | 0.009 | 0.151 | 0.004 | 0.001 | 0.000 | 0.005 | 0.000 | 0.010 |
15–19 | 0.529 | 0.085 | 0.045 | 0.000 | 0.048 | 0.000 | 0.000 | 0.033 | 0.000 | 0.045 |
20–24 | 0.497 | 0.108 | 0.054 | 0.000 | 0.071 | 0.000 | 0.000 | 0.051 | 0.000 | 0.054 |
25–29 | 0.476 | 0.068 | 0.032 | 0.180 | 0.054 | 0.010 | 0.056 | 0.043 | 0.002 | 0.045 |
30–34 | 0.433 | 0.051 | 0.022 | 0.370 | 0.036 | 0.013 | 0.000 | 0.042 | 0.000 | 0.035 |
35–39 | 0.440 | 0.041 | 0.018 | 0.518 | 0.022 | 0.011 | 0.004 | 0.040 | 0.000 | 0.029 |
40–44 | 0.403 | 0.037 | 0.015 | 0.512 | 0.017 | 0.009 | 0.000 | 0.040 | 0.000 | 0.023 |
45–49 | 0.416 | 0.031 | 0.013 | 0.534 | 0.012 | 0.006 | 0.072 | 0.036 | 0.003 | 0.022 |
50–54 | 0.403 | 0.026 | 0.011 | 0.576 | 0.008 | 0.005 | 0.151 | 0.030 | 0.004 | 0.020 |
55–59 | 0.488 | 0.021 | 0.010 | 0.647 | 0.004 | 0.003 | 0.327 | 0.022 | 0.007 | 0.020 |
60–64 | 0.508 | 0.016 | 0.008 | 0.629 | 0.003 | 0.002 | 0.328 | 0.017 | 0.006 | 0.016 |
65–69 | 0.511 | 0.012 | 0.006 | 0.665 | 0.002 | 0.001 | 0.411 | 0.012 | 0.005 | 0.012 |
70–74 | 0.521 | 0.010 | 0.005 | 0.545 | 0.001 | 0.001 | 0.327 | 0.010 | 0.003 | 0.009 |
75–79 | 0.540 | 0.008 | 0.004 | 0.462 | 0.001 | 0.000 | 0.185 | 0.008 | 0.002 | 0.006 |
80–84 | 0.520 | 0.005 | 0.003 | 0.667 | 0.000 | 0.000 | 0.156 | 0.006 | 0.001 | 0.004 |
85–89 | 0.361 | 0.003 | 0.001 | 0.682 | 0.000 | 0.000 | 0.146 | 0.003 | 0.000 | 0.002 |
90–94 | 0.471 | 0.001 | 0.000 | 0.712 | 0.000 | 0.000 | 0.000 | 0.001 | 0.000 | 0.000 |
95–99 | 0.205 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 |
Total | 0.569 | 0.277 | 0.304 | 0.062 | 0.407 | 0.033 | 0.373 | |||
Female | ||||||||||
0–1 | 0.672 | 0.003 | 0.002 | 0.000 | 0.005 | 0.000 | 0.000 | 0.000 | 0.000 | 0.002 |
1–4 | 0.666 | 0.010 | 0.007 | 0.000 | 0.006 | 0.000 | 0.000 | 0.000 | 0.000 | 0.007 |
5–9 | 0.644 | 0.010 | 0.007 | 0.133 | 0.002 | 0.000 | 0.000 | 0.000 | 0.000 | 0.007 |
10–14 | 0.533 | 0.010 | 0.005 | 0.087 | 0.003 | 0.000 | 0.000 | 0.002 | 0.000 | 0.006 |
15–19 | 0.300 | 0.049 | 0.015 | 0.226 | 0.008 | 0.002 | 0.052 | 0.008 | 0.000 | 0.017 |
20–24 | 0.357 | 0.037 | 0.013 | 0.323 | 0.012 | 0.004 | 0.317 | 0.011 | 0.003 | 0.020 |
25–29 | 0.337 | 0.023 | 0.008 | 0.378 | 0.010 | 0.004 | 0.536 | 0.010 | 0.005 | 0.017 |
30–34 | 0.329 | 0.020 | 0.006 | 0.373 | 0.008 | 0.003 | 0.424 | 0.012 | 0.005 | 0.015 |
35–39 | 0.367 | 0.018 | 0.006 | 0.364 | 0.008 | 0.003 | 0.476 | 0.013 | 0.006 | 0.015 |
40–44 | 0.331 | 0.016 | 0.005 | 0.391 | 0.006 | 0.002 | 0.428 | 0.014 | 0.006 | 0.014 |
45–49 | 0.389 | 0.014 | 0.005 | 0.361 | 0.004 | 0.002 | 0.354 | 0.013 | 0.005 | 0.012 |
50–54 | 0.511 | 0.011 | 0.006 | 0.440 | 0.003 | 0.001 | 0.398 | 0.011 | 0.004 | 0.011 |
55–59 | 0.473 | 0.010 | 0.005 | 0.455 | 0.002 | 0.001 | 0.462 | 0.008 | 0.004 | 0.009 |
60–64 | 0.468 | 0.009 | 0.004 | 0.432 | 0.001 | 0.001 | 0.497 | 0.005 | 0.003 | 0.007 |
65–69 | 0.460 | 0.008 | 0.004 | 0.340 | 0.001 | 0.000 | 0.545 | 0.003 | 0.002 | 0.006 |
