Intolerance of Uncertainty and Distorted thinking About the Future

Another common area I feel addiction has with obsessive compulsive disorder (OCD) is intolerance of uncertainty (IU).

In fact it is also associated with post traumatic stress disorder (PTSD)- there is actually a high co-morbidity  (at least around 40% comorbidity) with addiction and PTSD and it is one so-called co-morbidity that does not naturally dissipate like some others months into recovery such as Generalized Anxiety Disorder or Depression (the 14% rates of depression and GAD in recovery people are the same as for a normal population) but remains and often makes the symptomatic manifestations of addiction more severe, especially the tendency to engage in “fight or flight” reactions” to uncertainty and ambiguity.

I will blog more on this co-morbidity in later blogs.

The study we cite today in fact looks at IU in addicts who have suffered trauma (1).

Intolerance of uncertainty is a term that refers to a certain way in which some people perceive and respond to situations that are uncertain, and it has been found to be associated with the experience of PTSD symptoms.

Individuals who respond to uncertain or unpredictable situations in this way are considered to have an intolerance of uncertainty. People who are intolerant of uncertainty may begin to experience constant worry about what could happen in the future.

One study (1) demonstrated that negative emotion regulation strategy and intolerance of uncertainty can significantly explain the craving beliefs in addicts (especially those who have suffered a traumatic experience).

This result is consistent with that of Asadi Majareh, Abedini, Porsharifi and Nilkokar (2013) and Nasiri Shushi (2011).

Nasiri Shushi (2011) revealed that there is a significant difference among substance abuse and intolerance of ambiguity and tolerance of uncertainty in two groups of drug abusers.

The other results of this study showed that addicts have less tolerance of ambiguity and tolerance of uncertainty. In the implications of these results it should be expressed that tolerance of uncertainty is associated with cognitive features and addicts when they are faced with difficult situations act in very low levels of performance in terms of decision-making.

Studies carried out to investigate the characteristics of drug abusers suggest that they use substances to regulate a wide range of cognitive events. Undoubtedly unpleasant emotional states, particularly anxiety, depression and stress in addicts are associated with the cognitive consequences.”

The authors suggest that “Drug abusers are not able to tolerate the unpleasant situations and uncertainty in the stressful conditions and their sensitivity leads to mental and emotional problems, therefore, they more turn to substances to regulate their own cognitive experiences (Spada, Nikčević, Moneta, Wells, 2007).

The results of a study showed that individuals with lower tolerance to ambiguity find the ambiguous situations threatening… Many of them may find the substance use in the face of difficulties the only solution and therefore are not able to think or consider other solutions.”

“….While, those with high tolerance to ambiguity in face of unpleasant situation and uncertainty try to find a good solution to get rid of this condition as soon as possible…those with a low tolerance to ambiguity and uncertainty cannot find an appropriate solution…and consequently turn to undetected compromise strategies such as the use of the substance (Ahmadi-Tahoorsoltani and Najafy, 2012).”

I can relate to this study. As I still suffer from intolerance of uncertainty (IU) in recovery, and some years into recovery, it is safe to assume that I suffered form IU in addictive addiction also, if not more so?

For me dealing with an uncertain future can still provoke anxiety. In recovery groups, like AA, we often hear sensible suggestions such as do not “project into the future”, which basically means do not attempt to control future events by thinking about them because this is not only impossible but also anxiety inducing.

The main reason why I think me and other alcoholics cannot project into the future and reasonably reflect and deliberate possible outcomes is because we may have an intrinsic impairment in this regard.

We, or some of us, especially those who have suffered trauma in earlier years, may have IU, like OCD sufferers.

The number of times I rang my sponsor in early recovery to help me with projecting into the future was legion.

Having some one else to talk and share with helps us recruit the pre frontal part of the brain so that we can either see the sense in not not projecting into an unknown future or get help in reasoning through what is likely to occur then.

The difficulty I had and can still have is that my projection into the future is still negatively biased, it is still prompted by distress based cognitive distortions.

As we will see in later blogs these types of cognitive distortions proliferate across a wide range of addictive disorders such as eating disorders which we consider in our next blog.

Among this cognitive distortions is catastrophic thinking which is also distressed based. I will also blog on this at a later date. My head can still run away with itself and convince itself about something which is patently not the case. It can persuade me that this is person or that is doing this or that for these reasons. All of which on reflection are usually nonsense. For me this is like a type of delusion. It is a part of my condition that my head can trick me into believing a whole range of ideas that are delusional. Sometimes I realise this only weeks and months later.

And some people wonder why we turn our lives over to a power greater than ourselves!!?

All this distorted thinking is distressed based.

Which means there is chronically excessive stress chemicals like glucocorticoids being synthesized and whirling around one’s brain. If you give some one enough glucocorticoid there is a good chance they will end up in psychosis. In the 1950s glucocorticoids were used as an anti depressant until people started ending up in psychosis.

Ultimately when we engage in this negatively biased and distorted thinking we have potentially taken the first steps in a walk to relapse because that will eventually seem a whole lot better idea than psychosis?

