Back in 2002, a new research recruit was welcomed to Dr. Justin Feinstein’s neurophychology lab. This recruit had a peculiar condition which affected her ability to feel fear. The condition affected the amygdala – the area in the brain where fear is thought to originate. Up to this point in 2002, both life and researchers had tried to illicit a fear response from her without success. She had been exposed to experiences of sexual, emotional, mental and physical abuse without even a flinch from her. All of the experiences left her emotionless. They were akin to watching a kettle boil for her - nothing.  
In Dr. Feinstein’s lab, this was all about to change.  
This is the story on the origins of anxiety and your breath. 
Dr. Feinstein is a neurophysiologist, he is interested in examining the links between the body and the brain. During the early 2000s, Dr. Feinstein was researching the origins of fear. He wanted to know if fear was all in the head or was it in the body too? 
Dr. Feinstein had found long-forgotten research from 1951 on carbon dioxide therapy to help alleviate fear and anxiety in patients. He was curious about the research and he was seeking ways to reignite this research when he approached his new recruit. Her name is kept anonymous but she is known as SM to us today. 
That fateful day in the lab was to change SM’s life forever and our understanding of fear. SM sat down in a chair to receive a bolus dose of carbon dioxide. She simply had to sit there and breathe in a mixture of gas containing an extreme amount of carbon dioxide. One breath of this mixture later and S.M. experienced a severe panic attack for the first time in thirty years. 

I can't breathe! 

Fig. 1. Heightened fear and panic to 35% CO2 in three rare lesion patients with focal bilateral amygdala damage. The amygdala is highlighted by red-dashed circles on the magnetic resonance imaging scans in the top panel. A single vital capacity inhalation of 35% CO2 triggered a panic attack in all of the patients with amygdala 
(A), as well as significantly higher levels of self-reported fear 
(B). and panic 
(C), and a significantly higher rate of respiration 
(D). *p < .05; error bars represent the standard error of the mean. VAS, visual analogue scale. 
from Feinstein et al. (2022). 
Ripping the mask off and breathing hard, SM left the lab, not wanting to return – she was traumatised by the event. Emotional and physical abuse she experienced in her life couldn’t do it but carbon dioxide did it. Carbon dioxide provoked a fear response in SM for the first time in her adult life. During debriefing, she later told the researchers she “can’t breathe” and labelled the experience as the “worst” fear she ever felt in her life. 
The events on this fateful day set in motion a lifetime of research for Dr. Feinstein and other researchers around the world. He had just discovered for himself that fear can be provoked without a fully functioning amygdala. It was carbon dioxide that was the stimulus. This is to suggest that fear is not only in the brain but it’s in the body too, specifically fear is in your ability to regulate your breath. Dr. Feinstein’s research has since been confirmed by other researchers and patients like SM. 
AM and BG are twins with a similar condition to SM. They were put through a similar protocol by Dr. René Hurlemann in partnership with Dr. Feinstein. Both twins experienced similar carbon dioxide invoked fear in the absence of a normal functioning amygdala. 

Welcome to the Apnea induced Anxiety Model 

Fig 2. A model of the AiA from Feinstein et al (2022) 
Fast forward fifteen years and we are beginning to discover the connections between carbon dioxide and fear in the brain. Neurosurgery Researchers found that stimulation of the amygdala inhibits breathing and triggers apnea. When this research is applied to real-life, it means that a fear invoking thought or scenario stops your signal to breathe (inhibited breathing) and provokes a breath hold (apnea). The most interesting thing from this research was the discovery that breathing stopped without the person’s awareness - fear can literally ‘take your breath away’ without you knowing it! 
In March 2022, Dr. Feinstein wrote a review article on the links between carbon dioxide and fear. In the article, he proposed a model of Apnea-induced-Anxiety (AiA). 
The AiA model proposes how a fear inducing situation leads to a concurrent breath hold and de-sensitized awareness of that hold. As the stress-inducing stimulus subsides, you become overwhelmed by the high levels of carbon dioxide in your body and a panic alarm is signalled. This alarm can lead to adapted breathing patterns, anxiety states and panic attacks. 
The initial breath hold in response to a stressor is thought to be a benefit to humans. Think of it as your ‘playing dead’ response to a threat. The body and brain remain calm in the face of fear until the imminent danger passes. However, if this response is initiated regularly this positive adaptive behaviour can become a negative maladaptive behaviour. It’s a case of too much of a good thing is bad for you. 
Viewing anxiety through the AiA model we can see how long-term adapted breathing, fear and anxiety are all linked together. 

What we've always known... 

This review by Dr. Feinstein supports the practice of Breath Teachers for the past 70 years. As far back as the 1950’s, Dr. Buteyko, proposed that normal healthy people lower their threshold for carbon dioxide sensitivity in the long run. He thought that the lowered sensitivity to carbon dioxide can elicit a disease response in people, such as: anxiety, depression, asthma, cardiac disease and type 2 diabetes. 
Nowadays, Breath Coaches understand that adapted breathing patterns are more varied than just a lowered sensitivity to carbon dioxide. We also recognise that adapted breathing patterns may include: chronic mouth breathing, chest breathing, breathing with either a high or low breathing rate/volume and excessive tension in the breathing tissues. 
Adapted breathing patterns and a lowered threshold to carbon dioxide puts people ‘on the edge’ of a fear response all the time. Once a person experiences a significant stressor, they are much more likely to activate the Apnea induced Anxiety model. Over time, the recurring activation of the AiA can result in a adapted breathing patterns, a sensitivity to carbon dioxide and a sensitivity to a myriad of stressors. These people begin to experience life as a continuous loop of fear, anxiety and panic states. A life of stress and breathlessness become the norm for them. 
However, all is not lost... 

Breath Training is the Solution 

In writing this article I wanted to explain to you how anxiety works, as we know it today. 
And I also want you to know that in training your breath, you have a tool to reverse engineer this process. 
Breath training teaches you to breathe calmly, restore your breathing and it de-sensitizes you to carbon dioxide. When your breath is restored and your carbon dioxide threshold is elevated, you pull yourself back “from the edge”. As you are exposed to acute levels of stress, you remain calm and you remain aware of your response. The AiA model is not invoked because you can breathe calmly with awareness through the situation. There is less fear, less carbon dioxide exposure, less anxiety and less panic – if any at all. 
This skill is highly transferrable to all fear and anxiety provoking scenarios in life – in an ice bath, on a sports field, during an office meeting, in the heat of an argument with a loved one or even in a trauma-related situation. 
If you want to learn to train your breath to be free, calm and subtle, then take a look at my Breath Training Foundations programme or Breath Training for Health coaching package
Resources for this Article: 
Feinstein, Gould and Khalsa. (2022). Amygdala-driven apnea and the chemoreceptive origin of anxiety. Review. Biological Psychology. Article in Press 
Feinstein, J. S., Buzza, C., Hurlemann, R., Follmer, R. L., Dahdaleh, N. S., Coryell, W. H.,& Wemmie, J. A. (2013). Fear and panic in humans with bilateral amygdala damage. 
Nature Neuroscience, 16(3), 270–272. 
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