On the Mortality of Companies.

Using data from both the US and UK we examine the survival and mortality of companies in both the early stage or start-up and mature phases. The shape of the mortality curve is broadly similar to that of humans. Even small single cellular organisms such as rotifers have a similar shape. The mortality falls in the early stages in a hyperbolic manner until around 20-30 years when it begins to rise broadly according to the Gompertz exponential law. To explain in simple terms these features we adapt the MinMax model introduced by the authors elsewhere to explain the shape of the human mortality curve.

A joint explanation of infant and old age mortality.

Infant deaths and old age deaths are very different. The former are mostly due to severe congenital malformations of one or a small number of specific organs. On the contrary, old age deaths are largely the outcome of a long process of deterioration which starts in the 20s and affects almost all organs. In terms of age-specific death rates, there is also a clear distinction: the infant death rate falls off with age, whereas the adult and old age death rate increases exponentially with age in conformity with Gompertz's law. An additional difference is that whereas aging and old age death have been extensively studied, infant death received much less attention. To our knowledge, the two effects have never been inter-connected. Clearly, it would be satisfactory to explain the two phenomena as being two variants within the same explanatory framework. In other words, a mechanism providing a combined explanation for the two forms of mortality would be welcome. This is the purpose of the present paper. We show here that the same biological effects can account for the two cases provided there is a difference in their severity: death triggered by isolated lethal anomalies in one case and widespread wear-out anomalies in the second. We show that quite generally this mechanism leads indeed, respectively, to a declining and an upgoing death rate. Moreover, this theoretical framework leads to the conjecture that the severity of the death effects, whether in infancy or old age, is higher for organisms which comprised a larger number of organs. Finally, let us observe that the main focus of the paper is the drastic difference of the age-specific death rates (i.e., decreasing versus increasing) because this difference is found in many species, whereas the question of the best fit (e.g., Gompertz versus Weibull) is rather specific to human mortality.

Magnitude and significance of the peak of early embryonic mortality.

Embryonic development is of great importance because it determines congenital anomalies and influences their severity. However, little is known about the actual probabilities of success or failure and about the nature of early embryonic defects. Here, we propose that the analysis of embryonic mortality as a function of post-fertilization time provides a simple way to identify major defects. By reviewing the literature, we show that even small initial defects, e.g., spatial cellular asymmetries or irregularities in the timing of development, carry with them lethal effects in subsequent stages of embryogenesis. Although initially motivated by human study, in this contribution, we review the few embryonic mortality data available for farm animals and highlight zebrafish as a particularly suited organism for such a kind of study because embryogenesis can be followed from its very beginning and observed easily thanks to eggshell transparency. In line with the few other farm animals for which data are available, we provide empirical evidence that embryonic mortality in zebrafish has a prominent peak shortly after fertilization. Indeed, we show how subsequent mortality rates decay according to a power law, supporting the role of the early embryonic mortality peak as a screening process rapidly removing defective embryos.

Physical models of infant mortality: implications for defects in biological systems.

Reliability engineering concerned with failure of technical inanimate systems usually uses the vocabulary and notions of human mortality, e.g., infant mortality vs. senescence mortality. Yet, few data are available to support such a parallel description. Here, we focus on early-stage (infant) mortality for two inanimate systems, incandescent light bulbs and soap films, and show the parallel description is clearly valid. Theoretical considerations of the thermo-electrical properties of electrical conductors allow us to link bulb failure to inherent mechanical defects. We then demonstrate the converse, that is, knowing the failure rate for an ensemble of light bulbs, it is possible to deduce the distribution of defects in wire thickness in the ensemble. Using measurements of lifetimes for soap films, we show how this methodology links failure rate to geometry of the system; in the case presented, this is the length of the tube containing the films. In a similar manner, for a third example, the time-dependent death rate due to congenital aortic valve stenosis is related to the distribution of degrees of severity of this condition, as a function of time. The results not only validate clearly the parallel description noted above, but also point firmly to application of the methodology to humans, with the consequent ability to gain more insight into the role of abnormalities in infant mortality.

Coupling between death spikes and birth troughs. Part 1: Evidence.

In the wake of the influenza pandemic of 1889-1890 Jacques Bertillon, a pioneer of medical statistics, noticed that after the massive death spike there was a dip in birth numbers around 9 months later which was significantly larger than that which could be explained by the population change as a result of excess deaths. In addition it can be noticed that this dip was followed by a birth rebound a few months later. However having made this observation, Bertillon did not explore it further. Since that time the phenomenon was not revisited in spite of the fact that in the meanwhile there have been several new cases of massive death spikes. The aim here is to analyze these new cases to get a better understanding of this death-birth coupling phenomenon. The largest death spikes occurred in the wake of more recent influenza pandemics in 1918 and 1920, others were triggered by the 1923 earthquakes in Tokyo and the Twin Tower attack on September 11, 2001. We shall see that the first of these events indeed produced an extra dip in births whereas the 9/11 event did not. This disparity highlights the pivotal role of collateral sufferers. In the last section it is shown how the present coupling leads to predictions; it can explain in a unified way effects which so far have been studied separately, as for instance the impact on birth rates of heat waves. Thus, it appears that behind the apparent randomness of birth rate fluctuations there are in fact hidden explanatory factors.