70–74 | 0.526 | 0.006 | 0.003 | 0.247 | 0.001 | 0.000 | 0.605 | 0.002 | 0.001 | 0.005 |
75–79 | 0.449 | 0.006 | 0.003 | 0.232 | 0.001 | 0.000 | 0.503 | 0.001 | 0.001 | 0.003 |
80–84 | 0.351 | 0.004 | 0.001 | 0.370 | 0.000 | 0.000 | 0.337 | 0.001 | 0.000 | 0.002 |
85–89 | 0.087 | 0.002 | 0.000 | 0.147 | 0.000 | 0.000 | 0.285 | 0.000 | 0.000 | 0.000 |
90–94 | 0.011 | 0.001 | 0.000 | 0.520 | 0.000 | 0.000 | 0.590 | 0.000 | 0.000 | 0.000 |
95–99 | 0.751 | 0.000 | 0.000 | 0.000 | 0.000 | 0.000 | 0.402 | 0.000 | 0.000 | 0.000 |
Total | 0.277 | 0.105 | 0.081 | 0.023 | 0.126 | 0.046 | 0.174 |
Note: Columns 1, 4, and 7 correspond to proportionate reductions in age and cause-specific mortality. Columns 2, 5, and 8 correspond to the estimated maximum potential years of life gained for complete reduction, , and includes contributions from the main effects and interaction shown in equation 14. Columns 3, 6, and 9 correspond to the estimated realized years of life gained under Case 1 reductions by sex, age, and cause. Column 10 corresponds to the total estimated realized years of life by age and sex. Source: authors’ calculations.
Columns (2), (5), and (8) show that, among men in 2005, violent deaths were responsible for 1.28 years of life lost: 0.57 years from motor vehicle accidents, 0.30 years from homicides, and 0.41 years from suicides. Applying the mortality reductions shown in columns (1), (4), and (7) leads to a gain in life expectancy at birth for men of about 0.28 years from motor vehicle accidents, 0.06 years from homicides, and about 0.03 years from suicides, for a total of about 0.37 years of life gained (column 10). Even when we apply these large declines in age and cause-specific mortality rates, we are only able to recover about half, one-fifth and one-tenth of the potential years of life lost from motor vehicle accidents, homicides and suicides, respectively.
Of course, if the outcome of interest is simply the total gain in life expectancy at birth when violent death mortality is reduced by a targeted amount, then the calculation of a life table under this new scenario would suffice. Yet from a policy perspective, it is equally important to know for which ages and for which specific causes a change in mortality rates would produce the greatest gain in life expectancy at birth, as shown in Table 3.
3.3 Case 2
A closer look at Table 3 shows that the greatest loss of potential life years occurs between ages 15 and 34 for most of the violent deaths. Thus, we can imagine a new scenario in which we focus on reducing mortality rates at these particular ages. We show this case as a dashed line in Figure 1. Such declines might reflect the result of an aggressive and targeted public health and safety campaign. For example, we assume a decline of 95% in motor vehicle accidents, 60% in homicide, and 35% in suicide among 20–24 year old men (Table 4). We then estimate the highest gain in life expectancy at birth that would occur for the 20–24 year old age group.
Table 4.
