Vital rates from the action of mutation accumulation

The Penna model is a model of evolutionary ageing through mutation accumulation where traditionally time and the age of an organism are treated as discrete variables and an organism's genome by a binary bit string. We reformulate the asexual Penna model and show that, a universal scale invariance emerges as we increase the number of discrete genome bits to the limit of a continuum. The continuum model, introduced by Almeida and Thomas in [Int.J.Mod.Phys.C, 11, 1209 (2000)] ca...

Gompertz's law tells us that for humans above the age of 35 the death rate increases exponentially with a doubling time of about 10 years. Here, we show that the same law continues to hold even for ages over 100. Beyond 106 there is so far no statistical evidence available because the number of survivors is too small even in the largest nations. However assuming that Gompertz's law continues to hold beyond 106, we conclude that the mortality rate becomes equal to 1 at age 120...

Aging is thought to be a consequence of intrinsic breakdowns in how genetic information is processed. But mounting experimental evidence suggests that aging can be slowed. To help resolve this mystery, I derive a mortality equation which characterizes the dynamics of an evolving population with a given maximum age. Remarkably, while the spectrum of eigenvalues that govern the evolution depends on the fitness, how they change with the maximum age is independent of fitness. Thi...

Well protected human and laboratory animal populations with abundant resources are evolutionary unprecedented. Physical approach, which takes advantage of their extensively quantified mortality, establishes that its dominant fraction yields the exact law, whose universality from yeast to humans is unprecedented, and suggests its unusual mechanism. Singularities of the law demonstrate new kind of stepwise adaptation. The law proves that universal mortality is an evolutionary b...

What is aging? Mechanistic answers to this question remain elusive despite decades of research. Here, we propose a mathematical model of cellular aging based on a model gene interaction network. Our network model is made of only non-aging components - the biological functions of gene interactions decrease with a constant mortality rate. Death of a cell occurs in the model when an essential gene loses all of its interactions to other genes, equivalent to the deletion of an ess...

We combine the Penna Model for biological aging, which is based on the mutation-accumulation theory, with a sort of antagonistic pleiotropy. We show that depending on how the pleiotropy is introduced, it is possible to reproduce both the humans mortality, which increases exponentially with age, and fruitfly mortality, which decelerates at old ages, allowing the appearance of arbitrarily old Methuselah's.

Demographic data and recent experiments verify earlier predictions that mortality has short (few percent of the life span) memory of the previous life history, may be significantly decreased, reset to its value at a much younger age, and (until certain age) eliminated. Such mortality dynamics is demonstrated to be characteristic only of evolutionary unprecedented protected populations. When conditions improve, their mortality decreases stepwise. At crossovers the rate of decr...

The paper discusses a connection between asymmetric reproduction -- that is reproduction in a parent-child relationship where the parent does not mutate during reproduction --, the fact that all non-viral lifeforms bear genes of their reproduction machinery and how this could relate to evolutionary mechanisms behind aging. In a highly simplified model of the evolution process rules are derived under which aging is an important factor of the adaption in the evolution process a...

We study the dynamics of an age-structured population in which the life expectancy of an offspring may be mutated with respect to that of its parent. When advantageous mutation is favored, the average fitness of the population grows linearly with time $t$, while in the opposite case the average fitness is constant. For no mutational bias, the average fitness grows as t^{2/3}. The average age of the population remains finite in all cases and paradoxically is a decreasing funct...

Widespread population aging has made it critical to understand death rates at old ages. However, studying mortality at old ages is challenging because the data are sparse: numbers of survivors and deaths get smaller and smaller with age. We show how to address this challenge by using principled model selection techniques to empirically evaluate theoretical mortality models. We test nine different theoretical models of old-age death rates by fitting them to 360 high-quality da...