Periodic Reporting for period 1 - STressD (Stressfully Transmitted Diseases: How your partner’s past stress affects your current and future health)
Reporting period: 2017-05-01 to 2019-04-30
Exposure to unpleasant, uncontrollable, and unpredictable events are unavoidable aspects of life that can cause stress. In humans and other animals, chronic activation of an individual’s stress response systems – particularly in early life – can be costly, leading to poorer health and shorter life expectancy. There is also evidence that stress can be socially transmitted between individuals, with recent experimental work in a songbird (zebra finch) showing that the negative health consequences of early-life stress can be transmitted from an individual to their reproductive partner, almost like an infection. Specifically, early-life stress reduced the lifespan of the individual that experienced it as well as the lifespan of their reproductive partner who had not experienced early-life stress themselves. As these birds lived in benign laboratory environments, well-established mortality risk factors such as disease, starvation and predation could not explain why early-life individuals and their partners suffered accelerated ageing and premature death. Despite these findings, previous experimental studies on early-life stress have focused almost entirely on the exposed individuals and overlooked how early-life stress in an individual can affect the health and longevity of other individuals, particularly partners involved in long-term social relationships. Yet we know that social relationships are significant predictors of human mortality regardless of age, sex, and cause of death and one of the most important predictors of human health and well-being (being as strongly associated with health and longevity as smoking, blood pressure, obesity, physical exercise and other well-established health risk factors). Therefore, this project set out to generate novel insights into the largely unexplored question of how lifespan reduction caused by early-life stress is transmitted to other individuals (i.e. reproductive partners), thus shifting the focus of research on early-life stress, social interactions, and health beyond the level of the individual. The objectives of the project have been met, although the data collected during the project are still being analysed.
For the project it was hypothesized that social transmission of detrimental effects of early-life stress on lifespan could occur through different routes simultaneously. As early-life stress increases the activity of a key physiological stress response system (the hypothalamic-pituitary-adrenal, HPA axis), partners of early-life stressed individuals may also increase their HPA axis activity to match their early-life stressed partners to improve coordination of parental care activities between partners and increase reproductive success. The negative effects of early-life stress on lifespan may also be transmitted through ineffective social buffering of the HPA axis, which occurs when the presence of a social partner reduces an individual’s stress response and attenuates the negative effects of prolonged HPA axis activation. Increased HPA axis activation is associated with shortening of telomeres, structures at the ends of chromosomes that protect chromosomes from degradation. This means when telomeres shorten to a critical length it can halt cell division and trigger cell death. Thus, the project sought to obtain information on how early-life stressed individuals affect the behaviour, HPA axis activity, and telomere length of their partner to generate a more comprehensive picture of how early-life stress in one individual could decrease the lifespan of their partner.
The experiments used the zebra finch as a model species, and applied an integrative approach, combining physiological, behavioural, and life-history measures. Early-life stress was manipulated by controlled dosing of glucocorticoid hormones (a product of the HPA axis) to half of the subjects (matched numbers of males and females). After sexual maturity, reproductive pairs were created that had two control subjects, one early-life stressed and one control subject, or two early-life stressed subjects. Physiological samples were collected before and after reproduction to determine the degree to which HPA axis activity and telomere length of individuals and their partners changed. Parental care behaviours (e.g. coordination of parental care) were recorded during reproduction. A social buffering experiment was also carried out, where we observed how partners interacted when one pair member had experienced an acutely stressful event. Measures of HPA axis activity were also taken to determine whether it predicted stress buffering behaviours.
The first set of results are on parental behaviour, and indicate that early-life stress in either parent impaired male coordination but had negligible effects on male parental care effort, whereas early-life stress in one or both parents increased female parental care effort but had insignificant effects on female coordination. Reproductive success, however, was similar across pair types. Data on the change in HPA axis activity and telomere length, and social buffering experiment are currently being analysed.
The experiments used the zebra finch as a model species, and applied an integrative approach, combining physiological, behavioural, and life-history measures. Early-life stress was manipulated by controlled dosing of glucocorticoid hormones (a product of the HPA axis) to half of the subjects (matched numbers of males and females). After sexual maturity, reproductive pairs were created that had two control subjects, one early-life stressed and one control subject, or two early-life stressed subjects. Physiological samples were collected before and after reproduction to determine the degree to which HPA axis activity and telomere length of individuals and their partners changed. Parental care behaviours (e.g. coordination of parental care) were recorded during reproduction. A social buffering experiment was also carried out, where we observed how partners interacted when one pair member had experienced an acutely stressful event. Measures of HPA axis activity were also taken to determine whether it predicted stress buffering behaviours.
The first set of results are on parental behaviour, and indicate that early-life stress in either parent impaired male coordination but had negligible effects on male parental care effort, whereas early-life stress in one or both parents increased female parental care effort but had insignificant effects on female coordination. Reproductive success, however, was similar across pair types. Data on the change in HPA axis activity and telomere length, and social buffering experiment are currently being analysed.
The results of the parental care behaviour add an important dimension to a growing body of evidence on sex-dependent effects of early-life stress by showing that it can influence distinct aspects of male and female parental behaviour in a bi-parental species. The results on potential matching of HPA axis between partners, change in telomere length and effectiveness of stress buffering depending on own and partner’s early-life conditions will be novel and expected to shed light on the mechanisms by which early-life individuals affect their partner’s behaviour and physiology, bring new understanding on the potential trade-offs between health and reproductive success that arise from convergence of physiology during parental care, and provide first insight into how early-life stress may lower an individual’s capacity to buffer others against stress, thereby reducing an individual’s quality as a social partner.