Age Group |
Motor Vehicle Accidents | Homicide | Suicide | Total | ||||||
---|---|---|---|---|---|---|---|---|---|---|
−k𝒜j (1) |
(2) |
(3)= (1)×(2) |
−k𝒜j (4) |
(5) |
(6)= (4)×(5) |
−k𝒜j (7) |
(8) |
(9)= (7)×(8) |
(10)= (3)+(6)+(9) |
|
Male | ||||||||||
15–19 | 0.900 | 0.085 | 0.077 | 0.600 | 0.048 | 0.029 | 0.450 | 0.033 | 0.015 | 0.120 |
20–24 | 0.950 | 0.108 | 0.103 | 0.600 | 0.071 | 0.042 | 0.350 | 0.051 | 0.018 | 0.163 |
25–29 | 0.900 | 0.068 | 0.061 | 0.450 | 0.054 | 0.024 | 0.150 | 0.043 | 0.007 | 0.092 |
30–34 | 0.900 | 0.051 | 0.045 | 0.300 | 0.036 | 0.011 | 0.100 | 0.042 | 0.004 | 0.060 |
35–39 | 0.150 | 0.041 | 0.006 | 0.050 | 0.022 | 0.001 | 0.050 | 0.040 | 0.002 | 0.009 |
Total | 0.569 | 0.292 | 0.304 | 0.107 | 0.407 | 0.045 | 0.444 | |||
Female | ||||||||||
15–19 | 0.850 | 0.049 | 0.042 | 0.600 | 0.008 | 0.005 | 0.500 | 0.008 | 0.004 | 0.051 |
20–24 | 0.800 | 0.037 | 0.029 | 0.600 | 0.012 | 0.007 | 0.400 | 0.011 | 0.004 | 0.041 |
25–29 | 0.750 | 0.023 | 0.017 | 0.450 | 0.010 | 0.005 | 0.200 | 0.010 | 0.002 | 0.024 |
30–34 | 0.700 | 0.020 | 0.014 | 0.300 | 0.008 | 0.002 | 0.100 | 0.012 | 0.001 | 0.017 |
35–39 | 0.200 | 0.018 | 0.004 | 0.180 | 0.008 | 0.001 | 0.050 | 0.013 | 0.001 | 0.006 |
Total | 0.277 | 0.105 | 0.081 | 0.020 | 0.126 | 0.012 | 0.138 |
Note: Columns 1, 4, and 7 correspond to proportionate reductions in age and cause-specific mortality. Columns 2, 5, and 8 correspond to the estimated maximum potential years of life gained for complete reduction, , and includes contributions from the main effects and interaction shown in equation 14. Columns 3, 6, and 9 correspond to the estimated realized years of life gained under Case 1 reductions by sex, age, and cause. Column 10 corresponds to the total estimated realized years of life by age and sex. Source: authors’ calculations.
Case 2 yields a similar gain in life expectancy through these targeted age and cause-specific reductions as in Case 1. Moreover, in Case 2, reductions are targeted at ages in which the assumption of independence among causes of death is far more plausible. For males, targeted motor vehicle accident, homicide, and suicide reductions contribute about 0.29, 0.11, and 0.05 years of life expectancy, respectively (Table 4). Similarly for females, the corresponding gains are 0.11, 0.02, and 0.01 years of life expectancy. This leads to a total gain in life expectancy at birth of 0.44 years for males and 0.14 years for females.
In both cases, we utilize our common formulation to link changes in life expectancy with changes in the forces of mortality. For each case, we simply evaluate its particular change in cause-specific forces of mortality for every unit of time, δμi(s, t)/δt. One could certainly envision other cases of hypothesized mortality reduction, as well. Once δμi(s, t)/δt is evaluated in this new context, the same methodology developed in Section 2 applies.
4 Concluding Remarks
In this paper, we develop two important results. First, we provide a unifying framework for assessing the change in life expectancy given a change in age and cause-specific mortality. Two conceptualizations of mortality change are possible: a counterfactual assessment of a hypothetical change or a retrospective assessment of an observed change. Our framework, developed in Sections 2.3 and 2.4, shows how these conceptualizations can be easily implemented to assess changes in life expectancy with respect to time, both for all-cause and multiple cause of death. In doing so, we thus connect previous demographic research into a sound and parsimonious formulation.
Second, when we apply our methodology to a particular case of targeted age and cause-specific mortality reductions, we obtain an especially useful byproduct: the maximum potential years of life lost, specific to each age and cause, given current mortality. This quantity provides an estimate of the theoretical maximum years of life that could be potentially recovered if all deaths in this age and cause could be averted. In a particular case, only a proportion of deaths would be averted; then only this proportion of years of life would be recovered. For example, the estimated maximum years of life lost due to male 20–24 year old motor vehicle accidents is 0.11 years in 2005. If we could decline mortality in this cause and age group by 65%, we would recover 0.07 years of life expectancy at birth.
