Environment, damage and senescence: modelling the life-history consequences of variable stress and caloric intake
Article first published online: 16 MAY 2008
© 2008 The Author. Journal compilation © 2008 British Ecological Society
Volume 22, Issue 3, pages 422–430, June 2008
How to Cite
Mangel, M. (2008), Environment, damage and senescence: modelling the life-history consequences of variable stress and caloric intake. Functional Ecology, 22: 422–430. doi: 10.1111/j.1365-2435.2008.01410.x
- Issue published online: 16 MAY 2008
- Article first published online: 16 MAY 2008
- Received 7 November 2007; accepted 14 March 2008; Handling Editor: Pat Monaghan
- life-history theory;
- foetal programming;
- metabolic syndrome;
- 1Senescence is intimately connected with physiological state, which is affected by the environment. Two aspects of the environment – stress and caloric intake – are investigated in the context of senescence, particularly in the context of repair of damage caused by endogenous and exogenous stressors.
- 2In a simple life-history model, the organism is characterized by size (affecting reproductive success) and accumulated damage (affecting survival) at age. The modelled organism experiences an imprinting period, at the end of which it estimates the level of food and damaging sources in the environment. From those, an optimal life history is determined, assuming that reproduction is an allometric function of size.
- 3The optimal life history involves a behavioural trait (intensity of foraging) and an allocation process (amount of energy allocated to repair of damage). Subsequent to the imprinting period, the organism lives experiencing levels of stress or caloric intake that differ from those during the imprinting period. The mismatch is such that either the caloric intake is greater post-imprinting than during imprinting or environmental stress is smaller post-imprinting that during imprinting.
- 4Since reproduction is given allometrically and the organism cannot shrink, there is no reproductive senescence. In all cases, mortality increases with age. Senescence is caused by accumulated damage and we focus on the allocation of potential growth to repair and environmental mismatch.
- 5In the case of stress mismatch, the general qualitative result is that both the optimal level of activity and the allocation to repair are greater than their values in the case of no mismatch and they are positively correlated. For caloric mismatch, during the post-imprinting period the intensity of foraging is greater than that predicted if there were no mismatches. However, we predict either a negative correlation between genes characterizing activity and repair (for small mismatch), no correlation (for moderate mismatch) or positive correlation (for large mismatch). Furthermore, caloric mismatch is predicted to lead to a considerable reduction in lifetime reproduction, but stress mismatch is predicted to induce an increase in stress resistance throughout life with little cost to lifetime reproduction.