Friday, 25 May 2018

How Misreading Bodily Signals Causes Anxiety

It’s 9 AM Monday morning. You’ve just pulled into work and are ready to pitch your presentation to the senior management team. Your PowerPoint slides are damn near perfect and you’ve gone over the script dozens of times. You’ve got this.

As everyone gathers in the room, you’re suddenly flooded with a hit of adrenaline. The bad kind. In a flash you become acutely aware of what your body is doing: beads of sweat forming on your brow, a dry mouth that no amount of water can fix, and a steadily increasing heart rate thumping inside your chest.

This ability to perceive the signals of your body is known as interoceptive accuracy (IAc). There are, as the example demonstrated, different psychosomatic cues that you pick up within yourself during states of anxiety. But above all, a beating heart is the hardest one to ignore.

It’s for this reason that heartbeat perception, as brain scientists call it, is a direct proxy for measuring people’s IAc and reported anxiety and stress levels.

IAc and a beating heart

Having the ability to accurately detect your own heartbeat is critical for reappraising your anxiety on a moment to moment basis. We know that anxiety is as much in the body as it is in the mind, and that a (mis)perception of a fast heart rate can easily contribute to the catastrophization of a panicked state.

It’s why some of the most effective anxiety-related therapies, like progressive muscle relaxation and deep breathing, tend to focus on muting a physiological response followed by a cognitive reappraisal technique.

Now in terms of IAc, the longstanding view was that it is an inherited trait, similar to eye color or height. Your IAc is immutable, unchanging. But now there’s new evidence suggesting that the situation matters just as much as the person: While some people may have inherently bad interoceptive ability, we can’t ignore the influence of the broader context. And this, if it turns out to be true, is a definite win for anyone looking to reverse a certain anxiety-based predisposition.

The study and findings

A team of researchers led by Martin F. Whittkamp out of the University of Luxembourg  set out to investigate just how much of a role the environment plays in determining our ability to self-reflect on accurate biofeedback.

The researchers relied on two methods to measure IAc via heartbeat perception. The first, called the counting task is simply a comparison between actual measures of your heartbeat with your self-reported measures. Another method, called the heartbeat discrimination task, measures how accurately you can rate whether or not your heartbeat is in sync with an external stimulus such as a blinking light on a computer screen.

The team in this newest study compared the results of both a heartbeat counting task and discrimination task in two conditions: a resting state and a stress state. Mental stress was induced by having participants match the color of a flashing light bulb with a corresponding button as fast and accurately as possible. If this wasn’t stressful enough, the experimenter also chimed in with a few verbal cues urging the participant to perform better so as to not ruin the entire experiment.

In addition to comparing stress state IAc with resting state IAc, the researchers also designed a number of computational models. These models aimed to measure how much of one’s interoceptive accuracy is owed to individual ability versus the situation.

The results found that about 40% of a person’s IAc can be explained by his/her individual traits, while around 30% can be explained by the changing situation, leaving the remaining 30% to measurement error.

What this says is that your ability to detect and therefore modulate your bodily responses during an anxious state is not fixed. These signals are amenable to change. You can learn to more accurately perceive your beating heart in a high-stress environment. You can apply reappraisal techniques in mitigating your anxiety.

The findings of this study have the potential to inform research on stress and anxiety management. For example, having a general idea of how much your IAc is dependent on biological predisposition could provide leeway to pharmaceutical interventions to help combat debilitating responses to stressful situations.

For now there’s therapeutic power in knowing you can improve your IAc and work towards minimizing your anxiety.

References

Feldman, G., Greeson, J., & Senville, J. (2010). Differential effects of mindful breathing, progressive muscle relaxation, and loving-kindness meditation on decentering and negative reactions to repetitive thoughts. Behaviour Research And Therapy, 48(10), 1002-1011. doi: 10.1016/j.brat.2010.06.006

Knoll, J., & Hodapp, V. (1992). A Comparison between Two Methods for Assessing Heartbeat Perception. Psychophysiology, 29(2), 218-222. doi: 10.1111/j.1469-8986.1992.tb01689.x

Richter, D., Manzke, T., Wilken, B., & Ponimaskin, E. (2003). Serotonin receptors: guardians of stable breathing. Trends In Molecular Medicine, 9(12), 542-548. doi: 10.1016/j.molmed.2003.10.010

Wittkamp, M., Bertsch, K., Vögele, C., & Schulz, A. (2018). A latent state-trait analysis of interoceptive accuracy. Psychophysiology, 55(6), e13055. doi: 10.1111/psyp.13055

Image via mohamed_hassan/Pixabay.

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Thursday, 24 May 2018

Why We Don’t Remember Early Childhood?

Although early experiences are important for personal development and future life, as adults we recall nothing or very little of those early formative events, such as making first steps or learning first words. In fact, when adults are asked about their first memories they usually don’t recall events before the age of 2-3, with only fragmented recollection of events that happened between the age of 3 and 7. This phenomenon is often called childhood or infantile amnesia. It represents an inability of both children and adults to recall episodic memories (i.e., memories for particular events or stimuli that occur in a particular context) from infancy and early childhood, before the age 2-4.