An important limitation in this area of demographic research is the assumption of independence among causes of death. Whereas the assumption may hold for violent deaths among young adults, it is far more tenuous for other causes of death among older adults. For age groups 15 to 34, which we study in Section 3.3, violent deaths are the leading cause of death. The risk of death from other causes, notably leading causes among the elderly (cardiovascular disease, cancer, and stroke) is considerably smaller. For example, if a young adult’s motor vehicle accident death could have been averted, the decedent’s risk of death from other causes would likely changed very little. On the other hand, if an older adult’s diabetes death could have been averted, this decedent’s risk of death from other causes will likely change because of diabetes-related comorbidities.
Tsiatis (1975) showed in the absence of specified joint distribution of potential survival times, the model of potential survival times is not identifiable. Tsiatis (1975) further identified the problem and challenges of directly verifying a particular specification. The multiple-decrement life table model follows a competing risks framework (see Preston et al., 2001, Ch. 4) and the identification problem is a core concern. Thusfar, three approaches have been developed to solve the identification problem in competing risks models, but all of them require additional assumptions regarding the duration until death from different causes of death and a functional form for the mortality process (Honoré and Lleras-Muney, 2006). For example, Yashin et al. (1986) developed a multivariate stochastic process in which the different cause specific hazards were jointly dependent to formulate a solution for the dependent competing risk model of longitudinal data. Yashin et al. (2009) assumed a multivariate log-normal frailty model in their approach of a dependent competing risks model capturing negative correlations between causes of death. Llorca and Delgado-Rodríguez (2001) developed a Markov chain model to study the association between cardiovascular disease, coronary heart disease and cancer in Spain. Honoré and Lleras-Muney (2006) developed a solution for the competing risk model in a semi-parametric accelerated failure time model with grouped durations. All these approaches, however, require additional information that is unavailable from cross-sectional data at the population level. However, the unifying framework we present addresses the contribution of a cause of death to a change in life expectancy, and as noted by Yashin et al. (1986): “adjustment for cause dependency is more important … when estimating the resulting population life expectancy after elimination than when producing an estimate of the effect of a given disease (p.135).”
Our methodological and substantive results have immediate implications for health demography. Health demographers often require an assessment of possible gains in life expectancy that could result from a public health campaign aimed at reducing mortality for specific ages and causes of death. We provide a theoretical framework and simple tools2 that inform these important health policy decisions.
A Appendix
A.1 First Derivations
After applying the chain rule, the first term of equation 5 is equivalent to:
(A-1) |
The second term of equation 5 is equivalent to:
(A-2) |
Substituting equations A-1 and A-2 into equation 5 we obtain:
Thus,
(A-3) |
The relative change in life expectancy at birth, defined as é(0, t), is obtained by diving equation 6 by e(0, t):
(A-4) |
A.1.1 Discrete Case: Proportional Changes in Mortality
In the discrete case, the time unit change is equal to 1, δt = 1. Then, substituting the functional differential of μ(a, t), k μ(a, t), into equation A-4, the relative change in life expectancy at birth reduces to:
(A-5) |
Thus, from equation A-5 we derive the well known result of proportional change in life expectancy by Keyfitz (1977, p.413):
(A-6) |
A.1.2 Discrete Case: Absolute Change in Mortality
Let μ(a, t) and μ*(a, t) denote the force of mortality before and after some change in mortality. Under this two-time period scenario, the change in μ, δμ(a, t), is equal to μ*(a, t) − μ(a, t). Similarly, let p(a, t) and p*(a, t) be the probability of surviving from birth to age a before and after the change in the force of mortality, respectively. Recall that and . The change in p(a, t), δp(a, t) is equal to δp(a, t) = p*(a, t)−p(a, t).
Rearranging terms leads to the following:
(A-7) |
The then change in life expectancy at birth, δe(0, t) is equal to:
For changes in cause-specific mortality, the change in life expectancy at birth is:
(A-8) |
Dividing by e(0, t) yields the relative change in life expectancy at birth, é(0, t).
