Consequences of increased longevity for wealth, fertility, and population growth

We present, solve and numerically simulate a simple model that describes the consequences of increased longevity on fertility rates, population growth and the distribution of wealth in developed societies. We look at the consequences of the repeated use of life extension techniques and show that they represent a novel commodity whose introduction will profoundly influence key aspects of economy and society in general. In particular, we uncover two phases within our simplified model, labeled as 'mortal' and 'immortal'. Within the life extension scenario it is possible to have sustainable economic growth in a population of stable size, as a result of dynamical equilibrium between the two phases.Comment: 13 pages, 5 figures, uses elsart.cl

What are the effects of maternal and pre-adult environments on ageing in humans, and are there lessons from animal models?

An open issue in research on ageing is the extent to which responses to the environment during development can influence variability in life span in animals, and the health profile of the elderly in human populations. Both affluence and adversity in human societies have profound impacts on survivorship curves, and some of this effect may be traceable to effects in utero or in infancy. The Barker Hypothesis that links caloric restriction in very early life to disruptions of glucose-insulin metabolism in later life has attracted much attention, as well as some controversy, in medical circles. It is only rarely considered by evolutionary biologists working on phenotypic plasticity, or by biogerontologists studying model organisms such as C. elegans or Drosophila. One crucial mechanism by which animals can respond in an adaptive manner to adverse conditions, for example in nutrition or infection, during development is phenotypic plasticity. Here we begin with a discussion of adaptive plasticity in animals before asking what such phenomena may reveal of relevance to rates of ageing in animals, and in humans. We survey the evidence for effects on adult ageing of environmental conditions during development across mammalian and invertebrate model organisms, and ask whether evolutionary conserved mechanisms might be involved. We conclude that the Barker Hypothesis is poorly supported and argue that more work in human populations should be integrated with multi-disciplinary studies of ageing-related phenomena in experimental populations of different model species that are subjected to nutritional challenges or infections during pre-adult development

Rational Pension Reform

This paper is motivated by the idea to create, wherever possible, rational mechanisms that adapt pension systems automatically to a changed economic and demographic environment, rather than to leave such adaptations to discretionary high-profile pension reforms which all too often stir political opposition. The paper delineates the theory behind such rational mechanisms, shows the advantages and limits of „self-stabilizing“ pension systems, and compares the Swedish and the German approaches to rule-bound pension policy

Industrial energy use and the human life history

The demographic rates of most organisms are supported by the consumption of food energy, which is used to produce new biomass and fuel physiological processes. Unlike other species, modern humans use ‘extra-metabolic' energy sources acquired independent of physiology, which also influence demographics. We ask whether the amount of extra-metabolic energy added to the energy budget affects demographic and life history traits in a predictable way. Currently it is not known how human demographics respond to energy use, and we characterize this response using an allometric approach. All of the human life history traits we examine are significant functions of per capita energy use across industrialized populations. We find a continuum of traits from those that respond strongly to the amount of extra-metabolic energy used, to those that respond with shallow slopes. We also show that the differences in plasticity across traits can drive the net reproductive rate to below-replacement levels

Methodology for the development of a taxonomy and toolkit to evaluate health-related habits and lifestyle (eVITAL)

<p>Abstract</p> <p>Background</p> <p>Chronic diseases cause an ever-increasing percentage of morbidity and mortality, but many have modifiable risk factors. Many behaviors that predispose or protect an individual to chronic disease are interrelated, and therefore are best approached using an integrated model of health and the longevity paradigm, using years lived without disability as the endpoint.</p> <p>Findings</p> <p>This study used a 4-phase mixed qualitative design to create a taxonomy and related online toolkit for the evaluation of health-related habits. Core members of a working group conducted a literature review and created a framing document that defined relevant constructs. This document was revised, first by a working group and then by a series of multidisciplinary expert groups. The working group and expert panels also designed a systematic evaluation of health behaviors and risks, which was computerized and evaluated for feasibility. A demonstration study of the toolkit was performed in 11 healthy volunteers.</p> <p>Discussion</p> <p>In this protocol, we used forms of the community intelligence approach, including frame analysis, feasibility, and demonstration, to develop a clinical taxonomy and an online toolkit with standardized procedures for screening and evaluation of multiple domains of health, with a focus on longevity and the goal of integrating the toolkit into routine clinical practice.</p> <p>Trial Registration</p> <p>IMSERSO registry 200700012672</p

Revisiting mortality deceleration patterns in a gamma-Gompertz-Makeham framework

We calculate life-table aging rates (LARs) for overall mortality by estimating a gamma-Gompertz-Makeham (G GM) model and taking advantage of LAR’s parametric representation by Vaupel and Zhang [34]. For selected HMD countries, we study how the evolution of estimated LAR patterns could explain observed 1) longevity dynamics, and 2) mortality improvement or deterioration at different ages. Surprisingly, the age of mortality deceleration x showed almost no correlation with a number of longevity measures apart from e0. In addition, as mortality concentrates at older ages with time, its characteristic bell-shaped pattern becomes more pronounced. Moreover, in a GGM framework, we identify the impact of senescent mortality on shape of the rate of population aging. We also find evidence for a strong relationship between x and the statistically significant curvilinear changes in the evolution of e0 over time. Finally, model-based LARs appear to be consistent with point b) of the “heterogeneity hypothesis” [12]: mortality deceleration, due to selection effects, should shift to older ages as the level of total adult mortality declines

Metabolic syndrome and risk factors for cardiovascular disease: are nonagenarians protected?

This study assessed cardiovascular disease risk factors in three groups of human subjects aged 20–34 [young, 20 male (M)/33 female (F)], 60–74 (aged, 29M/29F), and > 90 years (nonagenarian, 47M/50F). Components of the metabolic syndrome, cardiovascular disease, and markers of inflammation and oxidative stress were assessed. Nonagenarians weighed less than the two other groups (P < 0.001); however, there was no difference in percent fat among the three groups. Aged individuals had the highest prevalence of the metabolic syndrome (P < 0.001) according to the Adult Treatment Panel III classification. Both fibrinogen and homocysteine concentrations were significantly higher in the nonagenarians compared to younger groups. However, there were no significant differences between groups in fasting insulin, high sensitive C-reactive protein, and plasminogen activator inhibitor 1 concentrations. There were also no relationships between inflammation/ oxidative stress and the metabolic syndrome or cardiovascular disease although nonagenarians appear to be protected from oxidative damage to DNA

Consumer perceptions of co-branding alliances: Organizational dissimilarity signals and brand fit

This study explores how consumers evaluate co-branding alliances between dissimilar partner firms. Customers are well aware that different firms are behind a co-branded product and observe the partner firms’ characteristics. Drawing on signaling theory, we assert that consumers use organizational characteristics as signals in their assessment of brand fit and for their purchasing decisions. Some organizational signals are beyond the control of the co-branding partners or at least they cannot alter them on short notice. We use a quasi-experimental design and test how co-branding partner dissimilarity affects brand fit perception. The results show that co-branding partner dissimilarity in terms of firm size, industry scope, and country-of-origin image negatively affects brand fit perception. Firm age dissimilarity does not exert significant influence. Because brand fit generally fosters a benevolent consumer attitude towards a co-branding alliance, the findings suggest that high partner dissimilarity may reduce overall co-branding alliance performance