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Image by Renate Vanaga

Stressfully Transmitted Diseases

How your partner's past affects your current and future health

Background

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 (the 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).

Research Objectives

This project sets 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).

Hypotheses

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.

Methods & Approach

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 glucocorticoid levels 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 (glucocorticoid levels) were also taken to determine whether it predicted stress buffering behaviours.

Results

Data are currently being analysed. Please keep checking back for updates!

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