When the force of mortality changes continuously over time, equation A-7 converges to equation 4, which is the basis for developing equations 6, 7, 8, and 9. We want to show:
Recall that for x ∈ ℝ. Let . Using equation A-7, the limit as h approaches zero corresponds to:
(A-9) |
The series converges to ez and the second term of equation A-9, , approaches zero as h becomes smaller, so
Recall μ is a continuous function. The first term of the limit in the above equation approaches zero as h approaches zero, while the exponential function approaches to one. Thus, the second term of equation A-9 approaches zero. From equation A-9, we conclude that when looking at continuous changes in mortality with respect to time, .
A.1.3 Continuous Case: Change in the gain in life expectancy
Both terms on the right hand side of equation 10 are particular cases of equation 6. Thus,
(A-10) |
because the ratio of functional differentials, , is equal to . Similarly,
(A-11) |
Substituting equations A-10 and A-11 into equation 10 leads to the main result of Beltrán-Sánchez et al. (2008) for linking decomposition approaches and cause-deleted life tables:
A.1.4 Varying Proportional Declines by Age and Cause of Death
Recall that . Applying equation A-8 to equation 12 leads to
Thus, we can split the change in life expectancy, e*(0, t)−e(0, t), into the sum of two parts: a main effect and interaction.
Using life table notation, the above terms can be estimated as
Footnotes
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
We thank Robert Aronowitz, David Asch, Christopher Croke, Bartek Czech, Charles Epstein, Douglas Ewbank, Brendan Hassett, Valerie Lewis, Samuel H. Preston, Jason Schnittker, Flaura Koplin Winston and the anonymous referees for helpful comments and suggestions. The authors thank the Robert Wood Johnson Foundation Health & Society Scholars program, University of Pennsylvania Population Studies Center (T32 HD 7242-26), and the Andrus Gerontology Center (T32 AG 37-33) at the University of Southern California for their financial support.
The following formula is developed assuming mortality changes continuously over time. When mortality changes over two discrete-time points, it gives rise to interaction terms that our formula ignores. (see A.1.2)
The R functions of the proposed method are available on the authors’ website: http://people.iq.harvard.edu/ssoneji/.
References
- Andreev E. Method Komponent v Analize Prodoljitelnosty Zjizni [The Method of Components in the Analysis of Length of Life] Vestnik Statistiki. 1982;9:42–47. [Google Scholar]
- Andreev E, Shkolnikov V, Begun A. Algorithm for Decomposition of Differences Between Aggregate Demographic Measures and its Application to Life Expectancies, Gini Coefficients, Health Expectancies, Parity-Progression Ratios and Total Fertility Rates. Demographic Research. 2002;7:499–522. [Google Scholar]
- Arriaga E. A Note on the Use of Temporary Life Expectancies for Analyzing Changes and Differentials of Mortality. Geneva: World Health Organization; 1982. Mortality in South and East Asia: A Review of Changing Trends and Patterns, Manila 1980, WHO/ESCAP, chap. pp. 559–562. [Google Scholar]
- Arriaga E. Measuring and Explaining the Change in Life Expectancies. Demography. 1984;21:83–96. [PubMed] [Google Scholar]
- Arthur B. Tech. rep. Laxenburg, Austria: International Institute for Applied Systems Analysis; 1981. The Analysis of Causal Linkages in Demographic Theory. [Google Scholar]
- Arthur WB. The Analysis of Linkages in Demographic Theory. Demography. 1984;21:109–127. [PubMed] [Google Scholar]
- Beltrán-Sánchez H, Preston S, Vladimir C-R. An Integrated Approach to Cause-of-Death Analysis: Cause-Deleted Life Tables and Decompositions of Life Expectancy. Demographic Research. 2008;19:1323–1350. doi: 10.4054/DemRes.2008.19.35. [DOI] [PMC free article] [PubMed] [Google Scholar]
- CDC. Tech. rep. Centers for Disease Control and Prevention; 2001. Comparability Across ICD Revisions for Selected Causes. http://www.cdc.gov/nchs/data/statab/comp2.pdf. [Google Scholar]
- Das Gupta P. Decomposition of differences between rates when the factors are nonmultiplicative with applications to the US life tables. Mathematical Population Studies. 1991;3:105–125. [Google Scholar]
