Posts tagged stress hormones
Articles and news from the latest research reports.
Boost your Immune System and Shake Off Stress by Taking a Walk in the Woods
Work, home, even in the car, stress is a constant struggle for many people. But it’s more than just exhausting and annoying. Unmanaged stress can lead to serious health conditions such as high blood pressure, heart disease, obesity and diabetes.
“The American lifestyle is fast-paced and productive, but it can be extremely stressful. If that stress is not addressed, our bodies and minds can suffer,” said Dr. Aaron Michelfelder, professor of Family Medicine at Loyola University Chicago Stritch School of Medicine.
Our bodies need sleep to rejuvenate and if we are uptight and stressed we aren’t able to get the rest we need. This can lead to serious physical and mental health issues, which is why it’s extremely important to wind down, both body and mind, after a stressful day.
According to Michelfelder, one of best ways to unwind and reconnect after a stressful day is by taking a walk. Though any walking is good, walking in the woods or in nature has been proven to be even better at reducing stress and improving your health.
“When we get to nature, our health improves,” Michelfelder said. “Our stress hormones rise all day long in our bloodstream and taking even a few moments while walking to reconnect with our inner thoughts and to check in with our body will lower those damaging stress hormones. Walking with our family or friends is also a great way to lower our blood pressure and make us happier.”
Research out of Japan shows that walking in the woods also may play a role in fighting cancer. Plants emit a chemical called phytoncides that protects them from rotting and insects. When people breathe it in, there is an increase in the number of “natural killer” cells , which are part of a person’s immune response to cancer.
“When we walk in a forest or park, our levels of white blood cells increase and it also lowers our pulse rate, blood pressure and level of the stress hormone cortisol,” Michelfelder said.
He also suggests reading, writing, meditating or reflecting to help calm the mind after long day. To help calm the body yoga and breathing exercises also are good.
“If you want to wind down, stay away from electronic screens as they activate the mind. Electronic devices stimulate brain activity and someone’s post on Facebook or a story on the evening news might cause more stress,” Michelfeder said.
How parents see themselves may affect their child’s brain and stress level
Self-perceived social status predicts hippocampal function and stress hormones
A mother’s perceived social status predicts her child’s brain development and stress indicators, finds a study at Boston Children’s Hospital. While previous studies going back to the 1950s have linked objective socioeconomic factors — such as parental income or education — to child health, achievement and brain function, the new study is the first to link brain function to maternal self-perception.
In the study, children whose mothers saw themselves as having a low social status were more likely to have increased cortisol levels, an indicator of stress, and less activation of their hippocampus, a structure in the brain responsible for long-term memory formation (required for learning) and reducing stress responses.
Findings were published online August 6th by the journal Developmental Science, and will be part of a special issue devoted to the effects of socioeconomic status on brain development.
"We know that there are big disparities among people in income and education," says Margaret Sheridan, PhD, of the Labs of Cognitive Neuroscience at Boston Children’s Hospital, the study’s first author. "Our results indicate that a mother’s perception of her social status ‘lives’ biologically in her children."
Sheridan, senior investigator Charles Nelson, PhD, of Boston Children’s Hospital and colleagues studied 38 children aged 8.3 to 11.8 years. The children gave saliva samples to measure levels of cortisol, and 19 also underwent functional MRI of the brain, focusing on the hippocampus.
Mothers, meanwhile, rated their social standing on a ladder on a scale of 1 to 10, comparing themselves with others in the United States. Findings were as follows:
- After controlling for gender and age, the mother’s self-perceived social status was a significant predictor of cortisol levels in the child. This finding is consistent with studies in animals. “In animal research, your stress response is related to your relative standing in the hierarchy,” Sheridan says.
- Similarly, the mother’s perceived social status significantly predicted the degree of hippocampal activation in their children during a learning task.
- In contrast, actual maternal education or income-to-needs ratio (income relative to family size) did not significantly predict cortisol levels or hippocampal activation.
The findings suggest that while actual socioeconomic status varies, how people perceive and adapt to their situation is an important factor in child development. Some of this may be culturally determined, Sheridan notes. She is currently participating in a much larger international study of childhood poverty, the Young Lives Project, that is looking at objective and subjective measures of social status along with health measures and cognitive function. The study will capture much wider extremes of socioeconomic status than would a U.S.-based study.
