Are You Anxious or Sad? If So, Probably Both
Between the top two most common mental illnesses in the US are anxiety and mood disorders, which includes depression. Often a depressed person will suffer from anxiety, but more often still an anxious person suffers from depression. However, anxiety and depression, while intricately entwined, are not one and the same. This paper aims to explore each and the relationship between the two mental disorders.
Depression is not merely a case of the blues. It is natural to feel sad sometimes. Problems arise when these sad feelings persist for weeks. Telltale signs of depression are lack of or excessive sleep, weight gain or loss, fatigue, physical pain, difficulty concentrating, decreased interest in things once found pleasurable, agitation, and suicidal idealizations. These symptoms must endure for at least two weeks for a diagnosis of clinical depression (1). There are different types of depression. Neurotic depression is characterized by anxious behavior and is generally a reaction to environmental conditions. Psychotic depression is shown by hallucinations and delusions (2). It can be difficult to tell the difference between clinical depression and a depressed mood, and even more difficult to draw the line to determine where one becomes the other.
The genetic origins of depression are still unknown. Representatives from the National Institute of Mental Health said, “We have not identified the genetic and neurobiological mechanisms underlying depression and mania, nor do we understand the mechanisms by which nongenetic factors influence these disorders” (1). No single gene can code for a mental state. Nearly all behavior is influenced but not determined by genes. Genes only code for macromolecules, not behaviors of the mind. However, this is not to say that genes do not play a role in depression. Females are twice as likely to become depressed as males – a difference thought to be genetic-related.
Researchers theorize that mental illness can arise from varying concentrations of neurotransmitters in the brain and their activity. One hypothesis for the cause of depression is excessive or deficient levels of noradrenaline and serotonin. It is thought that people with depression have low activity in the noradrenergic system, so they do not produce adequate amounts of noradrenaline. This neurotransmitter is related to serotonin, which is also believed to be related to depression in low levels. Serotonin regulates moods and is associated with impulse control. Those with high levels of serotonin are “confident, optimistic, relaxed, and neither aggressive nor impulsive,” while those with low levels of serotonin are “aggressive, competitive, and more impulsive, but may also be fearful and inhibited” (3). Other symptoms are a result of hypothalamus functional imbalances. The hypothalamus is responsible for hunger, so when it malfunctions, one loses one’s appetite, which is why depressed people experience weight loss (3). Another area of the brain involved with depression is the hypothalamic-anterior pituitary-adrenocortical axis. Those who are depressed have a hypersecretion of cortisol (4). Cortisol is a hormone that is released in response to stress, so it makes sense that a depressed person would have high levels of cortisol in their system because they are likely to be very stressed. Dopamine is another neurotransmitter thought to affect depression. It is responsible for regulating mental processes and can affect personality traits. People with high levels of dopamine partake in risky behavior, are impulsive, and change interests often, while those with low levels of dopamine are more stable but also have trouble taking pleasure in life. One of dopamine’s roles is to provide the body with pleasure (3). If depression is thought to be a result of chemical imbalances in the brain, then why hasn’t depression been cured?
The idea that neurotransmitters play a key role in depression was created along with antidepressant medications, and because these medications can sometimes be helpful, this idea is still being held as true even though there is no conclusive evidence to prove it. Antidepressants are obviously used to treat depression, but they can also be used to treat other illnesses (1). There seems to be a sort of hit or miss game that doctors must play with patients when prescribing antidepressants because no one really knows how they work or why they work. According to a study by Paykel, “Thirty to forty percent of patients will fail to respond to an adequate trial of an antidepressant, and an additional problem is partial response” (4). The most commonly prescribed antidepressants are SSRIs, or selective serotonin reuptake inhibitors, such as fluoxetine or sertraline. These medications increase serotonin levels by inhibiting serotonin from being reabsorbed by certain neurons, leaving more of it available outside of the nerve cells. Unfortunately it generally takes 4-6 weeks for the patient to feel the effects, so if the patient does not respond to the medication, then it will take another 4-6 weeks to figure out if he or she will respond to a different medication. Meanwhile, the patient is suffering and may even feel more hopeless after a failed antidepressant attempt. Moreover, there is no immediate medical relief from depression. Those with mild cases of depression might benefit from antidepressants alone, but for those with severe or chronic depression, it is best to couple medication with psychotherapy. In these severe cases, doctors may prescribe more than one antidepressant, generally a cocktail of antipsychotics and antidepressants. Only 66% of patients will have an immediate response to the medications, while 15% will fail to respond and therefore will not improve, possibly causing chronic depression. Of the 66%, one third will relapse during their attempted recovery. 75% of those who recover will suffer another episode within five years (1, 4). It is no wonder therapy is highly suggested to supplement antidepressant medications.
