Some neurological aspects of anxiety

At the end of my last blog, I talked about how taking charge and taking control are at the very heart of recovery of almost all ‘clinical’ problems. The most essential way of taking charge and ensuring strong mental health throughout life is through exercising mental control.

To help you exert the level of mental control you need for recovery, it is important to understand how your brain works at a physiological level.

As you will see in my biography, I came out of a background in brain research where I was studying aspects of normal learning and memory. This background encouraged me to think about how our brains work and led me, about 16 years ago, to develop a neurological theory and a set of solutions which I called ‘Smart Therapy’ about how we ‘learn’ anxiety or depression or anger or other forms of self-sabotage, and then how we ‘consolidate’ those anxious, depressive or self-sabotaging thoughts, feelings and images, over time into long-term memory (LTM) which then become very easily retrievable. The more retrievable these anxious or depressive thoughts and feelings are, the more they pop-up in consciousness and fill-up our mental space and the more we then see ourselves as ‘anxious’ or ‘depressed’ in our overall personality or identity.

For almost everyone, anxiety (or depression) starts following some type of stressful life event (SLE). It might be losing a job, divorce, moving schools, migrating, being bullied, developing an illness, losing a loved one, parental separation, being assaulted, or failing an important exam. When any of us experience an event that is going to have some pretty serious or threatening ramifications, our brains will pump out more of a certain hormone known as corticotrophin releasing factor (CRF) from the amygdale. Mostly CRF is released in the brain from the anterior pituatory gland, but when we encounter a SLE it is also released from the amygdale.

This is probably not that surprising, because our amygdale are the main areas of fear and threat detection in our brains, and we have just encountered a serious threat – so our brain would not want us to miss the next threat due to lack of attention. Indeed, when CRF is released from the amygdale it has a direct effect upon neurons, dropping the level of stimulation required to make them fire – so the neurons influenced by CRF fire much more readily than usual. The neurons become hyper-reactive, firing much more easily than they would without the presence of CRF.

The release of CRF in the amygdale causes a high level of brain agitation leading to the sorts of symptoms people typically experience following a SLE such as difficulty sleeping, reduced appetite, increased anxiety, lowered mood, lowered confidence and increased rumination on scary or depressive thoughts.

It is important to realise that this happens to everyone on the planet – whenever any of us experience a serious SLE our brains will have this physiological response. It is a normal response to deal with an abnormal threat – that will resolve of its own accord so long as undue attentional focus is not given to those scary or depressive ruminations (more on this in a moment). But, if it is the case that this is a normal response to an SLE then it is important to think about why only some people develop ‘clinical’ anxiety or ‘clinical’ depression following a SLE.

The answer that I have found to this question in my clinical practice of having seen more than two thousand people over the last two decades – is that it is people who have come from difficult backgrounds who are more likely to develop the ‘clinical’ symtoms of a self-reinforcing cycle of anxiety or depression partly because of the negative assumptions they hold about the world, themselves and other people (see last blog) and partly because they are already very brain-practised at encountering threat.

For example, people who have come from more cushioned backgrounds will still have SLEs, still get the CRF response of intense brain agitation, leading to trouble sleeping, increased heart rate, nausea and more scary or threatening thoughts, such as ‘what if…I stab you in the eye with my pen’. However, because people from more cushioned backgrounds have had less CRF-activation of the amygdale in the past and are therefore less practised at a hyper-vigilant brain response to threat plus their assumptions are generally positive, like the world is safe, others are friendly, and I am a good and capable person – then these people will dismiss scary thoughts as ‘silly’ and show absolutely no interest in them – recognising that all healthy, imaginative people have silly, scary thoughts from time to time.

On the other hand, people who have come from more difficult backgrounds will be more ‘primed’ towards threat (having experienced many more threats) so they will more readily, tune-into the CRF-activation of the amygdale and become quickly hyper-vigilant since they have learnt from their previous experience. On top of this, they will (also as a result of their earlier learning experience) hold more negative and self-doubting assumptions like people can be hostile and I’m a bad, untrustworthy person – leading them to take the same silly, scary thoughts more seriously.

In taking the thought more seriously, what I mean is that more attentional focus is brought to bear on that scary thought. This is the theory at the centre of my Smart Therapy approach. This attentional focus might involve examining the thought (to try to disprove the ‘scary’ thought) and this could take the form of mentally checking back over old memories to see whether there have ever been any other similar ‘violent’ instances. If other (even slightly similar) instances are found in LTM (such as I did elbow Vanessa is grade 5) then those scenarios will also be examined and ruminated upon at length. When these other similar instances are found they induce high levels of fear in the person, causing strong physiological sensations of anxiety and exacerbating self-doubt. Once frightened like this, it is easy to take the next step of behavioural avoidance by thinking ‘well, if I can’t be trusted not to stab you with my pen then I had better not go near any other possible weapons, I must stay right away from the knife block or I shouldn’t even be within reach of this stapler – in case I belt someone over the head with it’.