What the current study didn’t find was evidence that stress itself alters hippocampal function; no relationship was found between cortisol and hippocampal function, as has been seen in animals, perhaps because of the small number children having brain fMRIs. “This needs further exploration,” says Sheridan. “There may be more than one pathway leading to differences in long-term memory, or there may be an effect of stress on the hippocampus that comes out only in adulthood.”
(Source: eurekalert.org)
Stress Hormone Could Trigger Mechanism for the Onset of Alzheimer’s
A chemical hormone released in the body as a reaction to stress could be a key trigger of the mechanism for the late onset of Alzheimer’s disease, according to a study by researchers at Temple University.
Previous studies have shown that the chemical hormone corticosteroid, which is released into the body’s blood as a stress response, is found at levels two to three times higher in Alzheimer’s patients than non-Alzheimer’s patients.
“Stress is an environmental factor that looks like it may play a very important role in the onset of Alzheimer’s disease,” said Domenico Praticò, professor of pharmacology and microbiology and immunology in Temple’s School of Medicine, who led the study. “When the levels of corticosteroid are too high for too long, they can damage or cause the death of neuronal cells, which are very important for learning and memory.”
In their study, “Knockout of 5-lipoxygenase prevents dexamethasone-induced tau pathology in 3xTg mice,” published in the journal Aging Cell, the Temple researchers set up a series of experiments to examine the mechanisms by which stress can be responsible for the Alzheimer’s pathology in the brain.
Using triple transgenic mice, which develop amyloid beta and the tau protein, two major brain lesion signatures for Alzheimer’s, the Temple researchers injected one group with high levels of corticosteroid each day for a week in order to mimic stress.
While they found no significant difference in the mice’s memory ability at the end of the week, they did find that the tau protein was significantly increased in the group that received the corticosteroid. In addition, they found that the synapses, which allow neuronal cells to communicate and play a key role in learning and memory, were either damaged or destroyed.
“This was surprising because we didn’t see any significant memory impairment, but the pathology for memory and learning impairment was definitely visible,” said Pratico. “So we believe we have identified the earliest type of damage that precedes memory deficit in Alzheimer’s patients.”
Pratico said another surprising outcome was that a third group of mice that were genetically altered to be devoid of the brain enzyme 5-lipoxygenase appeared to be immune and showed no neuronal damage from the corticosteroid.
In previous studies, Pratico and his team have shown that elevated levels of 5-lipoxygenase cause an increase in tau protein levels in regions of the brain controlling memory and cognition, disrupting neuronal communications and contributing to Alzheimer’s disease. It also increases the levels of amyloid beta, which is thought to be the cause for neuronal death and forms plaques in the brain.
Pratico said the corticosteroid causes the 5-lipoxygenase to over-express and increase its levels, which in turn increases the levels of the tau protein and amyloid beta.
“The question has always been what up-regulates or increases 5-lipoxygenase, and now we have evidence that it is the stress hormone,” he said. “We have identified a mechanism by which the risk factor — having high levels of corticosteroid — could put you at risk for the disease.
“Corticosteroid uses the 5-lipoxygenase as a mechanism to damage the synapse, which results in memory and learning impairment, both key symptoms for Alzheimer’s,” said Pratico. “So that is strong support for the hypothesis that if you block 5-lipoxygenase, you can probably block the negative effects of corticosteroid in the brain.”
(Source: newswise.com)
Effects of stress on brain cells offer clues to new anti-depressant drugs
Research from King’s College London reveals the detailed mechanism behind how stress hormones reduce the number of new brain cells - a process considered to be linked to depression.
The researchers identified a key protein responsible for the long-term detrimental effect of stress on cells, and importantly, successfully used a drug compound to block this effect, offering a potential new avenue for drug discovery.
The study, published in Proceedings of the National Academy of Sciences (PNAS) was co-funded by the National Institute for Health Research Biomedical Research Centre (NIHR BRC) for Mental Health at the South London and Maudsley NHS Foundation Trust and King’s College London.
Depression affects approximately 1 in 5 people in the UK at some point in their lives. The World Health Organisation estimate that by 2030, depression will be the leading cause of the global burden of disease. Treatment for depression involves either medication or talking therapy, or usually a combination of both. Current antidepressant medication is successful in treating depression in about 50-65% of cases, highlighting the need for new, more effective treatments.
Depression and successful antidepressant treatment are associated with changes in a process called “neurogenesis”- the ability of the adult brain to continue to produce new brain cells. At a molecular level, stress is known to increase levels of cortisol (a stress hormone) which in turn acts on a receptor called the glucocorticoid receptor (GR). However, the exact mechanism explaining how the GR decreases neurogenesis in the brain has remained unclear.
