Causes of depression : Some types of depression run in families, indicating that a biological vulnerability to depression can be inherited. This seems to be the case especially with bipolar disorder. Studies have been done of families in which members of each generation develop bipolar disorder. The investigators found that those with the illness have a somewhat different genetic makeup than those who do not become ill. However, the reverse is not true. That is, not everybody with the genetic makeup that causes vulnerability to bipolar disorder has the illness. Apparently, additional factors, possibly a stressful environment, are involved in its onset. Major depression also seems to occur in generation after generation in some families, although not as strongly as in Bipolar I or II. Indeed, major depression can also occur in people who have no family history of depression. An external event often seems to initiate an episode of depression. Thus, a serious loss, chronic illness, difficult relationship, financial problem, or any unwelcome change in life patterns can trigger a depressive episode. Very often, a combination of genetic, psychological, and environmental factors is involved in the onset of a depressive disorder. Nothing in the universe is as complex and fascinating as the human brain. The over 100 chemicals that circulate in the brain are known as neurochemicals or neurotransmitters. Much of our research and knowledge, however, has focused on four of these neurochemical systems: norepinephrine, serotonin, dopamine, and acetycholine. In the new millennium, after new discoveries are made, it is possible that these four neurochemicals will be viewed as the "black bile, yellow bile, phlegm, and blood" of the twentieth century. Different neuropsychiatric illnesses seem to be associated with an over-abundance or a lack of some of these neurochemicals in certain parts of the brain. For example, a lack of dopamine at the base of the brain causes Parkinson disease. Alzheimer dementia seems to be related to lower acetylcholine levels in the brain. The addictive disorders are under the influence of the neurochemical dopamine. That is to say, drugs and alcohol work by releasing dopamine in the brain. The dopamine causes euphoria, which is a pleasant sensation. Repeated use of drugs or alcohol, however, desensitizes the dopamine system, which means that the system gets used to the drugs and alcohol. Therefore, a person needs more drugs or alcohol to achieve the same high feeling. Thus, the addicted person takes more and more to feel less and less high. The different types of schizophrenia are associated with an imbalance of dopamine (too much) and serotonin (poorly regulated) in certain areas of the brain. Finally, the depressive disorders appear to be associated with altered brain serotonin and norepinephrine systems. Both of these neurochemicals are lower in depressed people. Please note that I specified, "associated with" instead of, "caused by." I made this distinction because we really don't know whether low levels of neurochemicals in the brain cause depression or whether depression causes low levels of neurochemicals in the brain.

Symptoms of depression and mania : Not everyone who is depressed or manic experiences every symptom. Some people experience a few symptoms and some many symptoms. The severity of symptoms also varies with individuals. Depression Symptoms of Manic Depression : Persistently sad, anxious, or "empty" mood. Feelings of hopelessness, pessimism. Feelings of guilt, worthlessness, helplessness. Loss of interest or pleasure in hobbies and activities that were once enjoyed, including sex. Insomnia, early-morning awakening, or oversleeping. Decreased appetite and/or weight loss, or overeating and weight gain. Fatigue, decreased energy, being "slowed down." Thoughts of death or suicide, suicide attempts. Restlessness, irritability.

Other causes of depression : Certain medications that alter the levels of norepinephrine or serotonin can alleviate the symptoms of depression. Some medicines that affect both of these neurochemical systems appear to perform even better or faster. Other medications that treat depression primarily affect the other neurochemical systems. The most powerful treatment for depression, electroconvulsive therapy (ECT), is certainly not specific to any particular neurotransmitter system. Rather, ECT, by causing a seizure, produces a generalized brain activity that probably releases massive amounts of all of the neurochemicals. Women are twice as likely to become depressed as men. However, scientists do not know the reason for this difference. Psychological factors also contribute to a person's vulnerability to depression. Thus, persistent deprivation in infancy, physical or sexual abuse, clusters of certain personality traits, and inadequate ways of coping (maladaptive coping mechanisms) all can increase the frequency and severity of depressive disorders, with or without inherited vulnerability. The effect of maternal-fetal stress on depression is currently an exciting area of research. It seems that maternal stress during pregnancy can increase the chance that the child will be prone to depression as an adult, particularly if there is a genetic vulnerability. It is thought that the mother's circulating stress hormones can influence the development of the fetus's brain during pregnancy. This altered fetal brain development occurs in ways that predispose the child to the risk of depression as an adult. Further research is still necessary to clarify how this happens. Again, this situation shows the complex interaction between genetic vulnerability and environmental stress, in this case, the stress of the mother on the fetus.

