Summary: Researchers have found a strong link between stressful life events and deteriorating biological health. Analyzing blood concentrations of four key biomarkers in over 4,900 participants, the study reveals how stress disrupts the immune, nervous, and endocrine systems’ communication, increasing the risk of illnesses like cardiovascular disease and depression.
Chronic stressors like financial strain were particularly detrimental, with those experiencing such stress 59% more likely to be in the high-risk group for health issues. This groundbreaking research underscores the profound impact of stress on our biological systems, regardless of genetic predisposition.
Key Facts:
- Stressful events, including financial strain, significantly disrupt the healthy interaction of the immune, nervous, and endocrine systems.
- Individuals exposed to stress were 61% more likely to be in a high-risk health group, with each additional stressor increasing this likelihood by 19%.
- The study establishes that chronic stress can lead to poor biological health, independent of genetic factors.
Source: UCL
People who experience stressful life events or circumstances are more likely to have worse biological health, as indicated by biomarkers involved in the interaction between our immune, nervous and endocrine systems, according to a new study by UCL researchers.
The study, published in the journal Brain, Behavior and Immunity, found that not only major stressful experiences such as bereavement but chronic challenges such as financial strain were detrimental to the healthy interaction of these systems.
Communication between our immune, nervous, and endocrine systems is necessary to maintain good health. Disruption of these processes is linked to a wide range of mental and physical illnesses, from cardiovascular disease to depression and schizophrenia.
When a threat like stress occurs, signals between the immune, nervous, and endocrine systems are activated and spur physiological and behavioural changes.
In this new study, the researchers analysed blood concentrations of four biomarkers in 4,934 people aged 50 and over who were participants of the English Longitudinal Study of Ageing. Two of these were proteins involved in the innate immune response to inflammation (C-reactive protein and fibrinogen), and two were hormones involved in the physiology of the stress response (cortisol and IGF-1).
The team used a sophisticated statistical technique, latent profile analysis, to identify clusters of biomarker activity. Three groups were identified and labelled as low risk to health, moderate risk, and high risk. The researchers then looked at how earlier exposure to stressful circumstances might affect people’s likelihood of being in the high-risk group.
They found that exposure to stressful circumstances overall, ranging from being an informal carer to experiencing a bereavement or divorce in the last two years, was linked to a 61% increase in likelihood of belonging to the high-risk group four years later.
Separately, the effect was also cumulative, as the likelihood of belonging to the high-risk group increased by 19% for each stressor experienced, for those who experienced more than one stress-inducing circumstance.
People who reported only financial strain – the perception that they may not have enough financial resources to meet their future needs – were 59% more likely, four years later, to belong to the high-risk group.
Lead author, PhD candidate Odessa S. Hamilton (UCL Institute of Epidemiology & Health Care), said: “When the immune and neuroendocrine systems function well together, homeostasis is maintained and health is preserved. But chronic stress can disrupt this biological exchange and lead to disease.
“We found that financial stress was most detrimental to biological health, although more research is needed to establish this for certain. This may be because this form of stress can invade many aspects of our lives, leading to family conflict, social exclusion, and even hunger or homelessness.”
Experiencing stress over a prolonged period of time can disturb the communication between the immune and neuroendocrine systems. That is because our response to stress is similar to our response to sickness, activating some of the same pathways (for instance, both responses trigger the production of immune system signals called pro-inflammatory cytokines).
The researchers also looked at genetic variants previously found to influence our immune-neuroendocrine response and found that the association between stressful life circumstances and belonging to the high-risk group four years later remained true irrespective of genetic predisposition.
Funding: The research was supported by the National Institute on Aging, the UK’s National Institute for Health and Care Research (NIHR), the Economic and Social Research Council (ESRC), the Biotechnology and Biological Sciences Research Council (BBSRC) and UCL.
About this stress and health research news
Author: Mark Greaves
Source: UCL
Contact: Mark Greaves – UCL
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Immune-neuroendocrine patterning and response to stress. A latent profile analysis in the English longitudinal study of ageing” by Odessa S. Hamilton et al. Brain, Behavior and Immunity
Abstract
Immune-neuroendocrine patterning and response to stress. A latent profile analysis in the English longitudinal study of ageing
Psychosocial stress exposure can disturb communication signals between the immune, nervous, and endocrine systems that are intended to maintain homeostasis. This dysregulation can provoke a negative feedback loop between each system that has high pathological risk.
Here, we explore patterns of immune-neuroendocrine activity and the role of stress. Using data from the English Longitudinal Study of Ageing (ELSA), we first identified the latent structure of immune-neuroendocrine activity (indexed by high sensitivity C-reactive protein [CRP], fibrinogen [Fb], hair cortisol [cortisol], and insulin growth-factor-1 [IGF-1]), within a population-based cohort using latent profile analysis (LPA). Then, we determined whether life stress was associated with membership of different immune-neuroendocrine profiles.
We followed 4,934 male and female participants, with a median age of 65 years, over a four-year period (2008–2012). A three-class LPA solution offered the most parsimonious fit to the underlying immune-neuroendocrine structure in the data, with 36 %, 40 %, and 24 % of the population belonging to profiles 1 (low-risk), 2 (moderate-risk), and 3 (high-risk), respectively.
After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, higher exposure to stress was associated with a 61 % greater risk of belonging to the high-risk profile (RRR: 1.61; 95 %CI = 1.23–2.12, p = 0.001), but not the moderate-risk profile (RRR = 1.10, 95 %CI = 0.89–1.35, p = 0.401), as compared with the low-risk profile four years later.
Our findings extend existing knowledge on psychoneuroimmunological processes, by revealing how inflammation and neuroendocrine activity cluster in a representative sample of older adults, and how stress exposure was associated with immune-neuroendocrine responses over time.