Professor Carmine Pariante, from King’s College London’s Institute of Psychiatry and lead author of the paper, says: “With as much as half of all depressed patients failing to improve with currently available medications, developing new, more effective antidepressants is an important priority. In order to do this, we need to understand the abnormal mechanisms that we can target. Our study shows the importance of conducting research on cellular models, animal models and clinical samples, all under one roof in order to better facilitate the translation of laboratory findings to patient benefit.”
In this study, the multidisciplinary team of researchers studied cellular and animal models before confirming their findings in human blood samples. First, the researchers studied human hippocampal stem cells, which are the source of new cells in the human brain. They gave the cells cortisol to measure the effect on neurogenesis and found that a protein called SGK1 was important in mediating the effects of stress hormones on neurogenesis and on the activity of the GR.
By measuring the effect of cortisol over time, they found that increased levels of SGK1 prolong the detrimental effects of stress hormones on neurogenesis. Specifically, SGK1 enhances and maintains the long-term effect of stress hormones, by keeping the GR active even after cortisol had been washed out of the cells.
Next, the researchers used a pharmacological compound (GSK650394) known to inhibit SGK1, and found they were able to block the detrimental effects of stress hormones and ultimately increase the number of new brain cells.
Finally, the research team were able to confirm these findings by studying levels of SGK1 in animal models and human blood samples of 25 drug-free depressed patients.
Dr Christoph Anacker, from King’s College London’s Institute of Psychiatry and first author of the paper, says: “Because a reduction of neurogenesis is considered part of the process leading to depression, targeting the molecular pathways that regulate this process may be a promising therapeutic strategy. This novel mechanism may be particularly important for the effects of chronic stress on mood, and ultimately depressive symptoms. Pharmacological interventions aimed at reducing the levels of SGK1 in depressed patients may therefore be a potential strategy for future antidepressant treatments.”
(Source: kcl.ac.uk)
Researchers find out why some stress is good for you
Overworked and stressed out? Look on the bright side. Some stress is good for you.
“You always think about stress as a really bad thing, but it’s not,” said Daniela Kaufer, associate professor of integrative biology at the University of California, Berkeley. “Some amounts of stress are good to push you just to the level of optimal alertness, behavioral and cognitive performance.”
New research by Kaufer and UC Berkeley post-doctoral fellow Elizabeth Kirby has uncovered exactly how acute stress – short-lived, not chronic – primes the brain for improved performance.
In studies on rats, they found that significant, but brief stressful events caused stem cells in their brains to proliferate into new nerve cells that, when mature two weeks later, improved the rats’ mental performance.
“I think intermittent stressful events are probably what keeps the brain more alert, and you perform better when you are alert,” she said.
Kaufer, Kirby and their colleagues in UC Berkeley’s Helen Wills Neuroscience Institute describe their results in a paper published April 16 in the new open access online journal eLife.
The UC Berkeley researchers’ findings, “in general, reinforce the notion that stress hormones help an animal adapt – after all, remembering the place where something stressful happened is beneficial to deal with future situations in the same place,” said Bruce McEwen, head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology at The Rockefeller University, who was not involved in the study.
Kaufer is especially interested in how both acute and chronic stress affect memory, and since the brain’s hippocampus is critical to memory, she and her colleagues focused on the effects of stress on neural stem cells in the hippocampus of the adult rat brain. Neural stem cells are a sort of generic or progenitor brain cell that, depending on chemical triggers, can mature into neurons, astrocytes or other cells in the brain. The dentate gyrus of the hippocampus is one of only two areas in the brain that generate new brain cells in adults, and is highly sensitive to glucocorticoid stress hormones, Kaufer said.
Much research has demonstrated that chronic stress elevates levels of glucocorticoid stress hormones, which suppresses the production of new neurons in the hippocampus, impairing memory. This is in addition to the effect that chronically elevated levels of stress hormones have on the entire body, such as increasing the risk of chronic obesity, heart disease and depression.
Less is known about the effects of acute stress, Kaufer said, and studies have been conflicting.
To clear up the confusion, Kirby subjected rats to what, to them, is acute but short-lived stress – immobilization in their cages for a few hours. This led to stress hormone (corticosterone) levels as high as those from chronic stress, though for only a few hours. The stress doubled the proliferation of new brain cells in the hippocampus, specifically in the dorsal dentate gyrus.
