A Final Word and a New Page?

A Final Word – before I get all close up and personal next week  with our new format on Alcoholics Gide to Alcoholism which will now be blogs, 600 words or less, based on my own experience of addiction and recovery. Written specifically for those thinking of coming into or actually coming into recovery and their families.

I want to help explain in more simply terms this most profound of conditions – this strange illness of mind, body and spirit.

I will still blog on the latest neuroscientific,  neuropsychological and neurotheological insights into addiction and recovery on my other blog insidethealcoholicbrain.com – it was always intended that I was personal on one blog and a researcher on the other.

Now I am clearly letting you, my readers, know of my intentions.

I have to say I can’t wait to get my teeth into the new format.

I can’t tell you how much effort it has been over the last year, continuously writing research blogs?

I now believe most of what you need to know about addiction from a neurobiological, emotion and cognitive perspective can be found on these blogs if you look around them. We have covered much ground.

 

But there is more to this strange illness which can only be fully explained via sharing my story and hopefully you sharing your stories.

12 step groups primarily work via story sharing and fellowship/support, which allows newcomers to identify with the progression of an illness in others while identifying this progression in themselves.

Listening to these stories usually shows the newcomer what the solution is also.

The power of identification is why I am here, sober and in recovery since 2005.

I identified with what a bunch of strangers in a room in a parish chapel said about their illness, their struggles to live life on life’s terms, their descent in alcoholism and addiction, their rock bottoms and their turning points to eventually finding their solution to their problems.

The necessary psychic change happened in my first meeting – I suddenly realised what my problem was and where I could get the solution.

I found through their stories that I identified with these strangers, that I belonged for the first time, in this club. I had found my tribe for the first time ever in my life.

These people could help me. The first glimmers of hope.

Hopefully  identifying with what I write about will set you on your journey to recovery  or help you on the journey you have already started.

I want to hear from you!!

But I wanted to set out my comprehensive view of addiction so that one can find a whole view as regards addiction and recovery in one blog. I believe my theory of addiction and recovery stands up to the highest scrutiny and certainly reflects my own experience and the experience of hundreds and hundreds of alcoholics, addicts and those suffering other addictive behaviours.

There is so much more to addiction than the substance or behaviour used! Hopefully science will grasp that idea fully in time.

Neurobiology affects emotion which affects thinking. Go figure?

Maladaptive neurobiology and endocrinology affects impaired emotion regulation which distorts thinking in those suffering addictive behaviours.

 

Before that however, notification of another new Page! 

This page will be dedicated to addressing the co-occurrence of  other psychiatric conditions with addiction and addictive behaviours.

For example, conditions such as post traumatic stress disorder and generalized anxiety disorder and major depression are said to frequently co-occur with addictive disorders.

This page will be addressing how frequently these disorders actually co-occur with addiction, or whether their influence has been overstated.

How they should be treated, whether treatment for addiction can help with these disorders too or whether they should be treated separately and importantly whether these so-called co-morbid conditions are tributaries which feed into the overall disorder of addiction?

In other words, when we receive treatment specifically for addictive behaviours are we also treating the conditions which have canalized into addiction.

 

 

If so does medication help or hinder sobriety and recovery, especially if prescribed based on a misdiagnosis of addictive disorder showing as an affective disorder?

When considering relapse prevention, are we addressing behaviours and responses to negative emotions and stress reactivity which are common to all affective disorders?

Do these conditions all contribute to addiction severity?

Do they contribute to similar hyper amgydaloid reactivity, to the same cognitive distortions, to similar “fight of flight” responding, to common recruitment of more motoric parts of the brain when making decisions, to similar rumination, in effect to a similar profile of emotion dysregulation?

Do they all have common neurotransmitter deficits, similar dysregulated stress systems and reward networks?

Is addiction a unitary disorder whereby negative affect leads to an impulsive, urgent desire to regulate these emotions by external means such as substances and behaviours, whereas other affective disorders do not have this behavioural manifestation?

Is negative urgency a trait that distinguishes between addictive behaviour and other affective or psychiatric disorders?

These questions seem very pertinent in trying to understand if addiction is in fact a unitary disorder in it’s own right or whether it is a unitary disorder also affected by co-morbidity?

Are so-called co-morbidities really co-morbidities or are they substance induced disorders which dissipate in the early weeks of recovery?

Do they manifest as anxiety and depression in active addiction but disappear when a neuro-toxic substance is eliminated from one’s nervous system?

Or perhaps we continue to have anxiety type issues in recovery but do not appreciate this because we are managing these issues with 12 step recovery?

One way or the other, surely addiction is more than use of substance of behaviour despite negative consequences. Surely it is more than simply reducible to use of substance or behaviour alone?

If addiction is a unitary disorder how come we appear to share common distorted thinking and maladaptive behaviours as a range of other affective disorders?

Do the vast majority of us have various affective disorders which lead to chronic reliance on substances or behaviours?

Or is addiction a unitary disorder in it’s own right? A disorder neuro science and psychology knows little about – so little they relegate all it’s emotion dysfunction to that of co-morbidity?

The answers to these questions seem more urgent now than ever before?

