I come from a family of four siblings, two of whom are alcoholic and two who are not. I have often wondered why this is the case? Why is it the case that certain children of alcoholic parents will grow up to become alcoholics and why some will not? What is it that makes certain children vulnerable to alcoholism and other children, from the very same family, protected. What do these children have that protects them from later alcoholism?

This is especially important to know in terms of prevention strategies to help children at risk.

Throughout our blogs has been a thread suggesting alcoholics, and children of alcoholics, may have difficulties in processing and regulating emotions. Is this the vulnerability, is there a difference in affective/emotional circuitry in the brain?

We cite a very interesting article here  Affective circuitry and risk for alcoholism in late adolescence: Differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents

in setting out an argument that children of alcoholics who are at greater risk of later alcoholism may have inherited impairments in brain neural circuitry which is responsible for affective/emotional processing.

Children of alcoholics (COAs) are at elevated risk for alcohol use disorders (AUD), yet not all COAs will develop AUD. One aim of this study was to identify neural activation mechanisms that may mark protection or vulnerability to AUD in COAs.

 

 

Some differences between alcohol abusers and control samples may precede alcoholism onset and thus constitute markers of precursive risk. After all, behavioral and affective markers early in life can predict later alcoholism (Caspi et al., 1996; Mayzer et al., 2001). Thus, it is reasonable to hypothesize that pre-alcoholic differences in the functioning of relevant neural systems will be related to risk for alcoholism.

In hoping to identify neural activation mechanisms that may mark protection or vulnerability to AUD in children of alcoholic fathers, the guiding conceptual framework was that the functioning of affective and behavioral regulation networks in the brain may serve as such mechanisms.

Consistent with that framework, the resilient and vulnerable groups were distinguished from one another by remarkably consistent inverse or opposite patterns of activation in the brain in response to the processing of emotional stimuli and which were most apparent with regard to negative affective stimuli and the vulnerable group.

These results suggest separate pathways of risk and resilience in the COA’s. First, the COA group that was not prone to early problem drinking (the resilient group) had more activation of the orbital frontal gyrus (OFG) than controls in response particularly to negative affect stimuli, but also to some extent in response to positive affect stimuli. The OFG is involved in the monitoring and evaluation of the affective value of stimuli, allowing for appropriate behavioral responses (Kringelbach and Rolls, 2004; Rolls, 2004).

The resilient group also had increased left insula activation to negative words. The insula is involved in evaluating internally generated emotions and the monitoring of ongoing internal emotional state (Phan et al., 2002).

The present findings, then, are consistent with the hypothesis that resilient youth have enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth. Yet, in an important nuance, they did not suppress the emotional experience.

They were prepared to modify behavioral response while maintaining affective response to these stimuli. This pattern of response in resilient youth may represent increased flexibility in emotional and social behavior.  These youth may be exhibiting precisely an ability to delay external response to arousing stimuli, while internally processing those stimuli. In short, this may be a “reflective” pattern of approach to the world.

It is not difficult to speculate how this pattern might protect these at risk youth from substance misuse: they are able to respond to the emotional stimuli, but demonstrate enhanced monitoring that may allow for the inhibition of inappropriate responding, buying time for flexible response options based on well-processed information.

Interestingly, the vulnerable group displayed no differences from the control group in emotional monitoring and behavioral regulation systems (OFG and insula), suggesting that weakness in that system is not a risk factor. Rather, they demonstrated over-activation of DMPFC and an atypical under-activation of key emotion processing regions (particularly extended amygdala and ventral striatum). This pattern was more notable in regard to negative affect, it was also observed to a lesser extent with positive affect.

All of this may be consistent with a reactive approach to the world, in which affect is not fully processed.

Supporting this interpretation, neuroimaging studies have consistently shown the involvement of the DMPFC with conscious self-monitoring of emotional responses (Beauregard et al., 2001;Kuchinke et al., 2006; Levesque et al., 2003; Levesque et al., 2004; Phan et al., 2005). For example, during the voluntary suppression of negative affect in healthy adults, activation in the dorsal medial and lateral prefrontal cortex increased and that in the nucleus accumbens and extended amygdala decreased (Phan et al., 2005). It has been suggested that emotional information is conveyed from limbic regions to the prefrontal cortex allowing conscious, voluntary emotional self-regulation (Levesque et al., 2003; Levesque et al., 2004).

Therefore, one interpretation of the present findings is that the vulnerable youth were recruiting an emotional control system that was suppressing emotional response.

 

References

Heitzeg, M. M., Nigg, J. T., Yau, W. Y. W., Zubieta, J. K., & Zucker, R. A. (2008). Affective circuitry and risk for alcoholism in late adolescence: differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents. Alcoholism: Clinical and Experimental Research, 32(3), 414-426.