oons with social support, even if they weren’t at the top of the hierarchy, had lower levels of harmful stress hormones. The baboons that could count on other baboons to help them out in a fight, groom them and let them hold the baby, had less harmful stress hormones, even if they weren’t the alpha baboon. He also identified personality traits associated with low stress, even in the low ranking baboon. Certain baboons seemed to be unable to differentiate what was a danger and what was a non-threat in the environment. The “don’t sweat the small stuff” baboons thrived compared to their hyper-anxious buddies.
Like his baboon studies, many human studies have shown that a sense of loss of control in our lives is extremely stressful and children who live with constant violence and fear, suffer from the post-traumatic stress disorder. People who feel they can’t control their lives, who worry about the mortgage, the evil boss at work, or even the state of world events, run the risk of having stress hormones that are surging and impacting their immune systems in diseases that show up much later.
It takes a great deal of focus and attention to reduce stress and quit worrying.
Just saying “quit stressing out” or “relax” might even cause more stress.
We humans probably need more sleep, more time gazing out the window or watching rainfall, less time reading the news, less time watching TV or surfing the net, more classical music, more leisurely meals with large groups of friends and family, less shopping and errands, more realistic goals for our lives and more time grooming each other. Definitely more time grooming each other.
Mice With Depression-like Behaviors Reveal Possible Source Of Human Depression
Mice missing a specific protein from their brains react to stress differently. The genetically engineered mice develop an imbalance in a hormone involved in stress responses, and during stressful situations, they behave as if they are depressed. Genetic variations in the same protein may be a significant cause of human depression, according to researchers at Washington University School of Medicine in St. Louis.
Their report will be published in the Proceedings of the National Academy of Sciences, appearing on-line at the journal’s website during the week of Dec. 27 to 31, 2004, and in an upcoming print issue.
“A major obstacle to understanding depression has been finding what triggers its onset,” says Maureen Boyle, predoctoral fellow and first author of the report. “We felt it was important to look at elements that regulate the body’s stress system.”
In response to stress, the brain signals the adrenal gland to release hormones, including glucocorticoid, a hormone that preserves physiological equilibrium in many organs. Because proper levels of glucocorticoid are important for normal function, the brain closely monitors and regulates the hormone.
People with major depressive disorder release excessive amounts of adrenal hormones, including glucocorticoids, possibly because of their brains sense stress differently, according to the researchers.
“We wanted to find out if depression stems directly from the inability to sense glucocorticoid in the brain,” says senior author Louis Muglia, Ph.D., associate professor of pediatrics, of molecular biology and pharmacology, and of obstetrics and gynecology. “To test this, we developed an animal model that would tell us if changes in glucocorticoid receptor function could impart the animal equivalent of depression.”
The researchers engineered mice that lose glucocorticoid receptors from their forebrains, specifically from the cortex and hippocampus, beginning at about three weeks of age and continuing until they reach a 95 percent loss at six months. The team felt the gradual loss could simulate the time course typical for the human development of depression, which commonly begins in late adolescence.
During several stress-related tests, four- and six-month-old engineered mice showed an increase in behaviors suggestive of depression. The receptor-deficient mice also showed less interest in ple