- Das Gupta P. Decomposing the difference between rates when the rate is a function of factors that are not cross-classified. Genus. 1999;55:9–26. [Google Scholar]
- Goldman N, Lord G. A New Look at Entropy and the Life Table. Demography. 1986;23:275–282. [PubMed] [Google Scholar]
- Honoré B, Lleras-Muney A. Bounds in Competing Risks Models and the War on Cancer. Econometrica. 2006;74:1675–1698. [Google Scholar]
- Horiuchi S, Wilmoth J, Pletcher S. A Decomposition Method Based on a Model of Continuous Change. Demography. 2008;45:785–801. doi: 10.1353/dem.0.0033. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Keyfitz N. What Difference Would it make if Cancer were Eradicated? An Examination of the Taeuber Paradox. Demography. 1977;14:411–418. [PubMed] [Google Scholar]
- Llorca J, Delgado-Rodríguez M. Competing Risks Analysis Using Markov Chains: Impact of Cerebrovascular and Ischemic Heart Disease in Cancer Mortality. International Journal of Epidemiology. 2001;30:99–101. doi: 10.1093/ije/30.1.99. [DOI] [PubMed] [Google Scholar]
- Luenberger D. Optimization by Vector Space Methods. New York: Wiley; 1968. [Google Scholar]
- Pollard J. The Expectation of Life and its Relationship to Mortality. Journal of the Institute of Actuaries. 1982;109:225–240. [Google Scholar]
- Pollard J. Measuring and Explaining the Change in Life Expectancies. Demography. 1988;25:265–276. [PubMed] [Google Scholar]
- Pressat R. Contribution des Ecarts de Mortalite par Age a la Difference des Vies Moyennes. Population. 1985;4–5:765–770. [Google Scholar]
- Preston S. Relations Between Individual Life Cycle and Population Characteristics. American Sociological Review. 1982;47:253–264. [PubMed] [Google Scholar]
- Preston S, Heuveline P, Guillot M. Demography: measuring and modeling population processes. Malden, MA: Blackwell Publishing; 2001. [Google Scholar]
- Tsiatis A. A Nonidentifiability Aspect of the Problem of Competing Risks. Proceeding of the National Academy of Sciences. 1975;72:20–22. doi: 10.1073/pnas.72.1.20. [DOI] [PMC free article] [PubMed] [Google Scholar]
- United Nations. Tech. Rep. 74. New York: United Nations, Dept. of International Economic and Social Affairs; 1982. Levels and Trends of Mortality Since 1950. [Google Scholar]
- United States Department of Health, Education, and Welfare. United States Life Tables by Causes of Death: 1959–1961. vol. 1. Washington, D.C: U.S. Government Printing Office; 1968. [Google Scholar]
- University of California, Berkeley (USA) and Max Planck Institute for Demographic Research (Germany) Human Mortality Database. Tech. rep. 2006 http://www.mortality.org, data downloaded on April 1, 2006.
- U.S. Department of Health and Human Services. computer file, National Center for Health Statistics. Ann Arbor, MI: inter-university Consortium for Political and Social Research [distributor]; 2008. Multiple Cause of Death Public Use Files, 2005. [Google Scholar]
- U.S. Department of Health and Human Services. computer file, National Center for Health Statistics. Ann Arbor, MI: inter-university Consortium for Political and Social Research [distributor]; 2010. Mortality Data Files, 1968–1991. [Google Scholar]
- Vaupel J. How Change in Age-Specific Mortality Affects Life Expectancy. Population Studies. 1986;40:147–157. doi: 10.1080/0032472031000141896. [DOI] [PubMed] [Google Scholar]
- Vaupel J, Canudas-Romo V. Decomposing Change in Life Expectancy: A Bouquet of Formulas in Honor of Nathan Keyfitz’s 90th Birthday. Demography. 2003;40:201–216. doi: 10.1353/dem.2003.0018. [DOI] [PubMed] [Google Scholar]
- Yashin AI, Manton K, Stallard E. Dependent Competing Risks: A Stochastic Process Model. Journal of Mathematical Biology. 1986;24:119–140. doi: 10.1007/BF00275995. [DOI] [PubMed] [Google Scholar]
- Yashin AI, Ukraintseva S, Akushevich K, Arbeev G, Kulminski A, Akushevich L. Trade-off between Cancer and Aging: What Role do other Diseases Play? Evidence from Experimental and Human Population Studies. Mechanisms of Ageing and Development. 2009;130:98–104. doi: 10.1016/j.mad.2008.03.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Zhang Z, Vaupel J. The Threshold between Compression and Expansion of Mortality. Paper presented at the Population Association of America Annual Meeting.2008. [Google Scholar]
- Zhang Z, Vaupel J. The Age Separating Early Deaths From Late Deaths. Demographic Research. 2009;20:721–730. [Google Scholar]