In this page we will attempt to answer some of these questions.

We will address the reality that addiction shares a  multitude of cognitive distortions and maladaptive responses and behaviours with other affective disorders.

Why is this? Are these disorders different and how so?

Are there similar underlying neuro-mechanisms with all these disorders?

What it is about addiction that sets it out as a disorder separate from all other disorders?

For example, we believe addiction has a distress based impulsivity at its core which is based on a lack of emotion clarity and differentiation which results in risky (impulsive) maladaptive decision making. This appears to differentiate addiction from other affective disorders?

This makes addiction a disorder of “just one more…that’s all I need” – it is an affective disorder which results in a motivation to alter feelings via external means.

One may also be able to use certain scales such the Difficulties in Emotion Regulation DERS scale which appears to be able to differentiate between different disorders.

Ultimately, are all these disorders similar in their emotion dysregulation but not in the manifestation of this emotion dysregulation in terms of manifest behaviour?

Have we been diagnosing some affective disorders for years when they are often addictive disorders in disguise?

 

How do you know when Medicating becomes Self Medicating?

A recent blog in the After the Party Magazine  has raised some very pertinent questions about the issue of co-morbidity in alcoholics and addicts seeking recovery via 12 step groups and suggests the extent of this co-morbidity is much higher than may have been anticipated.

This blog raises important issues but ultimately may leave more questions than it answers?

The blog starts “You hear it in 12-step meetings all the time—people who were once on psych meds discovered they didn’t need them after getting sober and doing the steps. Now they’re evangelizing at every meeting in town about how their problem was really just spiritual. Maybe they were never mentally ill to begin with or maybe the steps really did banish their mental illness right out of their brains. But for me, and plenty of others I know, this isn’t the case.”

The author then continues ” If anyone has any questions about psychiatric meds AA has an official stance that’s in a pamphlet called The AA Member—Medications and Other Drugs. ”

I referred to this pamphlet on Monday’s blog Can you be Sober and in Recovery while on Medication?

As I mentioned then the pamphlet appears to be alerting AA members to the reality that certain members “must take prescribed medication for serious medical problems. However, it is generally accepted that the misuse of prescription medication and other drugs can threaten the achievement and maintenance of sobriety”.

As the author notes this pamphlet states ” “No A.A. member should ‘play doctor’; all medical advice and treatment should come from a qualified physician.”

It also states that “Some of us have had to cope with depressions that can be suicidal; schizophrenia that sometimes requires hospitalization; bipolar disorder, and other mental and biological illnesses.

“A.A. members and many of their physicians have described situations in which depressed patients have been told by A.A.s to throw away the pills, only to have depression return with all its difficulties, sometimes resulting in suicide.

“We have heard, too, from members with other conditions, including schizophrenia, bi-polar disorder, epilepsy and others requiring medication, that well-meaning A.A. friends discourage them from taking any prescribed medication. Unfortunately, by following a layperson’s advice, the sufferers find that their conditions can return with all their previous intensity. On top of that, they feel guilty because they are convinced that ‘A.A. is against pills.’ It becomes clear that just as it is wrong to enable or support any alcoholic to become readdicted to any drug, it’s equally wrong to deprive any alcoholic of medication, which can alleviate or control other disabling physical and/or emotional problems.”

The author then suggest that ” roughly 70% people I meet in AA are on meds. A lot people are quiet about it because they don’t want the backlash…”

Is the prevalence of people taking medication in 12 step groups this high? Or is this a sample bias?

Perhaps many of the people I know in AA have simply been keeping quiet about it? I am not convinced that this figure is accurate, based on my own observations?

If this figure is representative then what co-occurring conditions are these recovering people medicating?

There are obviously a host of co-occurring conditions  that recovering people suffer from – from physical, such as back pain, to epilepsy, to anxiety disorders to depression, bi-polar, borderline personality disorder, post traumatic stress disorder, schizophrenia …in fact the list goes on.

Is it  thus reasonable of us in AA and other 12 step groups to expect that all members are medication free or that the 12 steps can treat all co-occurring conditions?

It has been suggested in a AA survey  that over 60% of recovering individuals in 12 step groups seek outside professional help for co-occurring difficulties which suggest that the trajectory of alcoholism and addiction is not straightforward and includes other co-occurring problems which may add to the severity of psychological symptoms experienced.

A very pertinent question is whether these co-occurring conditions are parallel problems or are additional problems that affect one’s addiction recovery.

By this I mean if one suffers, as I do, from PTSD, do PTSD symptoms also add to relapse vulnerability, for example. I can say for myself that the two times I have had issues with relapse have been prompted by manifestation of PTSD symptoms, such as flashbacks.

For me, at least, my co-occurring condition of PTSD affects my recovery from alcoholism and substance addiction. It is inseparable – in fact my PTSD and childhood maltreatment has contributed to my addiction.  Although it doesn’t necessarily follow that my choice of  treatment, e.g. 12 step recovery will straighten out all the factors that contributed to this addiction.

Equally the 12 step and associated fellowship and program for living may help manage this condition too?

I have not relapsed in a decade so the 12 steps etc must be helping with co-occurring conditions as these conditions have to potential to prompt relapse?

