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

Bois, Alex; García‐Roger, Eduardo M.; Hong, Elim; Hutzler, Stefan; Irannezhad, Ali; Mannioui, Abdelkrim; Richmond, Peter; Roehner, Bertrand M.; Tronche, Stéphane

doi:10.1007/s10867-020-09559-0

Cited by 4 publications

(1 citation statement)

References 25 publications

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“…In fact, deaths due to congenital anomalies are not limited to young age but continue during the whole life. For instance, a congenital defect of heart valves may be of no consequence until the age of 60 or 70 when the defect becomes more serious because the valve's leaflets become stiffer, see [11].…”

Section: The Effects Of Congenital Defects and Of Aging Occur Jointlymentioning

confidence: 99%

A joint explanation of infant and old age mortality

Richmond¹,

Roehner²

2021

Preprint

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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, are higher for organisms which are comprised of 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.

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Section: The Effects Of Congenital Defects and Of Aging Occur Jointlymentioning

confidence: 99%

A joint explanation of infant and old age mortality

Richmond¹,

Roehner²

2021

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

A joint explanation of infant and old age mortality

Richmond

Roehner

2021

J Biol Phys

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Infant mortality across species. A global probe of congenital abnormalities

Bois

García‐Roger

Hong

et al. 2019

Physica A: Statistical Mechanics and its Applications

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Infant mortality, by which we understand the postnatal stage during which mortality is declining, is a manifestation and embodiment of congenital abnormalities. Severe defects will translate into death occurring shortly after birth whereas slighter anomalies may contribute to death much later, possibly only in adult age. While for many species birth defects would be nearly impossible to identify, infant mortality provides a convenient global assessment. In the present paper we examine a broad range of species from mammals to fish to gastropods to insects. One of the objectives of our comparative analysis is to test a conjecture suggested by reliability engineering according to which the frequency of defects tends to increase together with the complexity of organisms. For that purpose, we set up experiments specially designed to measure infant mortality. In particular, we two species commonly used as model species in biological laboratories, namely the zebrafish Danio rerio and the rotifer Brachionus plicatilis. For the second, whose number of cells is about hundred times smaller than for the first, we find as expected that the screening effect of the infant phase is of much smaller amplitude. Our analysis also raises a number of challenging questions for which further investigation is necessary. For instance, why is the infant death rate of beetles and molluscs falling off exponentially rather than as a power law as observed for most other species? A possible research agenda is discussed in the conclusion of the paper. Main observations and questions Agenda for future comparative research Appendix A: Previous studies of the mortality of rotifers Main features Comments about variability What conclusions can one draw with respect to infant mortality? Appendix B: Methodology of the rotifer experiment Procedures Operational definition of death Appendix C: Correct estimate of the initial death rateThis paper is the second leg of an exploration in three parts; the two others are Bois et al. (2019a,b). Despite the connections, the three papers can be read independently from each other.

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

Cited by 4 publications

References 25 publications

A joint explanation of infant and old age mortality

A joint explanation of infant and old age mortality

A joint explanation of infant and old age mortality

Infant mortality across species. A global probe of congenital abnormalities

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