These cognitive distortions (and there are many)  may even be at the heart of this condition of addictive behaviour.

They are also the consequence of an impaired ability to process emotions (and to avoid) them and thus regulate them. This leads to a tendency to fight or flight which only leads to an heightening of this anxiety, and an increased proliferation of distressing thoughts about future possiblilities, all of which can seem to become more and more catastrophic. How much these thoughts are specifically linked to trauma has to be further explored by research.

For me IU and thought action fusion, especially in early recovery caused as many problems as so-called defects of character. The only difficulty is that they are not mentioned in AA literature, or the Big Book. That does not mean that they do not exist simply because they were not discussed as psychological manifestations commonly known to alcoholics in the 1930s.

They are however known now, which is why I write this blog. To add to our sum of knowledge about this strange illness…

That is not to say having a reassuring sponsor and taking inventory cannot deal with these issues. It is useful however to be aware of them and to realise that not every one in recovery has suffered traumatic incidents. Those who have can have additional requirements in terms of recovery.

I always found it comforting to have a sponsor in the early days who was there and who could also relate to the trauma side of my alcoholism and addiction. It helped soothe me when I could not self soothe. Helped me realise I was not alone in this, that I could recover like this other trauma sufferer could. We can do stuff we can’t do alone.

Ultimately with such an impaired ability to see things reasonably and to make decisions rationally it is imperative to evoke a cardinal recovery rule for me, Accept, Let Go and Let God.

The most profound way to regulated emotions. To Let it Be.

I also used a thing I borrowed and rephrased from Jeffey Schwartz, a leading expert on OCD, how suggested OCD sufferers when in the grip of some obsession to say to themselves “It’s not me it’s my OCD”.

So if your head gets into a downward spiral over some event your head distorts into being and likely to happen in the dark, threatening, Gothic never never world of the future, say to your self “It’s not me it’s my illness.”

In the UK it is called the fanatic in the attic.

It does the thinking for you, if you allow it. Guaranteed.

 

References

Fizollahi, S., Abolghasemi, A., & Babazadeh, A. THE ROLE OF EMOTION REGULATION, DISSOCIATIVE EXPERIENCES AND INTOLERANCE OF UNCERTAINTY IN THE PREDICTION OF CRAVING BELIEFS IN DRUG ABUSERS WITH TRAUMATIC EXPERIENCE.

What is craving?

When I first came into recovery I used to get frightened by other abstinent  alcoholics proclaim that they were so glad they did not get the “wet tongue” when they saw alcohol or people drinking alcohol.  I used to feel ashamed as I did have an instantaneous “wet tongue” and still do  years later when I see people drinking alcohol. Is this a “craving” for alcohol, do I still want to drink? Do I still have an “alcoholic mind?“.

It used to churn me up, these so-called alcoholics who had no a  physiological response to alcohol-related “cues”.

What I have discovered is that I have an “alcoholic brain” and not a “alcoholic mind” and there is a huge difference. So if there are people out there relatively new to recovery, listen up. For chronic alcoholics there is an automatic physiological response when we see cues such as other people drinking. Automatic, habitual, it happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

Some researchers in science call this a craving. I disagree. I call this an physiological urge, distinct from craving. I think a craving is more akin to a “mental obsession” about alcohol.

It is hugely important for recovering persons that we distinguish between urges and craving, in a clear manner that science seems to have been unable to do! Lives can depend on this. We are so vulnerable in early recover that we need so sound direction on what is happening to us automatically and what we are encouraging to happen, consciously.

An urge for me is a physiological response to cues, external and internal (e.g. stress). A craving is different but interlinked.

If I have an urge and it becomes accompanied by automatic intrusive thoughts such as a drink would be nice, and maybe a suggestion on where to get this drink, this does not mean I want a drink. It is simply automatically prompted intrusive thoughts, the type of thought I used to get all the time and so became habitual, became stored away in an automatized addiction schema or addiction action plan.

If I realize this and simply  these thoughts go, i.e. do not react to them, then they lessen and dissipate altogether.

This is not a craving. I have not consciously and emotionally engaged with these intrusive thoughts.

So what I am saying is that there is no simple urge state that automatically leads to drink. We have to cognitively and emotionally react to it.

In my time in recovery, I have rarely heard of or witnessed  someone lured siren-like by a cue to a drink and when I have it is because he wanted to drink really, were testing their alcoholism, or that he was in huge emotional distress and went to “hell with it!”. As we will see below, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

In the first of a four part series of blogs we discuss “what is craving?” and consider whether the emotional dysregulation we consider to be at the heart of alcoholism and addiction also plays a role in both craving and relapse.

We start this series by considering the neurobiological accounts of craving and will then consider how well these accounts explain craving and relapse in abstinent, treatment seeking, or recovering alcoholics and addicts.

Part 1

What is craving?

Craving persists years into abstinence (1).

