Is there a neurobiological association between childhood trauma, alexithymia, and long-term nicotine smoking?

By Dr. Liji Thomas, MDReviewed by Danielle Ellis, B.Sc.Jan 11 2024

Nicotine use is recognized to be harmful on multiple levels, including brain and heart toxicity. A new study published in JAMA Network Open explores the risk for smoking presented by childhood trauma with subsequent failure of emotional regulation and the neural measures that reflect these risk factors.

Background

Not much is known about what drives long-term smokers to continue the habit. Functional magnetic resonance imaging (fMRI) provides a tool to assess brain function in relation to tobacco use. While many studies have focused on the functional state of the brain at rest, dynamic-state measures could help understand how brain areas coordinate over time or with changing circumstances.

Earlier research based on data from the Human Connectome Project (HCP) reported that the brain showed eight transient network states. These states show common features with the default mode network (DMN) and salience network (SN) states.

The latter are considered to underpin substance use disorders because they react to smoking-associated cues. In addition, they show greater functional coordination during withdrawal and in proportion to the craving experienced.

Temporal dynamics is another field of study that focuses on brain networks associated with substance abuse. This shows three DMN-related states: the frontoinsular DMN (FI-DMN), the canonical DMN, and the occipital sensorimotor DMN (DMN-OSM). These have the same functions but with different aspects.

Thus, the FI-DMN state is linked to meditative thinking as well as emotional self-referential thinking. This could include a more emotional aspect of self-referential thought, like remembering an emotional event. More time spent in this state correlates with increased time spent thinking about negative emotions.

Alexithymia is a term denoting “difficulty identifying or describing feelings and by externally oriented thinking.” Smokers have earlier been identified as having a greater risk of alexithymia, which also poses a risk for substance abuse/other mental disorders.

Alexithymia correlates with neurobiological differences among substance users but not healthy people. Childhood trauma is also linked with neurobiological differences, even among people with the same psychiatric condition. Alexithymia is thus associated with childhood trauma and is responsible for its outcomes, such as self-injury, psychiatric illness in adult life, and vaping.

There have been few studies on how brain functional states vary over time among smokers vs non-smokers and how these are affected by emotional dysregulation or childhood trauma. This led to the current study, which used fMRI coupled with questionnaires to explore childhood trauma and alexithymia.

It looked at temporal dynamic differences in all 8 brain states between smokers and non-smokers, aiming to detect such differences if they exist. Moreover, it explores how childhood trauma, alexithymia and smoking associated with DMN states in the brain.

The study was conducted at the National Institute on Drug Abuse in Baltimore, Maryland. Of the 204 participants, half smoked nicotine.

All participants were adults between 18 and 65 years. They were chronic smokers but had no history of other substance abuse.

What did the study show?

The findings showed that smokers showed significantly more shifts between the different brain states than controls. Smokers spent an average of 25 seconds more in the FI-DMN state compared to others. They also spent more time in DMN-OSM but less in SN and the frontoparietal network (FPN).

Earlier literature shows that nicotine is linked to increased sensorimotor processing, explaining the increased time in DMN-OSM. Conversely, substance use is linked to more DMN activity and increased sharing of information between the DMN and SN.

This coordination between the SN and DMN could explain why increased FI-DMN time is associated with a greater risk of craving and substance use. The FI-DMN is the outcome of functional coordination between both DMN and SN. Though these are separate networks, they work together to sustain nicotine dependence by producing craving and withdrawal symptoms.

“The present study offers novel insight into the temporal engagement of coordinated activity of [these] 2 networks that often work together to maintain nicotine dependence.”

In this group, increased alexithymia was linked to less time spent in this state. The analysis also showed that childhood trauma accounted for the time spent in the FI-DMN state only among smokers.

What are the implications?

Smokers spent more time in the FI-DMN state. However, those who had a history of childhood trauma spent less time in this state. Those smokers who spent less time in FI-DMN had higher alexithymia.

The neurobiological alterations in smokers were linked with childhood trauma only through symptoms, such as alexithymia in this case. This corroborates earlier findings showing reduced DMN-SN connectivity to be linked to alexithymia among substance users but not controls. This indicates that factors stemming from or associated with childhood trauma could drive altered neurobiology, posing a risk for substance abuse.

The authors conclude, “We suggest that too much or too little FI-DMN function may correspond with different aspects of emotional dysregulation (i.e., rumination and alexithymia, respectively), both of which contribute to nicotine craving and use.” Moreover, it is possible, judging from these data, that substance abuse may arise via multiple neurobiological mechanisms, sometimes linked to alexithymia as a result of trauma in early life.

Further research is necessary to detect the direct effects of nicotine on the brain networks and whether the increased time spent in FI-DMN is because of long-term smoking or the cause of this habit. It is also essential to understand whether the inverse correlation with alexithymia represents maladaptation and emotional dysregulation or trauma-induced neurobiological changes.