Treatments are available for depression - Antidepressant Medications : Selective serotonin reuptake inhibitors (SSRIs) are medications that increase the amount of the neurochemical serotonin in the brain. (Remember that brain serotonin levels are low in depression.) As their name implies, the SSRIs work by selectively inhibiting (blocking) serotonin reuptake in the brain. This block occurs at the synapse, the place where brain cells (neurons) are connected to each other. Serotonin is one of the chemicals in the brain that carries messages across these connections (synapses) from one neuron to another. The SSRIs work by keeping the serotonin present in high concentrations in the synapses. These drugs do this by preventing the reuptake of serotonin back into the sending nerve cell. The reuptake of serotonin is responsible for turning off the production of new serotonin. Therefore, the serotonin message keeps on coming through. This, in turn, helps arouse (activate) cells that have been deactivated by depression, and relieves the depressed person's symptoms. In the United States, SSRIs have been used successfully for a decade to treat depression. They have fewer side effects than the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs), which are discussed below. SSRIs do not interact with the chemical tyramine in foods, as do the MAOIs. Also, SSRIs do not cause orthostatic hypotension and heart rhythm disturbances, like the TCAs do. Therefore, SSRIs are often the first-line treatment for depression. Examples of SSRIs include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), citalopram (Celexa), and fluvoxamine (Luvox). SSRIs are generally well tolerated and side effects are usually mild. The most common side effects are nausea, diarrhea, agitation, insomnia, and headache. However, these side effects generally go away within the first month of SSRI use. Some patients experience sexual side effects, such as decreased sexual desire (decreased libido), delayed orgasm, or an inability to have an orgasm. Some patients experience tremors with SSRIs. The so-called serotonergic (meaning caused by serotonin) syndrome is a serious neurologic condition associated with the use of SSRIs. It is characterized by high fevers, seizures, and heart rhythm disturbances. This condition is very rare and has been reported only in very ill psychiatric patients taking multiple psychiatric medications. All patients are unique biochemically. Therefore, the occurrence of side effects or the lack of a satisfactory result with one SSRI does not mean that another medication in this group will not be beneficial. However, if someone in the patient's family has had a positive response to a particular drug, that drug would be the preferable one to try first. Dual Action Antidepressants : The biochemical reality is that all classes of medications that treat depression (MAOIs, SSRIs, TCAs, and atypical antidepressants) have some effect on both norepinephrine and serotonin, as well as on other neurotransmitters. However, the various medications affect the different neurotransmitters in varying degrees. Some of the newer antidepressant drugs, however, appear to have particularly robust effects on both the norepinephrine and serotonin systems. These drugs seem to be very promising, especially for the more severe and chronic cases of depression. (Psychiatrists, rather than family practitioners, see such cases most frequently.) Venlafaxine (Effexor) is one of these dual action compounds. It is a serotonin reuptake inhibitor that, at lower doses, shares many of the safety and low side effect characteristics of the SSRIs. At higher doses, this drug appears to block the reuptake of norepinephrine. Thus, venlafaxine can be considered an SNRI, a serotonin and norepinephrine reuptake inhibitor. Another newer antidepressant, mirtazapine (Remeron), is a tetracyclic compound (four-ring chemical structure). It works at somewhat different biochemical sites and in different ways than the other drugs. It affects serotonin, but at a post-synaptic site (after the connection between nerve cells.) It also increases histamine levels, which can cause drowsiness. For this reason, mirtazapine is given at bedtime and is often prescribed for people who have trouble falling asleep. Like venlafaxine, it also works by increasing levels in the norepinephrine system. Other than causing sedation, this medication has side effects that are similar to those of the SSRIs, but to a lesser degree in many cases. Atypical antidepressants are so named because they work in a variety of ways. Thus, atypical antidepressants are not TCAs or SSRIs, but they act like them. More specifically, they increase the level of certain neurochemicals in the brain synapses (where nerves communicate with each other). Examples of atypical antidepressants include nefazodone (Serzone), trazodone (Desyrel), venlafaxine (Effexor), and bupropion (Wellbutrin). The United States Food and Drug Administration (FDA) has also approved bupropion for use in weaning from addiction to cigarettes. This drug is also being studied for treating attention deficit disorder (ADD) or attention deficit hyperactivity disorder (ADHD). These problems affect many children and adults and restrict their ability to focus or concentrate on one thing at a time.