This article relies largely or entirely on a single source .(May 2021) |
In gerontology, late-life mortality deceleration is the disputed theory that hazard rate increases at a decreasing rate in late life rather than increasing exponentially as in the Gompertz law.
Late-life mortality deceleration is a well-established phenomenon in insects, [1] which often spend much of their lives in a constant hazard rate region, but it is much more controversial in mammals. [2] Rodent studies have found varying conclusions, with some finding short-term periods of mortality deceleration in mice, others not finding such. Baboon studies show no mortality deceleration.
An analogous deceleration occurs in the failure rate of manufactured products; this analogy is elaborated in the reliability theory of aging and longevity. [1] [3]
Late-life mortality deceleration was first proposed as occurring in human aging in Gompertz (1825) (which also introduced the Gompertz law), and observed as occurring in humans in Greenwood & Irwin (1939), and has since become one of the pillars of the biodemography of human longevity – see history; here "late life" is typically "after 85 years of age". However, a recent paper, Gavrilov & Gavrilova (2011), concludes that mortality deceleration is negligible up to the age of 106 in the population studied (beyond this point, reliable data were unavailable) and that the Gompertz law is a good fit, with previous observations of deceleration being spurious, with various causes, including bad data and methodological problems – see criticism.
According to a 2018 paper, statistical errors are the main cause of apparent mortality deceleration in humans. [4]
Three related terms are used in this context:
A brief historical review is given in Gavrilov & Gavrilova (2011 , 2. Mortality at Advanced Ages: A Historical Review (pp. 433–435)); a detailed survey is given in Olshansky (1998).
Late-life mortality deceleration was first proposed as occurring in human aging, in Gompertz (1825), which also introduced the Gompertz law. [5] It was observed and quantified in Greenwood & Irwin (1939), and reproduced in many later studies. Greenwood and Irwin wrote:
Following these studies, late-life mortality deceleration became one of the pillars of the theory of biodemography of human longevity, and models have incorporated it. It has been criticized at times, and recently has been very seriously criticized; see below.
This section relies largely or entirely on a single source .(March 2020) |
Statistical studies of extreme longevity are difficult for a number of factors. Firstly, because few people live to very old ages, a very large population is required for such studies, ideally all born and living in similar conditions (same country, same birth year). In small countries, a single birth year cohort is insufficiently numerous for statistics, and thus multiple years are often used. Secondly, due to the great ages, accurate records of persons living over 100 years require records dating from the late 19th or early 20th century, when such record-keeping was often not high-quality; further, there is a tendency to exaggerate one's age, which distorts data. Thirdly, granularity is an issue – ideally exact day of birth and death would be used; using only year of birth and death introduces granularity, which adds bias (as discussed below).
Gavrilov & Gavrilova (2011) examined single birth-year cohorts from the United States Death Master File, using the method of extinct generations, and found that the effect disappeared if various distorting factors were removed. Specifically, they conclude that mortality deceleration is negligible up to the age of 106 in the population studied (beyond this point, reliable data were unavailable) and that the Gompertz law is a good fit, with previous observations of deceleration being spurious, with various causes, discussed below.
Given that mortality deceleration in humans had been observed in various studies, but disappeared on the careful analysis (of single-year cohorts in the US) in Gavrilov & Gavrilova (2011), it is natural to ask what causes this discrepancy – why was mortality deceleration observed?
Gavrilov & Gavrilova (2011) propose several causes; notable, in each instance when such a factor is corrected or diminished, the fit with the Gompertz law becomes better.
Data quality:
Technical:
Methodology:[ some of these are different ways of saying the same thing ]
Several causes are proposed for late-life mortality: [1]
Late-life mortality deceleration can be modeled via modifications of the Gompertz law, using various logistic models.
The rates of late-life mortality are important for pensions. For example, the mortality rates in late life (after age 85) are of particular interest for the baby boom generation, which will reach this age starting in 2030, and for pensions funding calculations.
Late-life mortality rates are of basic importance for understanding aging, both for organisms generally and for humans specifically.
Human life expectancy is a statistical measure of the estimate of the average remaining years of life at a given age. The most commonly used measure is life expectancy at birth. This can be defined in two ways. Cohort LEB is the mean length of life of a birth cohort and can be computed only for cohorts born so long ago that all their members have died. Period LEB is the mean length of life of a hypothetical cohort assumed to be exposed, from birth through death, to the mortality rates observed at a given year. National LEB figures reported by national agencies and international organizations for human populations are estimates of period LEB.
Demography is the statistical study of human populations: their size, composition, and how they change through the interplay of fertility (births), mortality (deaths), and migration.
Senescence or biological aging is the gradual deterioration of functional characteristics in living organisms. Whole organism senescence involves an increase in death rates or a decrease in fecundity with increasing age, at least in the later part of an organism's life cycle. However, the resulting effects of senescence can be delayed. The 1934 discovery that calorie restriction can extend lifespans by 50% in rats, the existence of species having negligible senescence, and the existence of potentially immortal organisms such as members of the genus Hydra have motivated research into delaying senescence and thus age-related diseases. Rare human mutations can cause accelerated aging diseases.
Mortality rate, or death rate, is a measure of the number of deaths in a particular population, scaled to the size of that population, per unit of time. Mortality rate is typically expressed in units of deaths per 1,000 individuals per year; thus, a mortality rate of 9.5 in a population of 1,000 would mean 9.5 deaths per year in that entire population, or 0.95% out of the total. It is distinct from "morbidity", which is either the prevalence or incidence of a disease, and also from the incidence rate.
