Negative Emotions in Response to Daily Stress Take a Toll on Long-Term Mental Health
Our emotional responses to the stresses of daily life may predict our long-term mental health, according to a new study published in Psychological Science, a journal of the Association for Psychological Science.
Psychological scientist Susan Charles of the University of California, Irvine and colleagues conducted the study in order to answer a long-standing question: Do daily emotional experiences add up to make the straw that breaks the camel’s back, or do these experiences make us stronger and provide an inoculation against later distress?
Using data from two national surveys, the researchers examined the relationship between daily negative emotions and mental health outcomes ten years later.
Participants’ overall levels of negative emotions predicted psychological distress (e.g., feeling worthless, hopeless, nervous, and/or restless) and diagnosis of an emotional disorder like anxiety or depression a full decade after the emotions were initially measured.
Participants’ negative emotional responses to daily stressors — such as argument or a problem at work or home — predicted psychological distress and self-reported emotional disorder ten years later.
The researchers argue that a key strength of the study was their ability to tap a large, national community sample of participants who spanned a wide age range. The results were based on data from 711 participants, both men and women, who ranged in age from 25 to 74. They were all participants in two national, longitudinal survey studies: Midlife Development in the United States (MIDUS) and National Study of Daily Experiences (NSDE).
According to Charles and her colleagues, these findings show that mental health outcomes aren’t only affected by major life events — they also bear the impact of seemingly minor emotional experiences. The study suggests that chronic nature of these negative emotions in response to daily stressors can take a toll on long-term mental health.
In addition to Charles, co-authors on the study include Jennifer Piazza of California State University, Fullerton; and Jacqueline Mogle, Martin Sliwinski, and David Almeida of Pennsylvania State University.
Researchers shine light on how stress circuits learn
Researchers at the University of Calgary’s Hotchkiss Brain Institute have discovered that stress circuits in the brain undergo profound learning early in life. Using a number of cutting edge approaches, including optogenetics, Jaideep Bains, PhD, and colleagues have shown stress circuits are capable of self-tuning following a single stress. These findings demonstrate that the brain uses stress experience during early life to prepare and optimize for subsequent challenges.
The team was able to show the existence of unique time windows following brief stress challenges during which learning is either increased or decreased. By manipulating specific cellular pathways, they uncovered the key players responsible for learning in stress circuits in an animal model. These discoveries culminated in the publication of two back-to-back studies in the April 7 online edition of Nature Neuroscience, one of the world’s top neuroscience journals.
“These new findings demonstrate that systems thought to be ‘hardwired’ in the brain, are in fact flexible, particularly early in life,” says Bains, a professor in the Department of Physiology and Pharmacology. “Using this information, researchers can now ask questions about the precise cellular and molecular links between early life stress and stress vulnerability or resilience later in life.”
Stress vulnerability, or increased sensitivity to stress, has been implicated in numerous health conditions including cardiovascular disease, obesity, diabetes and depression. Although these studies used animal models, similar mechanisms mediate disease progression in humans.
“Our observations provide an important foundation for designing more effective preventative and therapeutic strategies that mitigate the effects of stress and meet society’s health challenges,” he says.
Breakthrough in neuroscience could help re-wire appetite control
Researchers at the University of East Anglia (UEA) have made a discovery in neuroscience that could offer a long-lasting solution to eating disorders such as obesity.
It was previously thought that the nerve cells in the brain associated with appetite regulation were generated entirely during an embryo’s development in the womb and therefore their numbers were fixed for life.
But research published today in the Journal of Neuroscience has identified a population of stem cells capable of generating new appetite-regulating neurons in the brains of young and adult rodents.
Obesity has reached epidemic proportions globally. More than 1.4 billion adults worldwide are overweight and more than half a billion are obese. Associated health problems include type 2 diabetes, heart disease, arthritis and cancer. And at least 2.8 million people die each year as a result of being overweight or obese.
The economic burden on the NHS in the UK is estimated to be more than £5 billion annually. In the US, the healthcare cost tops $60 billion.
Scientists at UEA investigated the hypothalamus section of the brain – which regulates sleep and wake cycles, energy expenditure, appetite, thirst, hormone release and many other critical biological functions. The study looked specifically at the nerve cells that regulate appetite.
The researchers used ‘genetic fate mapping’ techniques to make their discovery – a method that tracks the development of stem cells and cells derived from them, at desired time points during the life of an animal.
They established that a population of brain cells called ‘tanycytes’ behave like stem cells and add new neurons to the appetite-regulating circuitry of the mouse brain after birth and into adulthood.
Lead researcher Dr Mohammad K. Hajihosseini, from UEA’s school of Biological Sciences, said: “Unlike dieting, translation of this discovery could eventually offer a permanent solution for tackling obesity.
Loss or malfunctioning of neurons in the hypothalamus is the prime cause of eating disorders such as obesity.
Until recently we thought that all of these nerve cells were generated during the embryonic period and so the circuitry that controls appetite was fixed.
But this study has shown that the neural circuitry that controls appetite is not fixed in number and could possibly be manipulated numerically to tackle eating disorders.
The next step is to define the group of genes and cellular processes that regulate the behaviour and activity of tanycytes. This information will further our understanding of brain stem cells and could be exploited to develop drugs that can modulate the number or functioning of appetite-regulating neurons.
Our long-term goal of course is to translate this work to humans, which could take up to five or 10 years. It could lead to a permanent intervention in infancy for those predisposed to obesity, or later in life as the disease becomes apparent.”