Chemical Imbalance | Anti-Depressants
“I think antidepressants make doctors feel better. They allow us, like the colleagues we envy (opthalmologist come to mind), to isolate a problem and eradicate it. If you run a mixed practice, it is a wonderful thing to have a percentage of patients walk in, get better fast, and respond with gratitude. And if you are, like many psychotherapists, someone who was raised to think of him- or herself as bright but not handy, there is also a seductive satisfaction in mastering a mildly “technological” treatment.”
Peter Kramer, “Moments of Engagement.”
I include these pages on an NLP site given the prevalence of antidepressant medication in our society. It seems wise that the NLP therapist has at least a working knowledge of how they work and their subjective effects. In my private practice, it is very rare for me to see a client who is not already taking some form of psychiatric medication (they never come to me as a first choice).
Most commonly, the clients are taking some form of antidepressant either in isolation or in conjunction with another form of medication. It is not just people complaining of depression that are prescribed these drugs that Peter Kramer prefers to refer to as “thymoleptics”. Anti-depressant medications (mostly the SSRI’s but also clomipramine) are increasingly being prescribed for such conditions as OCD, bulimia, anorexia, PTSD, anxiety and panic disorders and this scope appears to be increasing. For example, within the last two years, a drug was scheduled for the treatment of “shopping addiction” (I’m not kidding!)
Psychiatric drugs can be largely divided into two categories: those that raise levels of
neurotransmitters and those that reduce levels of neurotransmitters. All the antidepressant drugs raise neurotransmitter levels, notably, serotonin (5-HT) and norepinephrine whilst the neuroleptic drugs (chlorpromazine, haloperidol, etc) tend to reduce dopamine.
Prozac (fluoxetine) is probably the world’s best known psychiatric drug and is part of a class of drugs called SSRI’s – correctly, a Selective Serotonin Reuptake Inhibitor (but increasingly called a “Serotonin Specific Reuptake Inhibitor”). Other commonly prescribed drugs in this class are Paroxetine, Citalopram and Sertraline.
These drugs are believed to work by inhibiting the reuptake of serotonin from the synapse of the neuron, thus creating an overall rise in levels of this monoamine across the synapses of the brain.
Typically, SSRI’s have a long half-life (7-9 days) – this refers to the length of time that they
exist in the body. Because of this, they are usually taken once a day. A common misperception of these drugs is that they create a “high” much in the same way as a dose of amphetamine might – whilst researching a freelance article for a local newspaper in 1996, I interviewed a number of people in rave clubs about the drug users perceptions of Prozac. I found that at this time, Prozac was freely sold as a “rave drug” not just to get a [imaginary] high but in the belief that taking a single dose of Prozac would “protect the brain from the side effects of MDMA”. This is a notion I have seen often repeated in many of the pro-ecstasy type literature – what is missed from this literature is just what is supposed to protect the brain from the side effects of the Prozac?
These drugs do not work immediately and the depressive can usually expect a 2-6 week lag between taking the first dose and a reduction of symptoms. The actual reason for this lag is not yet fully understood, especially with regards to the initial rocket of serotonin levels with an hour of taking the first dose.
Because of the nature of the way they work, these drugs will only exert an effect if taken regularly. I have found it common for some clients to be “yo-yo” SSRI consumers – they take it whenever they remember and infrequently. Neurologically speaking this is a disaster, throwing the brain’s homeostatic mechanisms further into chaos and bringing no positive benefit to the consumer.
The other typical pattern is the consumer that takes the drug for a few weeks, feels better and then stops taking it – because he feels better. As the drug leaves the system and his brain returns to its normal depressed state (assuming no other intervention has taken place) he starts taking it again, and so on.
A typical side effect profile of the SSRI`s are:
- Nausea, vomiting, dyspepsia, abdominal pain, constipation, reduced appetite
- Dry mouth, blurred vision
- Nervousness, anxiety, headache, confusion
- Palpitations, tremor, dizziness, drowsiness
- Fever, sweating
- Sexual dysfunction
- Movement disorders, tics, dyskinesias
- Abnormal liver function, aplastic anaemia, CVA, abnormal bleeding, hair loss
Realistically, the most common side effect the consumer can expect is initial nausea (usually subsides after a few days) and delayed orgasm (or inability to orgasm) – this latter effect has led some doctors to prescribe this drug for symptom relief of premature ejaculation.
There is increasing evidence to suggest that the SSRI`s can also induce permanent neurological disorders such as tardive dyskinesia, especially when taken in conjunction with another class of drugs such as the neuroleptics.
What is not accounted for by the “side effect profile” is the sociological effect of organizing a society in such a way that the mass “side effects of living” can be mopped up by a chemical. Already in schools, we are seeing psychopharmacology replacing effective leadership, discipline and teaching and in culture, we are increasingly seeing people rely on psychotechnology for their happiness.
I have observed a disturbing but unhalting trend in long-stay care institutions where
anti-depressant drugs have replaced much of the care previously supplied by human contact. (Addendum April 2002 – recently a close friend pointed out that in fact isn’t the outside, ie the streets, the towns – the biggest long stay care institution that we possess?)