Longevity may refer to especially long-lived members of a population, whereas life expectancy is defined statistically as the average number of years remaining at a given age. For example, a population's life expectancy at birth is the same as the average age at death for all people born in the same year.
Maximum life span is a measure of the maximum amount of time one or more members of a population have been observed to survive between birth and death. The term can also denote an estimate of the maximum amount of time that a member of a given species could survive between birth and death, provided circumstances that are optimal to that member's longevity.
In actuarial science and demography, a life table is a table which shows, for each age, the probability that a person of that age will die before their next birthday. In other words, it represents the survivorship of people from a certain population. They can also be explained as a long-term mathematical way to measure a population's longevity. Tables have been created by demographers including John Graunt, Reed and Merrell, Keyfitz, and Greville.
Longevity claims are unsubstantiated cases of asserted human longevity. Those asserting lifespans of 110 years or more are referred to as supercentenarians. Many have either no official verification or are backed only by partial evidence. Cases where longevity has been fully verified, according to modern standards of longevity research, are reflected in an established list of supercentenarians based on the work of organizations such as the Gerontology Research Group (GRG) or Guinness World Records. This article lists living claims greater than that of the oldest living person whose age has been independently verified, Japanese woman Tomiko Itooka, aged 116 years, 188 days, and deceased claims greater than that of the oldest person ever whose age has been verified, French woman Jeanne Calment, who died aged 122 years and 164 days. The upper limit for both lists is 130 years.
The Gompertz curve or Gompertz function is a type of mathematical model for a time series, named after Benjamin Gompertz (1779–1865). It is a sigmoid function which describes growth as being slowest at the start and end of a given time period. The right-side or future value asymptote of the function is approached much more gradually by the curve than the left-side or lower valued asymptote. This is in contrast to the simple logistic function in which both asymptotes are approached by the curve symmetrically. It is a special case of the generalised logistic function. The function was originally designed to describe human mortality, but since has been modified to be applied in biology, with regard to detailing populations.
Biodemography is a multidisciplinary approach, integrating biological knowledge with demographic research on human longevity and survival. Biodemographic studies are important for understanding the driving forces of the current longevity revolution, forecasting the future of human longevity, and identification of new strategies for further increase in healthy and productive life span.
The reliability theory of aging is an attempt to apply the principles of reliability theory to create a mathematical model of senescence. The theory was published in Russian by Leonid A. Gavrilov and Natalia S. Gavrilova as Biologiia prodolzhitelʹnosti zhizni in 1986, and in English translation as The Biology of Life Span: A Quantitative Approach in 1991.
The compensation law of mortality states that the relative differences in death rates between different populations of the same biological species decrease with age, because the higher initial death rates in disadvantaged populations are compensated by lower pace of mortality increase with age. The age at which this imaginary (extrapolated) convergence of mortality trajectories takes place is named the "species-specific life span". For human beings, this human species-specific life span is close to 95 years.
The Gompertz–Makeham law states that the human death rate is the sum of an age-dependent component, which increases exponentially with age and an age-independent component. In a protected environment where external causes of death are rare, the age-independent mortality component is often negligible. In this case the formula simplifies to a Gompertz law of mortality. In 1825, Benjamin Gompertz proposed an exponential increase in death rates with age.
Advanced maternal age, in a broad sense, is the instance of a woman being of an older age at a stage of reproduction, although there are various definitions of specific age and stage of reproduction. The variability in definitions is in part explained by the effects of increasing age occurring as a continuum rather than as a threshold effect.
Enquiry into the evolution of ageing, or aging, aims to explain why a detrimental process such as ageing would evolve, and why there is so much variability in the lifespans of organisms. The classical theories of evolution suggest that environmental factors, such as predation, accidents, disease, and/or starvation, ensure that most organisms living in natural settings will not live until old age, and so there will be very little pressure to conserve genetic changes that increase longevity. Natural selection will instead strongly favor genes which ensure early maturation and rapid reproduction, and the selection for genetic traits which promote molecular and cellular self-maintenance will decline with age for most organisms.
Following is a list of topics related to life extension:
Biodemography is the science dealing with the integration of biological theory and demography.
The paternal age effect is the statistical relationship between the father's age at conception and biological effects on the child. Such effects can relate to birthweight, congenital disorders, life expectancy and psychological outcomes. A 2017 review found that while severe health effects are associated with higher paternal age, the total increase in problems caused by paternal age is low. Average paternal age at birth reached a low point between 1960 and 1980 in many countries and has been increasing since then, but has not reached historically unprecedented levels. The rise in paternal age is not seen as a major public health concern.
Negligible senescence is a term coined by biogerontologist Caleb Finch to denote organisms that do not exhibit evidence of biological aging (senescence), such as measurable reductions in their reproductive capability, measurable functional decline, or rising death rates with age. There are many species where scientists have seen no increase in mortality after maturity. This may mean that the lifespan of the organism is so long that researchers' subjects have not yet lived up to the time when a measure of the species' longevity can be made. Turtles, for example, were once thought to lack senescence, but more extensive observations have found evidence of decreasing fitness with age.
The mutation accumulation theory of aging was first proposed by Peter Medawar in 1952 as an evolutionary explanation for biological aging and the associated decline in fitness that accompanies it. Medawar used the term 'senescence' to refer to this process. The theory explains that, in the case where harmful mutations are only expressed later in life, when reproduction has ceased and future survival is increasingly unlikely, then these mutations are likely to be unknowingly passed on to future generations. In this situation the force of natural selection will be weak, and so insufficient to consistently eliminate these mutations. Medawar posited that over time these mutations would accumulate due to genetic drift and lead to the evolution of what is now referred to as aging.