Kirby discovered that the stressed rats performed better on a memory test two weeks after the stressful event, but not two days after the event. Using special cell labeling techniques, the researchers established that the new nerve cells triggered by the acute stress were the same ones involved in learning new tasks two weeks later.
“In terms of survival, the nerve cell proliferation doesn’t help you immediately after the stress, because it takes time for the cells to become mature, functioning neurons,” Kaufer said. “But in the natural environment, where acute stress happens on a regular basis, it will keep the animal more alert, more attuned to the environment and to what actually is a threat or not a threat.”
They also found that nerve cell proliferation after acute stress was triggered by the release of a protein, fibroblast growth factor 2 (FGF2), by astrocytes — brain cells formerly thought of as support cells, but that now appear to play a more critical role in regulating neurons.
“The FGF2 involvement is interesting, because FGF2 deficiency is associated with depressive-like behaviors in animals and is linked to depression in humans,” McEwen said.
Kaufer noted that exposure to acute, intense stress can sometimes be harmful, leading, for example, to post-traumatic stress disorder. Further research could help to identify the factors that determine whether a response to stress is good or bad.
“I think the ultimate message is an optimistic one,” she concluded. “Stress can be something that makes you better, but it is a question of how much, how long and how you interpret or perceive it.”
Foetal exposure to excessive stress hormones in the womb linked to adult mood disorders
Exposure of the developing foetus to excessive levels of stress hormones in the womb can cause mood disorders in later life and now, for the first time, researchers have found a mechanism that may underpin this process, according to research presented today (Sunday) at the British Neuroscience Association Festival of Neuroscience (BNA2013) in London.
The concept of foetal programming of adult disease, whereby the environment experienced in the womb can have profound long-lasting consequences on health and risk of disease in later life, is well known; however, the process that drives this is unclear. Professor Megan Holmes, a neuroendocrinologist from the University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science in Scotland (UK), will say: “During our research we have identified the enzyme 11ß-HSD2 which we believe plays a key role in the process of foetal programming.”
Adverse environments experienced while in the womb, such as in cases of stress, bereavement or abuse, will increase levels of glucocorticoids in the mother, which may harm the growing baby. Glucocorticoids are naturally produced hormones and they are also known as stress hormones because of their role in the stress response.
“The stress hormone cortisol may be a key factor in programming the foetus, baby or child to be at risk of disease in later life. Cortisol causes reduced growth and modifies the timing of tissue development as well as having long lasting effects on gene expression,” she will say.
Prof Holmes will describe how her research has identified an enzyme called 11ß-HSD2 (11beta-hydroxysteroid dehydrogenase type 2) that breaks down the stress hormone cortisol to an inactive form, before it can cause any harm to the developing foetus. The enzyme 11ß-HSD2 is present in the placenta and the developing foetal brain where it is thought to act as a shield to protect against the harmful actions of cortisol.
Prof Holmes and her colleagues developed genetically modified mice that lacked 11ß-HSD2 in order to determine the role of the enzyme in the placenta and foetal brain. “In mice lacking the enzyme 11ß-HSD2, foetuses were exposed to high levels of stress hormones and, as a consequence, these mice exhibited reduced foetal growth and went on to show programmed mood disorders in later life. We also found that the placentas from these mice were smaller and did not transport nutrients efficiently across to the developing foetus. This too could contribute to the harmful consequences of increased stress hormone exposure on the foetus and suggests that the placental 11ß-HSD2 shield is the most important barrier.
“However, preliminary new data show that with the loss of the 11ß-HSD2 protective barrier solely in the brain, programming of the developing foetus still occurs, and, therefore, this raises questions about how dominant a role is played by the placental 11ß-HSD2 barrier. This research is currently ongoing and we cannot draw any firm conclusions yet.
“Determining the exact molecular and cellular mechanisms that drive foetal programming will help us identify potential therapeutic targets that can be used to reverse the deleterious consequences on mood disorders. In the future, we hope to explore the potential of these targets in studies in humans,” she will say.
Prof Holmes hopes that her research will make healthcare workers more aware of the fact that children exposed to an adverse environment, be it abuse, malnutrition, or bereavement, are at an increased risk of mood disorders in later life and the children should be carefully monitored and supported to prevent this from happening.
In addition, the potential effects of excessive levels of stress hormones on the developing foetus are also of relevance to individuals involved in antenatal care. Within the past 20 years, the majority of women at risk of premature delivery have been given synthetic glucocorticoids to accelerate foetal lung development to allow the premature babies to survive early birth.
