This is an appendum to yesterday’s blog –

Ultimately, as this study (1) alludes to, there is a vital role for amygdaloid activity in both anxiety disorders and in alcoholism. It seems, however, to be suggesting that this amygdaloid hyperactivity is mainly prevalent in withdrawal and protracted abstinence.

It does not mention that amygdaloid hyper reactivity may continue to be present in long term recovery or even be evident in pre morbidity?

In other words, this amygdaloid hyperactivity may play a role in terms of a vulnerability to later alcoholism too.

Especially when one considers that alcoholism has been said to be highly co-morbid with other disorders which can also be viewed as based on amygdaloid hyperactivity such as in Generalized Anxiety Disorder, Major Depression, PTSD, etc.

Also given research findings that the majority of alcoholics have experienced some childhood maltreatment such as emotional, mental, physical or sexual abuse or have experienced trauma incidents in childhood there may be an amygdaloid hyperactivity “pre morbidly” also, even prior to substance or alcohol use. It may be a vulnerability factor in the aetiology of alcoholism in fact.

So are we being outlandish to suggest that alcoholism and perhaps other addictive behaviours are also amygdaloid disorders just like other affective, anxiety and mood disorders?

Is the sometimes thorny issue of co-morbidity may be clouding the role of a hyper reactive amygdaloid region of the brain across a range of disorders and manifesting in similar behaviours?

It is often said in term of  anecdote that alcoholics, even in recovery, are fear-based thinkers. Isn’t it reasonable to suggest that it is the influence of the amygdaloid in this, isn’t it this threat-based hyperactivity “doing the thinking” instead of the more reasonable and evaluative prefrontal cortex region of the brain.

It may be that both addictive and anxiety/mood/affective disorders share commonalities in that a hyper reactive amygdala makes sufferers more inclined to over react emotionally and to have related cognitive distortions when faced with threat in the environment. In fact, they may be inclined to experience situations as threat and which induce anxiety when there is no  real or limited threat? There reactions are disproportionate to the environmental of cognitive challenge?

These sufferers may be living in a near constant state of “emergency” when there is no emergency?

We  suggest this amygdaloid hpyerpactivity has similar manifestations in a range of disorders.  It can be shown in relation to the tendency to choose lesser short term immediate gain over greater, long term gain as shown in delay discounting and other  behavioural/emotion tasks and across all these respective disorders.

This hyper-reactive amgydaloid seems to result in a distress based impulsivity which effects decision making too and this is seen in a range of disorders.

Other commonalities such as intolerance of uncertainty, catastrophic thinking etc also seen across a range of affective disorders may also result of an over reactive amygdaloid region being in charge of behaviour instead of the prefrontal cortex.

It would seem in all these disorders that decisions are made to relieve inherent distress and not based on the recruitment of the prefrontal cortex  as a hyperactive amgydala does not recruit the prefrontal cortex when distressed, it recruits “fight or flight” reactions  and “emergency’ type thinking which immediately “offline” the prefrontal cortex in thinking and decision making.

It is thus important we feel to treat the distress at the heart of all addictive behaviours rather  than be bogged down too much in issues surrounding co-morbidity.

It may be that even the similar manifestations of certain co-morbidities get canalized in a general addiction relapse risk and this heightened emotional and stress reactivity should be treated before all else as it can lead to relapse.

In treating this relapse risk we may be getting at the heart of what needs to be treated more generally, regardless of supposed co-morbidity? Namely the errant emotion regulation, decision making deficits, distorted thinking, distress based impulsivity and compulsivity, and emotion processing deficits which accompany hyper reactivity in the amygdaloid region of the bran.

In other words, the distress at the heart of addictive behaviour!

References

1. Gilpin, N. W., Herman, M. A., & Roberto, M. (2015). The central amygdala as an integrative hub for anxiety and alcohol use disorders. Biological psychiatry,77(10), 859-869.