What makes some children of alcoholics vulnerable, and some resilient?

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.

Obviously environment has an impact on vulnerability but does an inherited protectiveness help prevent this sometimes dysfunctional and abusive childhood environment of alcoholic parenting from having the same impact as those children who have inherited a genetic vulnerability?

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.


Thoughtful little girl


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.



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.


Abusive Childhoods Increase Risk of Later Alcoholism

Sitting in AA meetings over a number of years I have been struck by the amount of stories I have heard about fellow AAs having had abusive childhoods and have always wondered how much this sort of maltreatment in childhood contributes to later alcoholism.

In my research I have found that child maltreatment has been frequently identified in the life histories of adolescents and adults in treatment for substance use disorders, as well as in epidemiological studies of risk factors for substance use and abuse.

Ample evidence exists for higher rates of substance abuse and dependence among maltreated individuals (1) so much so that alcoholism and addiction for many represent a developmental cascade.

In clinical samples undergoing treatment for substance use disorders, between one third and two thirds evince child abuse and neglect histories (2-7).

In a survey in The USA, of over 100,000 youth in 6th though 12th grade, Harrison, Fulkerson, and Beebe (1997)  found that those reporting either physical or sexual abuse in childhood were from 2 to 4 times more likely to be using drugs than those not reporting abuse; the rates were even higher for youth reporting multiple forms of child maltreatment (8).

Similar findings (9,10) have been reported by Rodgers et al. (2004) and Moran, Vuchinich, and Hall (2004). Among youth with Child Protective Services documenting maltreatment, Kelly, Thornberry, and Smith (1999) reported one-third higher risk for drug use among those with an abuse history(11).




In a large epidemiological study, Fergusson, Boden, and Horwood (2008) showed physical abuse and particularly sexual abuse to be related to illicit drug use, as well as abuse and dependence (12).

It also appears that  extreme economic deprivation characterizes many maltreating families who are residing in impoverished areas with substantial neighborhood disorganization and ample availability of drugs in the community(13).

Hawkins, Catalano, and Miller’s (1992) highlighted poor and inconsistent family management practices, high family conflict, and poor bonding to family as risks for adolescent substance abuse, and these factors also are characteristic of the dysfunction in maltreating families in which abuse and neglect occur.

These features are consistent with the progression of developmental failures exhibited by maltreated children (14).

Consequently, compromised adaptation in the social and academic arena contributes to association with deviant peers, who escalate the access to and modeling of substance abuse, contributing to early onset of drug use.


For many the propensity for later alcoholism and drug addiction are determined in part by genetic inheritance but all genetic transmission also relies on environmental conditions.

It would appear that abusive childhoods and emotional deprivation provide fertile grounds.



1.  Rogosch, F. A., Oshri, A., & Cicchetti, D. (2010). From child maltreatment to adolescent cannabis abuse and dependence: A developmental cascade model.Development and psychopathology22(04), 883-897.

2.  Bayatpour M, Wells RD, Holford S. Physical and sexual abuse as predictors of substance abuse and suicide among pregnant teenagers. Journal of Adolescent Health. 1992;13:128–132.

3. Cavaiola AA, Schiff M. Behavioral sequelae of physical and/or sexual abuse in adolescents. Child Abuse & Neglect.1988;12:181–188.

4. Dembo R, Dertke M, Borders S, Washburn M, Schmeidler J. The relationship between physical abuse, sexual abuse and tobacco, alcohol, and illicit drug use among youths in a juvenile detention center. International Journal of the Addictions.1988;23:351–378

5. Edwall GE, Hoffman NG, Harrison PA. Psychological correlates of sexual abuse in adolescent girls in chemical dependency.Journal of Adolescent Chemical Dependency. 1989;1:53–68.

6. Pribor EF, Dinwiddie SH. Psychiatric correlates of incest in childhood. American Journal of Psychiatry. 1992;149:52–56.

7. Schaefer MR, Sobieragi K, Hollyfield RL. Prevalence of child physical abuse in adult male veteran alcoholics. Child Abuse & Neglect. 1988;12:141–150.

8. Harrison PA, Fulkerson JA, Beebe TJ. Multiple substance use among adolescent physical and sexual abuse victims. Child Abuse & Neglect. 1997;21:529–539.

9. Harrison PA, Fulkerson JA, Beebe TJ. Multiple substance use among adolescent physical and sexual abuse victims. Child Abuse & Neglect. 1997;21:529–539.

