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Writer's pictureSula Windgassen

How our brain jumps to negative conclusions: examples from chronic urinary tract infections & IBS



Often after we’ve had experiences of bad things happening, our brain comes up with negative conclusions predictions. This article explains a bit about the physiology behind this and how to change it.


Our brain: A calculation machine

Our brain is more than a reactive organ. It is constantly processing and making pre-emptive calculations to anticipate our needs and what is best for our safety, survival and thriving. It is remarkable at what it does but it sure does get a lot of data. A lot of thoughts, a lot of feelings (physical and emotional) and a lot of external stimulus and input on an ongoing basis.

The brain is constantly comparing data incoming with previously stored data to work out what we need to do (if anything). Only a minority of the time is that a conscious process.

When something bad happens

Bad things happen to differing degrees all the time. From burning your toast to cutting your hand, to health complications. There is a continuum of “bad things” and your brain is likely to be less concerned with things on the lower end of your respective spectrum.

That is unless it has started to become less tolerant to any sense of threat. This can be a result of a range of things: personality, an overwhelming period of bad things happening, a change in perceived support or resources – a combination thereof.

In the middle of our brain there are some specific areas dedicated to threat processing (amygdala, hypothalamus and hippocampus). The amygdala is probably the best known of these to be associated with threat processing in particular. A significant thing about these regions is that they are also involved in processing pain and sensory signals [1,2]. It stands to reason that the more activated they are due to perceived threat, the more likely we are to experience pain or uncomfortable sensations.

The hippocampus is also involved in processing memories. It is an area that has been shown to reduce in size in those who have experienced chronic trauma and post traumatic stress disorder [3]. When all is functioning well, the hippocampus can help regulate that fight/flight/freeze stress response. But when it is impaired, it’s capacity to do so is diminished. Herein we can see how the brain starts becoming “wired” towards threat detection and hypervigilant.

Recent research also highlights the role of the prefrontal cortex (in the front and top area of the brain), known to be one of the key regions of the “thinking” as opposed to emotional and sensory brain. A review highlighted that activity in the PFC plays an important role in “threat learning circuitry” [4]. Just as areas of the PFC are involved in threat detection, they also seem to be involved in threat “extinction” i.e. teaching the brain to no longer be afraid of a particular threat/stressor. Such research find that this area of the brain communicates to other areas of the brain that are predominantly involved in emotion and sensory processing and downregulates activity.

What this means is that cognitively reappraising the threat, can reduce the sense of threat.

What does cognitively reappraising the threat look like? And is it possible when there are still threats?

To answer I’m going to pull examples of threat detection modes being activated in two conditions I commonly work with:

Irritable Bowel Syndrome: Someone with IBS has started to experience gut symptoms. For this example let’s say that is frequent loose stools and cramping. They worry that they won’t have adequate control over their bowels and take lots of precautions to prevent that. They are constantly feeling depleted by symptoms but feel like they are failing to do things well. The symptoms are threatening but also stressors of everyday life have become increasingly threatening (or stressful, to use less sciency terms).

Chronic urinary tract infections: Someone with chronic UTI will have had bacterial infection in the bladder. They may be managing this with long term antibiotics and now they don’t have full symptom relief but hope that the bacterial infection is being sufficiently targeted by the antibiotics. Every twinge of bladder sensation makes them feel like the infection could be getting worse. They don’t want to drink alcohol or eat too much spicy food in case that kicks off symptoms again.

We can see a number of areas for each condition where there is hypervigilance to potential threats that is initiated from fundamental threats. E.g. foods can irritate the bladder. Bowel urgency can come out of the blue.

The thing is, now the brain wants to grasp for as much control as possible and minimise the likelihood of threats occurring. So what does it council us to do? Avoid. Avoid as many threats as possible.

Now the thing about this research paper [4] is that it highlights that avoidance can keep threat circuitry going as there are no alternative opportunities for updating the threat calculation. As such avoidance can generalise out, making your world smaller and smaller.

Cognitively reappraising when threats are still there

We may assume that there should be a zero % likelihood of a threat happening again before we can start learning to reduce a sense of bad things will happen, but this is not real life. Also it’s not productive for us to recalibrate our threat sensing down to 0. We just don’t want it to be stuck at 100.

The best way I’ve found to help reappraise a sense of threat when working clinically (as of course evidenced by copious amounts of research), is to afford yourself the opportunity to have a different experience. The brain (and body) updates best on full, 360, 4 dimensional experience.

In IBS the threat calculation is currently towards the end of “I have 0 control of holding in if I get an urge to go”

In cUTI the threat calculation is currently towards the end of “If I create any bladder irritation it will cause a big symptom flare up”

We can see why it feels so vulnerable in both case.

To create some opportunities to reappraise this, we start off with low stakes experimentation.

In IBS this might look like, going to the toilet when hit with sudden urgency, but pausing at the door before pulling your trousers down and rushing to sit on the loo. Then seeing if this is comfortable, next time if you can pause outside the door and then at the foot of the stairs. Each time your brain is learning that you have more control than initially feared. You can count on it to auto-calculate the fear gauge down as a result.

In cUTI it might be having a small bit of food with minimal spice or not spice but something else that feels a bit worrisome. Or it may be having a fizzy drink instead of alcohol if this is also avoided. What it will be specifically, depends on the degree of avoidance. Often I find that my clients with cUTI have become withdrawn from a lot of things for a range of different worries. Leaving the house can be shrouded with threat of having a flare up. In this case, the experiment might be leaving the house but just walking round the block. And then building up from there. In fact, I have one incredible client I was just exploring how far she had come with this being the starting point.

As she reflected, the initial feared activities are a lot less feared (or not at all) now. The brain (and nervous system) has recalibrated accordingly. All you need to do to physiologically recalibrate, is set the right conditions.

Want to try this out?

If you’re interested in more resources and learning more about concepts like this, check out the Body Mind Connect membership

Before you finish reading, you might like to consider these questions

  • What has your body learnt is not safe?

  • How does it respond when you think about doing it or experiencing it?

  • How does this impact your life?

  • Would you like to change this?

References

[1] Bertram, T., Hoffmann Ayala, D., Huber, M., Brandl, F., Starke, G., Sorg, C., & Mulej Bratec, S. (2023). Human threat circuits: Threats of pain, aggressive conspecific, and predator elicit distinct BOLD activations in the amygdala and hypothalamus. Frontiers in Psychiatry, 13, 1063238.

[2] Price, D. D. (2002). Central neural mechanisms that interrelate sensory and affective dimensions of pain. Molecular interventions, 2(6), 392.

[3] Lambert, H. K., & McLaughlin, K. A. (2019). Impaired hippocampus-dependent associative learning as a mechanism underlying PTSD: A meta-analysis. Neuroscience & Biobehavioral Reviews, 107, 729-749.

[4] Alexandra Kredlow, M., Fenster, R. J., Laurent, E. S., Ressler, K. J., & Phelps, E. A. (2022). Prefrontal cortex, amygdala, and threat processing: implications for PTSD. Neuropsychopharmacology, 47(1), 247-259


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