Precise definitions of craving have remained elusive (2-5). Two general categories are based on conditioning and cognitive mechanisms (6) but are not mutually exclusive.

A Neuroadaptive Model of Craving – Scientists believe that a gradual and, perhaps, permanent adaptation of brain function (i.e., neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence (7,8).

Conditioning Models – The “conditioning” models posit that cues elicit the same physiological and psychological response as drug consumption itself  with these ‘respondent’ conditioning theories predicting that responses to drug-related cues either reflect aversive abstinence symptoms or mimic drug effects  have dominated explanatory models in cue reactivity studies (9).

The definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms craving and persistent risk, and emphasises risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors (10).

This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

The Incentive Sensitisation (IS) Model (11), addiction is the result of neural sensitisation of reward circuits (centred in the ventral striatum (VS)) by the neurotransmitter dopamine. Positive reinforcement mechanisms lead to a non-associative learning process, referred to as sensitization, in which repeated confrontation with a substance-related cue (which acts as a reinforcer) results in the progressive amplification of a response (substance seeking).

This ‘sensitisation’ or hypersensitivity may be independent of negative withdrawal symptoms or an individual’s general negative emotional state and leads to compulsive substance-seeking and substance-taking. These mechanisms of positive reinforcement leave addicts vulnerable to relapse when confronted with substance-related cues that trigger a pathological “wanting”. In short, IS produces a bias of attentional processing towards substance-associated stimuli and a pathological wanting of alcohol or substances. Sensitisation and attentional bias have been demonstrated in various studies (12,13).

Negative reinforcement model of addiction Basic negative reinforcement models pose that addictive behaviour is the consequence of persistent negative affect (NA). This NA is associated with maladaptive changes in the brain’s stress and reward circuits, which leave addicts vulnerable to cue-associated stimuli prompting a desire to relieve their negative emotional states (14).

One prominent stress-based negative reinforcement model, the Hedonic Dysregulation (HD) Model, mainly associated with Koob and le Moal (14), In sum, the HD model posits that, in substance dependent individuals,  an overactive stress  axis creates a progressive allostasis in the brain reward systems which underlies transition from substance use to addiction and creates a persistent state of NA (altered and excessive stress) and emotional reaction to “cues”. These changes continue to persist even when an addicted individual experiences a state of protracted abstinence.

Persistent NA increases their incentive salience and desire to use substances in an attempt to relieve this NA.

Evidence for the involvement of both the reward and the stress system of the brain  comes from imaging studies of addicted individuals during withdrawal or protracted abstinence, which have shown decreases in dopamine D2 receptor density (hypothesized to reflect hypodopaminergic function) (15) as well as alteration in brain stress systems, such as increase in CRF and glucocorticoids (16).

These models to me appear to be describing urges based on cues and the effect of cues with stress/emotional distress. This last one can impact on recovery and relapse mentioned in another blog.

The question remains however whether these neurobiological models predict relapse in abstinent alcoholics and addicts?

 

References 

1.  Anton, R. F. (1999). What is craving. Alcohol Research and Health23(3), 165-173.

2. LUDWIG, A.M., AND STARK, L.H. Alcohol craving: Subjective and situational aspects. Quarterly Journal of Studies on Alcohol 35:899–905, 1974.

3. KOZLOWSKI, L.T., AND WILKINSON, D.A. Use and misuse of the concept of craving by alcohol, tobacco, and drug researchers. British Journal of Medicine 82:31–45, 1987.

4.  KOZLOWSKI, L.T.; MANN, R.E.; WILKINSON, D.A.; AND POULOS, C.X. “Cravings” are ambiguous: Ask about urges and desires. Addictive Behaviors 14:443–445, 1989

5.  SITHARTHAN, T.; MCGRATH, D.; SITHARTHAN, G.; AND SAUNDERS, J.B. Meaning of craving in research on addiction. Psychological Reports 71:823–826, 1992.

6. SINGLETON, E.G., AND GORELICK, D.A. Mechanisms of alcohol craving and their clinical implications. In: Galanter, M., ed. Recent Developments in Alcoholism: Volume 14. The Consequences of Alcoholism. New
York: Plenum Press, 1998. pp. 177–195.

7. Robinson, T.E., & Berridge, K.C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research, 18, 247-291

8. Koob GF, Le Moal M. Drug abuse: hedonic homeostatic dysregulation. Science. 1997;278:52–58

9.  Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.

10.  Morse RM, Flavin DK (1992). “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism“. JAMA 268 (8): 1012–4

11. Robinson, T. E., & Berridge, K. C. (2008). The incentive sensitization theory of addiction: some current issues. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3137-3146

12. Leyton M. Conditioned and sensitized responses to stimulant drugs in humans. Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007;31:1601–1613.

13. Franken, I. H. (2003). Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(4), 563-579

14. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

15. Volkow ND, Wang GJ, Fowler JS, et al. Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature. 1997;386:830–3.

16.. Koob GF, Le Moal M. Addiction and the brain antireward system. Annu Rev Psychol. 2008;59:29–53