How is depression treated?
Depression can be treated with either drugs or talking treatment, or with both of these strategies. Antidepressant medicines work by enhancing the action of certain neurotransmitters in the brain. The most important ones are serotinin and norepinephrine. Their function is to transfer nerve impulses from one nerve cell to another, like ferries transporting trucks from one side of a river to the other, so they can continue.
The antidepressant drugs mechanisms of action is in most cases either inhibition of the reuptake of the transmitter into the cell which sent the impulse (reuptake inhibition), or inhibition of the enzyme that is responsible for the degradation of the transmittors (enzyme inhibition).
By doing this, the drugs improve the access to the neurotransmitters.
The antidepressant medicines belong to either of two categories. The first generation of antidepressants is called trycyclic antidepressants and they are psycho-chemically rather similar to eachother.
The second generation of antidepressants started about 1985 and is a more diversified group, with until today 4 – 5 subgroups of medicines. This new group is by far the most commonly used.
The new (second) generation of antidepressant
The second generation of antidepressants dominates the prescriptions.
SSRI is the most common type of pharmacological treatment against depression. This means ”selective serotonin reuptake inhibitors”, which describes the way these drugs work: They inhibit the reuptake of serotinin to the nerve cell that is sending the signal. By doing so, they cause an increased amount of serotonine in the space (synapse) between the cells.
SSRI:s are f.eks. fluoxetine (Prozac), sertraline (Zoloft) and escatilopram (Lexapro).
SNRI means ”serotonin norepinephrine reuptake inhibitors”. This group of antidepressants enhance the reuptake of both of the two neurotransmitters which are of critical importance in depression, serotonin and norepinephrine. By doing so, they are said to have ”dual action”. Drugs in this group are f.eks. venlafaxine (Effexor) and duloxetine (Cymbalta).
MAO-inhibitors inhibit an enzyme called monoaminoxidase (MAO), which is involved in the degradation of neurotransmitters. By doing so, they increase the amount of active neurotransmitters in the brain. These medicines are not used in the first line, since they can interfere with other drugs and with food that contains tyramine, such as cheese, meat and alcoholic beverages. MAO-inhibitor is f.eks. moklobemide (Aurorix)
Mirtazapine (Remeron) is an antidepressant that doesn't fit into any of the groups mentioned. The mechanism of action is not settled, probably it acts by inhibiting receptors of adrenerg type. This causes increased access to norepinephrine. Mirtazapine has somnolence as a common adverse reaction and should be taken before going to bed.
Bupropion (Wellbutrin) is yet another substance in the new generation of antidepressants. It belongs to the chemical class of aminoketones. Its action is thought to be inhibition of the reuptake of norepinephrine and also of dopamine. Besides being an antidepressant, it is used as smoking cessation aid.
The old (first) generation of antidepressants
Tricyclic antidepressants are the first generation of antidepressants. Prominent members of this group are klomipramine (Anafranil), imipramine (Imipramil) and amitriptyline. They typically cause more adverse reactions than the new generation of antidepressants, such as dry mouth, blurred vision and low blood pressure. Also they are far more dangerous when overdosed. The adverse reactions are the main reasons why they are not so much used any more and why Prozac and other drugs of the new generation of antidepressants have become so successful.
But there is still some use, especially for the treatment of more severe or treatment resistant depressions, when newer antidepressant are not sufficient. The tricyclic antidepressants are regarded as somewhat ”stronger” than the second generation.
They are called tricyclic because the chemical structure of these substances is built up by three rings. Most of them work by inhibiting the reuptake of both serotonin and norepinephrine.
The matter of time in depression treatment
All antidepressant drugs, without exception, have a delay of their effects. Typically the effects on mood starts after two to four weeks of treatment and then grows over another two to four weeks. It is important that this is explained and understood by the patient. It means that the effects should not be evaluated earlier than after about 4 weeks of treatment. It is also important than when doing so, the patient has been taking full dose for the last weeks.
The onset can be sudden. In some cases the patient is relatively unaffected after 3 weeks of treatment, but significantly improved after 4 weeks. Some patients describe an onset over a day or two.
Support from family, friends and the doctor is important while waiting for the effects to come.
When anxiety is prominent, a drug against anxiety (anxiolytic) can be added to the treatment. That kind of drug works within hours, some even within minutes. If so, the patient gets an immediate relief from the anxiety, while the sadness yet isn't very much reduced.
Typically a bensodiazepine such as oxazepam is chosen to treat the anxiety component of the depression. The anxiety component is, however, varying from case to case. Typically a drug against anxiety is prescribed only for the first weeks of treatment, until the antidepressant medicine starts to work.
This is an old treatment mainly used in bipolar disorders. But it can also be prescribed as a last line drug for unipolar depressions. The mechanism of action is not established. Its use is limited by adverse reactions such as kidney affection, skin conditions and diarrhea.
This expression has become connected with antidepressant medications. But it is not true that they give feelings of ”happiness”. They make the person feel normal, and that's good enough. That is, they cure the resistant feeling of unhappiness that is at the centre of the depression, and regain the persons normal emotional responsiveness.
That includes the capacity to feel happy as a normal response to happy life events.