“While this glucocorticoid treatment is essential, the dose, number of treatments and the drug used, have to be carefully monitored to ensure that the minimum effective therapy is used, as it may set the stage for effects later in the child’s life,” Prof Holmes will say.
Puberty is another sensitive time of development and stress experienced at this time can also be involved in programming adult mood disorders. Prof Holmes and her colleagues have found evidence from imaging studies in rats that stress in early teenage years could affect mood and emotional behaviour via changes in the brain’s neural networks associated with emotional processing.
The researchers used fMRI (Functional Magnetic Resonance Imaging) to see which pathways in the brain were affected when stressed, peripubertal rats responded to a specific learned task.
Prof Holmes will say: “We showed that in stressed ‘teenage’ rats, the part of the brain region involved in emotion and fear (known as amygdala) was activated in an exaggerated fashion when compared to controls. The results from this study clearly showed that altered emotional processing occurs in the amygdala in response to stress during this crucial period of development.”
(Image: iStockphoto)
Stressed-Out Tadpoles Grow Larger Tails to Escape Predators
When people or animals are thrust into threatening situations such as combat or attack by a predator, stress hormones are released to help prepare the organism to defend itself or to rapidly escape from danger—the so-called fight-or-flight response.
Now University of Michigan researchers have demonstrated for the first time that stress hormones are also responsible for altering the body shape of developing animals, in this case the humble tadpole, so they are better equipped to survive predator attacks.
Through a series of experiments conducted at field sites and in the laboratory, U-M researchers demonstrated that prolonged exposure to a stress hormone enabled tadpoles to increase the size of their tails, which improved their ability to avoid lethal predator attacks.
"This is the first clear demonstration that a stress hormone produced by the animal can actually cause a morphological change, a change in body shape, that improves their survival in the presence of lethal predators. It’s a survival response," said Robert Denver, a professor of molecular, cellular and developmental biology and of ecology and evolutionary biology.
The team’s surprising findings are detailed in a paper to be published online March 5 in the journal Proceedings of the Royal Society B. First author of the paper is Jessica Middlemis Maher, a former U-M doctoral student, now at Michigan State University, who conducted the work for her dissertation.
Scientists have long known that environmental changes can prompt animals and plants to alter their morphology and physiology, as well as the timing of developmental events. For example, tadpoles can accelerate metamorphosis into frogs in response to a drying pond, a high density of predators or a lack of food.
The term “phenotypic plasticity” is used to describe modifications by animals and plants in response to a changing environment.
"There’s been a lot of interest in phenotypic plasticity among developmental biologists and evolutionary ecologists for more than 70 years, but there’s been relatively little focus on the mechanisms by which the environmental signal is translated into a functional response," Denver said.
"We’ve known, for example, that tadpoles can change their body shape in response to predation risk. But until now, nobody knew the basic physiological mechanisms mediating that response. That’s what’s novel about this study."
(Image: Wikimedia Commons)
Early stress may sensitize girls’ brains for later anxiety
High levels of family stress in infancy are linked to differences in everyday brain function and anxiety in teenage girls, according to new results of a long-running population study by University of Wisconsin-Madison scientists.
The study highlights evidence for a developmental pathway through which early life stress may drive these changes. Here, babies who lived in homes with stressed mothers were more likely to grow into preschoolers with higher levels of cortisol, a stress hormone. In addition, these girls with higher cortisol also showed less communication between brain areas associated with emotion regulation 14 years later. Last, both high cortisol and differences in brain activity predicted higher levels of adolescent anxiety at age 18.
The young men in the study did not show any of these patterns.
"We wanted to understand how stress early in life impacts patterns of brain development which might lead to anxiety and depression,” says first author Dr. Cory Burghy of the Waisman Laboratory for Brain Imaging and Behavior. "Young girls who, as preschoolers, had heightened cortisol levels, go on to show lower brain connectivity in important neural pathways for emotion regulation — and that predicts symptoms of anxiety during adolescence."
To test this, scans designed by Dr. Rasmus Birn, assistant professor of psychiatry in the UW School of Medicine and Public Health, showed that teenage girls whose mothers reported high levels of family stress when the girls were babies show reduced connections between the amygdala or threat center of the brain and the ventromedial prefrontal cortex, a part of the brain responsible for emotional regulation. Birn used a method called resting-state functional connectivity (fcMRI), which looks at the brain connections while the brain is at a resting state.
The study was published in Nature Neuroscience.