Depression cannot be attributed simply to genetics or chemical imbalances. Environmental factors must also be taken into account. Depression following the death of a loved one or other stressful life events is not uncommon. For children, a non-supportive environment can lead to low self-esteem, self-depreciation, and self-criticism, which are grounds for depression. Also, depression in children can develop from a stressful home environment, such as parents going through a divorce, or physical, sexual, or emotional abuse (4). Children with depression will suffer disruptions in their development and have dysfunctional relationships with those around them. Adults may develop depression due to behaviors and thought patterns reminiscent of childhood abuse. Sufferers of depression are “characterized by their interpretation of external events not in general, but in personal terms that are often unfavourable to themselves. This means that their analysis of incoming information, definition of problems, and ways of seeking and implementing solutions are distorted” (3). They will think negatively about themselves and basically anything in their lives. Their perception is twisted in such a way that they believe their actions are pointless, their lives are worthless, and they will always feel this way. It seems only fitting that depression is the complex result of interactions between neurotransmitters, genetics, environmental factors and social situations.
Of course, this is to say nothing of anxiety’s role in depression. Frequently, depression and anxiety go hand in hand. The main forms of anxiety are generalized anxiety disorder (GAD), post-traumatic stress disorder (PTSD), obsessive-compulsive disorder (OCD), social phobia, and panic disorder. Generalized anxiety is not unbearable, just constantly present. Sufferers show signs of nervousness and anguish at the thought of seemingly innocuous triggers and in anticipation of certain events. About 30% of GAD patients also suffer from major depression. PTSD develops as a result of a traumatic experience. A person with OCD has obsessive thoughts and must perform compulsive rituals so as to alleviate their anxiety. This can lead to major depression. Those with social phobia feel anxious when interacting with strangers. Out of those who suffer from major depression, 24-28% also have social phobia. Panic disorder is characterized by the fear of having a panic attack, whose symptoms include nausea, difficulty breathing, increased heart rate, shivering, tremors, chest pain, and feeling like one is dying. These symptoms may persist for hours. 10-30% of people suffering from panic attacks will also suffer from depression. Clearly, people with anxious disorders will also suffer from depressive disorders – “an estimated 60% of depressed people also suffer from severe anxiety states” (3). Does one cause the other or do they merely correlate?
Much like depression, anxiety can be a result of genetics, chemical imbalances, social and environmental factors. People suffering from anxiety can learn anxious behavior from their parents or might develop it as a result of a stressful home life. Personality traits similar to those of depression can also cause anxiety, such as low self-esteem. Low self-esteem is often an outcome of poor parenting and associated attachment issues. Also, certain medications can cause anxiety as a side effect, including some antidepressants, such as Wellbutrin. As with depression, neurotransmitter deficiencies and dysfunctional activity can lead to anxiety disorders. Because serotonin is associated with impulse control, low levels of it can lead to the impulsiveness of certain anxiety disorders, such as panic disorder and OCD. The neurotransmitter noradrenaline can play a role in anxiety. The noradrenaline system and the sympathetic nervous system are activated under stressful situations – fight or flight situations -- and can therefore cause anxiety (3).
Even some of the same medications as depression are used to treat anxiety. This is no surprise since the two disorders are so closely related. SSRIs can be effective in combating anxiety because with increased levels of serotonin, a person is less impulsive and aggressive (3). For more intense forms of anxiety, however, stronger medications are required, usually in addition to an antidepressant. Most commonly prescribed is a class of psychoactive drugs called benzodiazepines, such as lorazepam or clonazepam. These medications are sedatives and muscle relaxants and are especially effective in treating panic disorder. Unlike depression, there are medications for anxiety that can provide relatively instant relief.
Since depressed people are less functional in society than people with anxiety, physicians generally focus on treating the depression first. However, “Longitudinal and epidemiological studies suggest that anxiety tends to precede depression in both adolescents and children and adults, raising the possibility that depression is in some sense secondary to anxiety. It may be that they share a common temperamental basis, such as emotionality” (4). It is possible that a person becomes depressed as a consequence of their anxiety. If one suffers from social phobia and is not treated for it, he or she is likely to develop distorted perceptions on how to deal with their anxiety, such as suicide. Negative and destructive thoughts resulting from anxiety can lead to depression. Interestingly, from personal experience, anxiety and depression seem to occur opposite each other. When I am suffering a depressive episode, I have little anxiety, but when I am pulling out of a depression, my anxiety greatly increases. Anxiety and depression are blatantly related. Unfortunately researchers have yet to discover hard scientific evidence to prove the relation.
1. Berrios, German E. and Christopher M. Callahan. Reinventing Depression. New York: Oxford University Press, 2005.
2. Brown, George W. and Tirril Harris. Social Origins of Depression. New York: The Free Press, 1978.
3. Wasserman, Danuta. Depression: The Facts. New York: Oxford University Press, 2006.
4. Goodyer, Ian M. Unipolar Depression: A Lifespan Perspective. New York: Oxford University Press, 2003.