Sigmund Freud was the first researcher to develop the theory of infantile amnesia, as he had observed that his patients rarely had been able to recall memories of events that took place during the first years of life. He believed that childhood memories are being repressed and thus forgotten. Still, modern theories focus on cognitive and social development as an important predictor of childhood amnesia. One possible explanation of childhood amnesia is the lack of neurological development, i.e., the development of brain parts that are in charge of storage and retrieval of episodic memories. For instance, some researchers believe that the development and functioning of the prefrontal cortex (cortex area at the front of the brain) is crucial for the creation of contextualized memories. Moreover, the prefrontal cortex and hippocampus are assumed to be crucial for the development of autobiographical memories. Importantly, these two brain structures develop around the age of 3 or 4.

The lack of neurological maturation, i.e., maturation of brain structures required for creation, storage, and recall of memories during infancy and early childhood might explain the phenomenon of childhood amnesia. According to this explanation, childhood amnesia occurs not due to the loss of memories over time (the forgetting explanation), as Freud had suggested, but rather due to the lack of storing of these memories in the first place. The lack of stored memories, according to this theory, is due to brain immaturity.

Some evidence has suggested that amnesia for events taking place in early childhood (before the age of 2) could be at least partly explained by difficulties with verbally recalling memories that were encoded before language acquisition. In line with this is the fact that the majority of words (the vocabulary) are acquired between the age of 2 years and 6 months and 4 years and 6 months. This is the time period that the earliest memories can be recalled.

Childhood amnesia seems not to be an exclusively human phenomenon. Indeed, some researchers have observed something like infantile amnesia in animals (for instance, rodents). The discovery of amnesia in animals has pointed to the possibility of investigating the underlying mechanisms of childhood amnesia, such as neurological events, by using animal models. The animal studies have addressed the importance of some parts of brain and their development in relation to the childhood amnesia. For instance, they have indicated that high rate of neurogenesis in hippocampus as observed in infancy might explain the accelerated forgetting of contextual fear memories. It seems that integrating of new neurons into the existing circuit might destabilize and weaken the existing memories.

Some researchers believe that it is unclear whether childhood amnesia occurs due to the failure of memory retrieval or failure of their storage. Forgetting might be described as a linear function of the time passing since the event. Since there is a long time span between the early events and recall in adulthood, it might be assumed that early events are simply forgotten. Still, some researchers disagree. This is because they have found that subjects recall far less memories for events occurring between the age of 6 and 7 as would be expected by simply extrapolating the forgetting curve. Thus, forgetting could not completely explain the phenomenon of childhood amnesia. This is why a neurogenic hypothesis of childhood amnesia has been developed.

According to its inventors, a neurogenic hypothesis explains childhood amnesia through the continuous adding of new neurons (neurogenesis) in the hippocampus, as already mentioned above. According to this hypothesis, high levels of postnatal neurogenesis (which occurs in both humans and some animals) in the hippocampus prevents the creation of long-lasting memories. This hypothesis has been experimentally tested in animal models (mouse and rat). The findings emerging from these models have proposed that high levels of neurogenesis jeopardize the formation of long-term memories, possibly by replacement of synapses in pre-existing memory circuits. In addition, the same findings indicate that the decline in hippocampal neurogenesis corresponds with the emerging ability to form stabile memories.

Thus, according to these animal studies, the theory of neurogenesis appears to be a logical explanation for childhood amnesia.

Although the early theory regarding the forgetting or repressing of memories might look like a good explanation of childhood amnesia, more recent findings demonstrate that something else is happening in our brain that contributes to this phenomenon. Whether this is the lack of development in some brain parts, or the continuous synthesis of new neurons, or both, remains to be further investigated. Childhood amnesia cannot be explained by simple forgetting.

References

Newcombe, N., Drummey, A., Fox, N., Lai, E., Ottinger-Alberts, W. (2000) Remembering Early Childhood: How Much, How, and Why (or Why Not). Current Directions in Psychological Science. 9 (2): 55–58.

Hayne, H., Jack, F. (2011) Childhood amnesia. Wiley Interdisciplinary Reviews. Cognitive Science. 2(2): 136-145. doi: 10.1002/wcs.107

Simcock, G., Hayne, H. (2003) Age-related changes in verbal and non-verbal memory during early childhood. Developmental Psychology. 39: 805–814. PMID: 12952395

Madsen, H.B., Kim, J.H. (2016) Ontogeny of memory: An update on 40 years of work on infantile amnesia. Behavioural Brain Research. 298(Pt A):  4-14. 10.1016/j.bbr.2015.07.030

Wetzler, S.E., Sweeney, J.A. (1986) Childhood amnesia: An empirical demonstration. In Autobiographical memory (ed. DC Rubin), pp. 191–201. Cambridge University Press, New York, NY.

Josselyn, S.A., Frankland, P.W. (2012) Infantile amnesia: a neurogenic hypothesis. Learning and Memory. 19(9): 423-433. doi: 10.1101/lm.021311.110

Image via VABo2040/Pixabay.

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Wednesday, 23 May 2018

Tuesday, 22 May 2018

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Monday, 21 May 2018

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Friday, 18 May 2018

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Thursday, 17 May 2018

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Wednesday, 16 May 2018

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Tuesday, 15 May 2018

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Monday, 14 May 2018

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