Depression and Cortisol
Learn more about Depression and Cortisol
Depression is one of the most common mental disorders in the United States. It can cause the affected person to suffer greatly and function poorly at work, at school, and in the family. Depression can lead to suicide. Close to 800 000 people die due to suicide every year. Suicide is the second leading cause of death in 15-29-year-olds. Depression is caused by an imbalance of brain chemicals called neurotransmitters. It is more likely to occur due to periods of stress and as people age.
Neurotransmitters are chemicals, which allow the transmission of signals from one nerve cell to another with the purpose of activating a receptor. They are mostly made in the GI tract but have the bulk of their effects on the brain. Neurotransmitters carry signals, which tell our body how to respond to our environment and thoughts. They help modulate our mood, sleep, memory, learning, eating habits, sexual desire, concentration, and emotional well-being. Neurotransmitters can be classified as excitatory or inhibitory. Excitatory neurotransmitters facilitate the firing of other nerves, while inhibitory neurotransmitters inhibit the firing of other nerves.
Serotonin is an inhibitory neurotransmitter. It controls our mood, sleep, appetite, sexual desire, concentration and learning ability. Serotonin plays a role in depression. Decreased serotonin associated with stress has been shown to be associated with depression, anxiety, eating disorders, obsessive-compulsive disorder, suicide, migraine headaches, fibromyalgia, and irritable bowel syndrome. Serotonin is important in thyroid hormone functioning. Low serotonin levels decrease the production of active T3 and T4. When serotonin levels are low, TSH levels are not elevated in individuals with hypothyroidism.
Glutamate is an excitatory neurotransmitter. It is the most common neurotransmitter in the central nervous system. It is crucial for learning and long-term memory.
GABA (Gamma-Aminobutyric Acid), which is made from glutamate, is an inhibitory neurotransmitter. Its primary role is to exert an inhibitory effect on excitatory neurotransmitters, which can cause anxiety. Individuals with too little GABA can develop anxiety disorders.
Acetylcholine plays a role in attention, memory, learning, and REM (rapid eye movement) sleep. It has excitatory and inhibitory effects and acts in the brain and muscles. Acetylcholine stimulates voluntary (skeletal) and involuntary muscles (smooth muscles), e.g. the gastrointestinal system. It is found in sensory neurons and predominates the autonomic parasympathetic nervous system.
Neurotransmitters are important in the stress response and allow us to cope with stress. Unfortunately, with prolonged stress, neurotransmitter imbalances arise, which leads to anxiety, depression, and other psychological disorders.
Everyone suffers from the blues or being anxious at some time in their lives. When we have to take an exam, for example, we may be filled with dread, particularly if we have not studied enough. Even the most cheerful person can have moments of sadness triggered by memories, financial losses, or loss of a loved one. However, even though we refer to these mood changes as anxiety and depression, these normal episodes are quite different from clinical anxiety and depression, which have longer-lasting and more serious symptoms.
Anxiety and depression occur when a person becomes aware that the demands of the environment are greater than his or her capacity to deal with them. When taxing events are too frequent, or prolonged, even a person with excellent coping skills will begin to experience the effects of chronic stress. At this point, stress can become a danger to one’s mental health, and if it is not dealt with, it can destroy one’s sense of well-being. Unfortunately, it appears that stress is actually increasing. In 2008, according to the American Psychological Association, 47% of adults reported a significant increase in stress since 2007.
Cortisol and Depression
Of those individuals who are clinically depressed, about one-half will have an excess of cortisol in their blood. Cortisol is believed to be related to clinical depression since the high levels usually reduce to a normal level once the depression disappears.
When the endocrine system is functioning properly, the hypothalamus monitors the amount of cortisol that is released by the adrenal gland. When cortisol levels rise, the hypothalamus slows down its influence on the pituitary gland by decreasing the production of CRH. Conversely, when cortisol levels drop, the hypothalamus stimulates ACTH production and the release of cortisol. However, in depressed individuals, the hypothalamus may continuously influence the pituitary to produce ACTH without regard for cortisol levels.
Other research concerning cortisol has shown that the timing of the release of this hormone may be problematic in those who are depressed. People who are not depressed tend to have secretions of cortisol at certain times of the day. Normally, cortisol levels are highest at approximately 8:00 a.m. and lowest during the night. This normal cycling of cortisol levels does not occur in some people who are depressed. For instance, they might have a consistently high or low level of cortisol throughout the day or high levels in the middle of the night.
With prolonged stress, cortisol decreases the amino acid tryptophan, which is necessary for serotonin production. Cortisol stimulates an enzyme that destroys tryptophan called tryptophan oxygenase, which leads to a decrease in serotonin production. Serotonin prevents depression and allows one to feel happy. It also has an effect on appetite, sleep, and sexual desire. Most antidepressants block the destruction and re-uptake of serotonin, which temporarily increases serotonin levels.
Elevated cortisol levels associated with prolonged stress decrease the body’s ability to make serotonin, which then initiates feelings of unhappiness. Eventually, the adrenal glands burn out and the production of cortisol declines, leading to worsening of depression. When cortisol declines, the ability to mobilize glucose for energy decreases, as well. This decline leads to fatigue, impaired brain function and further imbalance of neurotransmitters. The lack of cortisol activates the SNS, which leads to more anxiety and an inability to handle stress.
The Link between Depression and Anxiety
Depression and anxiety are two faces of the same problem. Medical statistics confirm that depression and anxiety often occur together; therefore, they are now viewed as being closely connected. Over 70% of patients who suffer from depression also have anxiety. Similarly, more than 50% of people with an anxiety disorder also have some form of depression. Treatments for depression are often effective against anxiety, and vice versa. Both treatments are targeted towards restoring balance to brain neurotransmitters.
Two recent studies with rats showed that injecting rats daily with high levels of cortisol for three weeks caused the rats to become anxious and depressed. The rats became more fearful to explore, less inclined to fight. They tended to give up sooner than non-stressed, depressed rats when put in a tank of water to swim. These studies show that a combination of depressive and anxious behavior is produced directly by high levels of cortisol. Evidence for cortisol being the culprit also comes from human clinical studies. For example, patients with Cushing’s syndrome, whose adrenal glands produce excess cortisol, often have depression and anxiety. In addition, patients who are on high doses of cortisol to treat conditions such as lupus and rheumatoid arthritis can develop depression after prolonged therapy. It is clear that repeated or chronic exposure to stress, rather than short-term stress, puts an individual at risk of developing depression and anxiety.
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