Then other attentional focus strategies can easily come into play. The anxious person might visualize themselves having committed a terrible assault on another person, and examine whether or not they feel ‘sufficient’ regret or remorse. If there is any room for doubt then this will be examined over and over each time leading to higher and higher levels of anxiety or distress.

This is how you build a self-reinforcing cycle of anxiety. Although the original frightening thought will vary person to person, I am describing here the usual way ‘clinical’ anxiety develops. What is important here is to know what is happening in the brain and why, and therefore how to stop the development of anxiety in its tracks.

According to my Smart Therapy approach: Whenever we pay attention to something we are telling our brain to learn it and remember it. If we pay attention to maths for 10 hours per day, we will lay huge amounts of maths equations and maths theories down into LTM. The more LTM we have laid down the more likely we are to access and retrieve those memories and therefore the more maths thoughts seem to just ‘pop’ into our mind with barely any provocation. Not only this, but the more we have maths thoughts and images, the more we would regard ourselves as a maths type-of-person – over time, maths would become a deep part of our identity.

This is no different with anxiety or depressive rumination – we can learn them just as effectively by paying them undue attention. In this way, anxiety and depression are not brain dysfunctions, genetic mutations or pathologies that need fixing up with medications – they are simply well-practised brain habits that we have learnt. We can learn maths, or reading or to play the guitar and we can learn anxiety or depression or anger just as effectively.

Indeed, it is not just that there is no pathology – it is that our brain is doing exactly what it ought to do – that is it is learning what it is being directed to learn. It is paying attention and then laying down traceable memories that are able to be easily retrieved. It is just that we are learning and retrieving distressing material that we would prefer not to learn or recall. But, our brains will learn just as effectively whatever we focus upon, whatever the targetted material.

It is important to understand this process from a neurological perspective also – so please bear with me through some of this information.

Although some areas of our brains are not flexible, much of our thinking, attentional and memory areas are highly flexible. With better imaging techniques we are now able to observe brain changes at the single synapse level.

For example, we know that when we pay attention (represented in the brain by synchronous neural firing between PFC areas and distal brain structures) then dendritic spines pop-up all over our dendrites in large ‘spiny’ neurons. The more we pay attention, the more they pop up.

These dendritic spines are thought to be the material representation of actual learning and memory in the brain. Each one, as soon as it pops up and sends attractor chemicals to draw an axon in its vicinity to synpase with it, has the machinery to function as an independent synapse – then capable of inputting (or not inputting) charges into the main body of the neuron and thereby influencing whether or not other neurons are activated further downstream.

Dendritic spines are made of Actin-F (the most flexible and ‘plastic’ material in the human brain) and they can pop-up for seconds and then retract and disappear or they can last for minutes, hours, months or years depending upon the amount of traffic they receive. More traffic leads to more robust shapes and higher levels of consolidation. With stronger learning, gene activation will occur and proteins will be synthesized resulting long-term potentiation and the formation of LTM. Whereas less traffic leads to more spindly and less robust shapes, where spines are easily dismantled and retracted and the synapses broken apart, with a corresponding weakening of memory.

Of course, in a sense we already know this. Even if we are extremely good at statistics and consistently get over 90% we only have to stop practising it for a few months and we can barely remember anything about it. If we don’t use it we lose it – even with extremely well-practised childhood memories they lose their detail and become harder to access over time – developing an ‘unreal’ aspect to them where we might not be sure if we remember something happening or if we were told it happened or if we saw a picture of it happening.

This has some relevance to ‘clinical’ anxiety or depressive rumination. As I have already outlined, after a SLE and a CRF response we all get more brain agitation and that culminates in more scary and threatening thoughts. People from a more difficult background are more likely to take these scary or depressive thoughts more seriously and they then pay excessive attention to them, examining them, checking them, recalling them, picturing them, feeling them and generally worrying about them. They often do this for hours everyday. As would be expected, their dendritic spines are madly popping-up all over the place, making endless synaptic connections all about anxiety. The more connections are built and the more they are retrieved and practised over and over in a constant anxiety rehearsal – the more anxiety is seen as part of the identity of the person. The person will say things like “I’m just an anxious person – I’ve always been like this”.

Of course to fix up this problem, we have to learn the mental control to stop focussing or paying attention to all these distressing thoughts, images, memories or feelings. How to do this, is what I will talk about in my next blog.

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