Medicating Anxiety: Should I take Anxiety Pills? Pros, Cons, Side Effects, and Consequences
We haven’t mentioned medication throughout the book (Overcome Anxiety: A Self Help Toolkit for Anxiety Relief and Panic attacks), but some of you may have taken medication in the past for your anxiety, be considering taking medication in the future, or may be taking medication now.
Medication can play an important role in overcoming anxiety, particularly in helping to cope with the symptoms of anxiety. The approach this book has suggested is that we should face our anxiety and fears in order to change the structure and function of the brain, along with our thinking and behaviour. Build a solid foundation, calm the mind, deal with action thoughts and feelings, and take action. Avoiding situations or tasks that make us anxious keeps us stuck in old patterns. When we do this life can become a vicious circle of anxiety-based thinking behaviour. Medication can help us to cope at times, but it isn’t designed to change our brain, the way we think, or what actions we take. It is normally used to remove or reduce severe suffering in the short-term.
So while medication can be helpful in reducing anxiety, the medication won’t provide you with the tools you need to change your brain. In order to do that - to weaken old negative patterns of thinking and grow more helpful thinking patterns - you need to take the opportunity to learn from experience and take action. Some medications can help with the restructuring of the brain when you’re actively working to overcome your anxiety, while some can interfere with the ability of the brain to change and learn, keeping you stuck where you are. However, the effects of the medication can differ from individual to individual and also depend on the type of anxiety the individual is experiencing and what triggered it.
It is important to say at this point, that you should always listen to the advice of the G.P. or medical professional that is responsible for your care. However, the following information may be useful when discussing current or potential treatment. So consider this part of the book to be information and not professional help or advice to strictly adhere to. You must talk to the professionals that are responsible for you care before you make any decisions. Okay, that’s the end of the disclaimer, now let’s talk about the different types of medications available.
There are three main categories of anxiety medications and all come with different side effects that you should weigh up and discuss with your doctor or GP:
- SSRIs and SNRIs
We will now briefly discuss how these medications work and what you can expect from taking them.
Benzodiazepines (Valium, Xanax, Ativan, and Klonopin)
Benzodiazepines, unlike most other anxiety medications, provide almost immediate relief from anxiety symptoms and are often prescribed for severe anxiety and insomnia. It’s thought that benzodiazepines work by increasing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA), which has the effect of calming down the activity of the amygdala and therefore reducing the physiological anxiety response (fight, flight, or freeze).
This category of medications may cause immediate side effects that include sedation, nausea, or muscle weakness. Benzodiazepines should never be combined with alcohol, as this can be fatal. Long-term use of benzodiazepines may impair a number of cognitive skills; including verbal learning and memory, and these impairments may continue even after an individual has stopped taking the medication. Prolonged use of benzodiazepines tends to lead to dependence, so increased dosages may be needed to for the medication to continue to be effective, and symptoms of withdrawal are likely if the medication is discontinued. The withdrawal symptoms may include insomnia, agitation, anxiety, headache, and loss of appetite. Because of the nature of these withdrawal symptoms, individuals may believe that their anxiety is returning, causing what is known as rebound anxiety. Therefore, in order to avoid these withdrawal symptoms, benzodiazepines are normally reduced slowly before being stopped,
In order to manage and overcome the problems anxiety causes through avoidance behaviour, we normally have to learn through experience; exposing ourselves to the very situations, activities, and tasks that make us anxious. To do this we must activate the neurons that are involved in that pathway of anxiety in order to generate new learning and rewire the brain. However, because benzodiazepines calm anxiety by reducing reactivity of the amygdala, it makes activating and changing these pathways difficult. So it is unsurprising that research has indicated those who benefit most from therapy or training for anxiety are those who do not take benzodiazepines. The amygdala cannot learn when it is being sedated.
So benzodiazepines can be useful for treating and reducing anxiety for a short period of time, but are likely to hamper the learning and rewiring process of learning to overcome anxiety through experience and exposure. Consideration should also be given to the adverse side effects of ths category of medications and their possible long-term impact.
SSRIs (Zoloft, Prozac, Celexa, Lexapro, and Paxil) and SNRIs (Effexor, Pristiq, and Cymbalta)
Selective serotonin reuptake inhibitors (SSRIs) and Serotonin norepinephrine reuptake inhibitors (SNRIs) are more often associated with the treatment of depression and referred to as antidepressants. However, they have also been found to treat anxiety effectively, particularly when an individual has also been diagnosed with depression.
These medications don’t tend to provide immediate relief, they are normally taken for a few weeks before any benefits are noticed. Some people may even feel more anxious initially after taking SSRIs or SNRIs and therefore doses are normally raised very gradually for individuals when first prescribed. SSRI side effects can include nausea, nervousness, dry mouth, dizziness, headaches, sexual difficulties, and weight gain or weight loss. SNRIs have similar side effects, but are more likely to include loss of appetite and agitation, and less likely to include weight gain or loss. This category of meditations aren’t thought to be addictive but can cause withdrawal symptoms; including dizziness, headache, sensory disturbances (such as tingling or pins and needles), agitation, anxiety, and sweating. Therefore it’s important to gradually reduce the use of them, and always under the care of a GP or medical practitioner.