This “psychological crutch” is an area that is worth addressing with the client who has been consuming such medication for some time. However, be advised that although SSRI`s are not supposed to have a withdrawal syndrome, sudden withdrawal of the drugs can be quite traumatic, both for physiological and psychological reasons. In addition, the non-medical NLPerson has to consider both the ethics and legalities of suggesting to anyone to stop taking any prescribed medication. Always liaise with the prescribing doctor if tempted to suggest cessation of any medication. Remember, a drug doesn’t need to be addictive in order to have a withdrawal syndrome!
In addition, it is well worth noting the research about state-dependent learning. If the
effective resources are anchored into the medicated state, provision for this will need to be made for the transition into the non-medicated state if the symptoms and behaviours that existed before the drugs were taken are not to recur.
The sudden boom in antidepressant prescribing really occurred with the advent of Prozac in the mid-80’s. Prior to this time medical prescribers only really had the older tricyclics or the MAO Inhibitors at their disposal. The MAO Inhibitors were potentially toxic when combined with certain foodstuffs and the tricyclics were almost always fatal when taken in sufficient overdose (especially when combined with alcohol). This lead to a bit of a dilemma for the doctors who would be supplying potentially fatal drugs to the very people who were most likely to use them for this purpose.
Prozac, on the other hand, which has comparatively low toxicity in overdosage meant that the patients who were the most at risk of deliberate self-endangerment could be prescribed a drug of low risk. As researchers began to notice that other concurrent symptoms such as anxiety and OCD could be reduced too with the SSRI’s, prescription rates began to rapidly increase.
The next generation of SNRI’s (Serotonin and Norepinephrine Reuptake Inhibitors) are specific to an additional transmitter Norepinephrine. Research suggests that it doesn’t really matter which transmitter of the two is raised by an antidepressant, despite the initial promise of such SNRI drugs such as Venlafaxine to be more efficient than the SSRI’s by acting on not one, but two neurotransmitter systems.
The older drugs, the tricyclics, were discovered somewhat by accident. Patients receiving a drug treatment for tuberculosis began to become rather happier. These patients were found to have an increase in energy, improvement in appetite and a restored sense of well being after receiving the drug Iproniazid which suppressed the reproduction of the tuberculosis bacilli. Iproniazid was subsequently found to be an effective tricyclic medication, though seldom prescribed these days following a bout of negative publicity associating it with hepatic jaundice.
Tricyclic medications that are still commonly used are: amitriptyline, imipramine, clomipramine, dothiepin and lofepramine. Some of the tricyclic drugs have sedating properties, such as dothiepin, and so may be the prescribing doctor’s treatment of choice where insomnia presents a particular problem. All the tricyclics will raise levels of serotonin and norepinephrine but also impact on other neurotransmitter systems, lacking the specificity of the SSRI’s and SNRI’s. Clomipramine is receiving a revival with the discovery that it is more potent than the SSRI’s and appears to exert a specific action in the treatment of obsessive-compulsive disorder.
Having a less specific action than the “clean” drugs, the SSRI`s, a typical side effect profile
of a tricyclic antidepressant is:
- Dry mouth, sedation, blurred vision
- Constipation, nausea, difficulty passing water
- Cardiovascular side effects – arrhythmias, postural hypotension, fast pulse, fainting
- Rashes and hypersensitivity reactions
- Behavioural disturbances, mania and hypomania, confusion
- Interference with sexual function
- Blood sugar changes, increased appetite and weight gain
- Convulsions, movement disorders and dyskinesias
- Fever and blood disorders
Prolonged administration can also cause permanent neurological syndromes such as tardive dyskinesia and tics. One problem of the tricyclic antidepressants is their suppression action on the cholinergic pathways in the brain, especially those of the autonomic nervous system. This leads to an activation of the “fight or flight” response leading to the nervous system to be “geared up” for action, thus leading to anxiety and jitteriness. Prolonged consumption of these drugs has been suggested to permanently damage these pathways.
Less commonly used these days are the monoamine oxidase inhibitors (MAOI’s). These drugs are potent antidepressants when used in sufficient doses and exert their function by blocking the action of the enzyme that breaks down the mono-amines (such as serotonin and norepinephrine). Their major problem lies in the fact they also inhibit the action of the breakdown of tyramine. This is a substance found in foods such as yeast extracts, smoked fish and cheese and an excess in the body will cause a colossal rise in blood pressure. Seldom used these days, their use is almost exclusively in “atypical depression” (the “form” of depression that Prozac was initially developed for) and for people who have not “responded” to other types of antidepressants.
Where SSRI’s prevent the reuptake of serotonin and MAOI’s inhibit the breakdown of serotonin, a mixture of these two drugs produces a catastrophic effect. The 5-HT syndrome (5-HT = serotonin) occurs with the resultant overload in the brain of this neurotransmitter, usually resulting in a very unpleasant death (I have myself seen this occur twice whilst working in Accident and Emergency). This syndrome resembles neuroleptic malignant syndrome and is characterised by coma, severe muscle rigidity (resulting is a serious rise in blood pressure and body temperature), seizures and cardiac disturbances. For this reason, a long “drying out” is required if someone is switched from an SSRI’s to a MAOI or vice versa.