10. Moran PB, Vuchinich S, Hall NK. Associations between types of maltreatment and substance use during adolescence. Child Abuse & Neglect. 2004;28:565–574.

11. Kelly BT, Thornberry TP, Smith CA. In the wake of child maltreatment. Washington, DC: Office of Juvenile Justice and Delinquency Prevention; 1997. pp. 1–15.

12.  Fergusson DM, Boden JM, Horwood LJ. Exposure to childhood sexual and physical abuse and adjustment in early adulthood.Child Abuse & Neglect. 2008;32:607–619.

13.  Hawkins JD, Catalano RF, Miller JY. Risk and protective factors for alcohol and other drug problems in adolescence and early adulthood: Implications for substance abuse prevention. Psychological Bulletin.1992;112:64–105.

14. Cicchetti D, Valentino K. An ecological transactional perspective on child maltreatment: Failure of the average expectable environment and its influence upon child development. In: Cicchetti D, Cohen DJ, editors. Developmental psychopathology: Vol. 3. Risk, disorder, and adaptation. 2nd ed. New York: Wiley; 2006. pp. 129–201

Alcoholics as secret overachievers!

A recent article suggests that  some people may have a genetic predisposition to alcoholism. Dr Alexander Niculescu  and his team, identified 11 “risk” genes (1) that can predict which people are more at prone to becoming alcoholic. For those with a family history of alcoholism, the danger is even greater. All of this can be detected with a simple genetic test.

“Having a family history already suggests that there is a genetic risk that’s being transmitted. Those people should not expose themselves to temptation and drink even small amounts, as they are more prone to go down a slippery slope of higher amounts of alcohol and full-blown alcoholism,” Dr Niculescu said.

Dr Niculescu said these gene variants also have a lot to do with drive and compulsions, which can be used for positive things like professional achievement. “What we are discovering at the biological level is that there is this physiological robustness and drive that goes hand in hand with predisposition or compulsion to alcoholism and if you manage to avoid getting sucked into alcoholism and just use your biological endowments and drive for other things, you might be an overachiever in other areas.”

In the conclusion to the article it states that  it is likely at its core a disease of an exogenous agent (alcohol) modulating different mind domains/dimensions (anxiety, mood and cognition) precipitated by environmental stress on a background of genetic vulnerability (2).

In simple language, this is what we have been suggesting in this blog. Alcohol acts on underlying mechanisms  relating to anxiety, mood, cognition, which we view under the umbrella term of emotional regulation and processing deficits.

It also shows how genetic vulnerability may overlap with other psychiatric disorders, overlap does not mean the same as.





The oft cited co-morbidities which supposedly co-occur alongside alcoholism are in fact not co-morbidity in our view  but intrinsic to the condition. Although this argument and article at least acknowledges there is a growing debate about what constitutes co-morbidity and pathology in alcoholism.

For us alcoholism is these so-called “co-morbidities” mixed with the deleterious effects of chronic alcohol on these deficits and which are commonly exacerbated pre-morbidity or before the actual start of alcohol use by traumatising or distressing early childhood experiences which have been known to result in both stress and emotional dysregulation which in turns leads to a heightening of the rewarding effect of alcohol (or drugs) as stress chemicals increase dopamine in reward networks such as the nucleus accumbens. Alcoholics find a “solution” to their emotional difficulties in the the heightened, calming effects of alcohol and eventually find in the course of time and chronic use that they cannot do without it.

For us genetically, this research is showing what manifestly, in terms of emotional and behavioural problems, is being shown by cognitve, affective and clinical neuroscience.

It also explains why so many recovering alcoholics surprise us and themselves, especially those underachievers at school of which I am one, with their vigour, intelligence and achievements in recovery once they have climbed out of their own personal hell of active alcoholism.

It also explains how they physically survived ordeals which would have killed most. 


Levey, D. F., Le-Niculescu, H., Frank, J., Ayalew, M., Jain, N., Kirlin, B., … & Niculescu, A. B. (2014). Genetic risk prediction and neurobiological understanding of alcoholism. Translational psychiatry4(5), e391.

Niculescu AB 3rd, Schork NJ, Salomon DR. Mindscape: a convergent perspective on life, mind, consciousness and happiness. J Affect Disord2010; 123: 1–8. |