SSRIs and SNRIs are known as reuptake inhibitors because they block the process of reuptake—or reabsorption—of neurotransmitters by neurons. In earlier chapters of the book we described how neurons transport signals between each other over a space called the synaptic cleft. In order to do this, the neurons release neurotransmitters that are used as a bridge between the two neurons. After a neuron releases a neurotransmitter, the neurotransmitter doesn’t normally remain in the synaptic space, but gets reabsorbs for use in the future. SSRIs and SNRIs block this reabsorption (reuptake) enabling the neurotransmitter to remain active in the space for longer. So medications that block reuptake, increase the activity of neurons in the pathways they target.
What is the difference between SSRIs and SNRIs? Well SSRIs target neurons that use serotonin, while SNRIs target neurons that use either serotonin or norepinephrine. Therefore SNRIs have an effect on a greater number of neurons. It is thought that serotonin has a role in sleep regulation, appetite, and digestion. The early versions of medications that increased serotonin levels often caused drowsiness, weight gain and nausea, but in more recent times the medications have been modified to target specific serotonin receptors (which is why why the term ‘selective’ is used) and the side effects have been greatly reduced. Progressive versions of SSRIs have developed, with each newly named SSRI thought to be more selective in targeting specific serotonin receptors (for example, first Prozac, followed by Celexa, and then Lexapro). SNRIs also target neurons that use norepinephrine as a neurotransmitter. It’s believed that norepinephrine influences the amygdala, hippocampus, thalamus and prefrontal areas of the cortex and plays a role in regulating systems in the body involved in heart rate, breathing, and blood flow to the muscles. However, only as medical research and technology advances will we really understand which areas of the brain are influenced and their exact effects on specific neural pathways.
Originally it was thought that this category of medications worked simply by increasing serotonin and norepinephrine levels, consistent with the idea that depression and anxiety was caused by chemical imbalances in neurotransmitters. However, as the symptoms don’t improve immediately when taking SSRIs and SNRIs, but take a few weeks, researchers began to look for other possible reasons for their effectiveness. It’s now known that when these medications are taken daily for a few weeks they begin to change the structure of the neurons by growing new dendrites, increasing the number of receptors, and developing new connections between neurons - neuroplasticity in action.
As a result, it’s possible that SSRIs and SNRIs help with the restructuring of the brain and aid the rewiring of neural circuits that play a role in anxiety. Therapists often report that clients who are taking SSRIs and SNRIs respond positively to therapy that is focused on changing anxious thought patterns. So combining these medications with psychotherapy often produces quicker, more positive outcomes, than when psychotherapy is used alone. However, this also tells us that care should be taken when taking these medications as they appear to promote neural growth, and this can include unhelpful thought patterns too. When you fertilize a garden, both flowers and weeds grow. So it’s important when taking these medications that to carefully consider what we training our brain to think and do when taking these medications.
Recent BBC Article on SSRIs: http://bbc.in/2e4LLZv (added19th Oct 2016)
Beta-Blockers (Inderal, Tenormin, Toprol)
Rather than targeting anxiety itself, beta-blockers are used to influence the physiological symptoms of anxiety, such as increased heart rate, raised blood pressure, shaking, and trembling. They do this by blocking certain receptors for adrenaline. So the amygdala still sends out signals to energise the fight or flight system, and adrenaline is still released, but the signals are blocked. So beta-blockers don’t stop anxious thoughts developing in the cortex or impact directly on the amygdala, but they reduce the symptoms, ensuring that adrenaline won’t be able to effectively trigger the physiological reactions to anxious thoughts and feelings. As a result, beta-blockers can be helpful to individuals who are very aware of, and particularly sensitive to, the physical symptoms of anxiety, relieving them of some of their stress symptoms.
There is no evidence that beta-blockers are addictive, but there hasn’t been much research on the side effects of taking beta-blockers over the long-term. Some studies do suggest long-term use can cause impaired memory, although not when used infrequently. If used daily, beta-blockers can cause physiological dependence, so when they are discontinued there may be some withdrawal symptoms, such as sweating and increased blood pressure and heart rate. As many of the symptoms of discontinuing beta-blockers resemble anxiety, it can sometimes lead people believing that they anxiety is returning or getting worse. So beta-blockers shouldn’t be stopped suddenly, but gradually and under the care of a medical professional.
There is some evidence that beta-blockers can be helpful in preventing fear that has been triggered by traumatic or severely anxious experiences from developing into anxiety-provoking memories. This is a particular problem for those who suffer from post traumatic stress disorder (PTSD), who experience vivid fearful memories or traumatic flashbacks, in which they keep reliving or vividly remembering a catastrophic event. It is thought that adrenaline may play a role in intensifying the brain’s memories in particularly stressful situations, turning them into ‘super-memories’. Research has suggested that giving beta-blockers to people just after a very stressful or traumatic event may reduce future PTSD symptoms, depending on the timing and amount of medication given.