I will explain this further, below, in relation to the various sponsors I have had in recovery.

I do not medicate for this condition nor have I sought outside help although I  have considered outside help many times. Perhaps I am edging closer to that.

Equally I believe the process of recovery has helped me recover from PTSD, has made me aware of triggers, etc.

How prevalent is PTSD in addiction? Do others suffer in recovery from this co-occurring condition too?

Approximately 35% to 50% of people in addiction treatment programs have a lifetime diagnosis of posttraumatic stress disorder (PTSD), and 25% to 42% have a current diagnosis (Back et al., 2000; Brady, Back, & Coffey, 2004; P. J. Brown, Recupero, & Stout, 1995; Cacciola, Alterman, McKay, & Rutherford, 2001; Dansky et al., 1996;Jacobsen, Southwick, & Kosten, 2001; Mills, Lynskey, Teesson, Ross, & Darke, 2005;Ouimette, Ahrens, Moos, & Finney, 1997).

Is this the case in 12 step groups?

In order to examine the extent of co-morbidity in recovery I will briefly run through some of the sponsors I have had in recovery, and their co-occurring conditions – self acknowledged or not.

First sponsor – bi polar, not medicated, but also treated via outside professional help – accepts that he will occasionally have very dark days as part of his recovery. His choice is not to medicate as he feels it is a chemical straightjacket although he accepts the right of others to take medication for this condition.

Second sponsor – borderline personality disorder – not medicated – has sought professional outside help.

Third sponsor – no co-occurring conditions  – but would suggest his religiomania contributes to his absolute conviction that recovering people do not need medication of any sort that God can heal everything.

Fourth and fifth  sponsors both PTSD but not fully acknowledged nor treated outside of 12 steps.

All in long term recovery of 12 plus years.

From this very small survey it is clear that there is a common co-occurrence with other conditions, acknowledged or otherwise. There is also extensive childhood abuse of various types.

All of them have not or do not take medication. They may be in some way also be treated by the 12 steps.

I have also sponsored a person with  schizophrenia who needs to take medication because of returning psychosis if he fails to take medication.

What I am saying is that some individuals with obvious co-occurring conditions also choose not to medicate as well and feel their general “recovery” is treated by the steps and fellowship, often together with outside help. Having a co-occurring condition does not mean one automatically takes medication for this condition? Many do not?

This is why I queried the “70%” are on meds above. I do not necessarily disagree that those suffering co-morbid conditions is the majority but would query why so many take medication?

Are some of these on medication assisted treatment to curb urges and cravings too?

In terms of so-called co-occurring disorders such as anxiety and mood disorders such as generalized anxiety disorders (GAD) and major depression (MDD), research has shown that these symptoms often dissipate in the early weeks of recovery.

This had led researchers like Mark Shuckit to call these substance induced disorders and to suggest that co-occurring disorders such as GAD and MDD are distributed in recovery populations as they are in normal population at around 15% prevalence.

This is why I think some 12 steppers are “anti med” as they often see the symptoms of GAD and MDD dissipate in early recovery and thus believe the steps are treating these disorders successfully.

Although these disorders are but temporary substance induced disorders for many, however, for 15%, at least, these conditions of  GAD and MDD are possibly what they suffer from too in recovery.

Regardless of that caveat if we add this 15% to up to 50% who suffer PTSD and the possibility of the occurrence of other conditions such as borderline, bi polar, etc we get closer to the 62% figure of AA respondents that an AA survey in 2012 states  received some type of treatment or counseling, such as medical, psychological, spiritual, etc., (and 82% of those said it played an important part in their recovery from alcoholism).

Whether these conditions require medication is a matter for the person and their sponsor in discussion with medical professionals and not some layperson “medical expert” as often abounds in AA and other 12 step groups.

The issue here is not simply co-morbidity  but whether this co-morbidity is an intrinsic part of the aetiology of addiction from a vulnerability to a relapse  factor. In other words, have other conditions meshed into the overall condition of addiction? Can they be treated by the same treatment?

Regardless,  they often have to be treated  separately.

To conclude it seems that 12 step groups need to appreciate that co-occurring conditions, self acknowledged or not, play an important part in recovery and relapse as well as in the aetiology of addiction.

How effectively the medication used can be dissected from the condition of addiction is still debatable for many?

In short, many feel being on medication impedes full recovery.

How we define full recovery is open to question? Recovery can be measured using many variables related to quality of life. If medication using members feel their lives are steadily improving then who are we to judge?

Equally just because one suffers a condition does not inevitably mean it must be medicated, some of the examples above have “treated”  their co-occurring conditions via the 12 step program of recovery.

I think ardent fans of the right to medication should appreciate that there is a valid counter argument – they may have the same rights to their point of view as the author of this  blog?

All of us has the right to think as they wish and to express their views also.

Live and Let Live may be apropos, we all have the right to be wrong, Love of others is our code.

Alcoholics are such absolutist thinkers, all or nothing, black and white thinkers at times. Recovery is also considering others and their points of view?

Personally speaking if I sponsor, I take it on a case by case basis.

I have had only one sponsee out of 7 who has been on medication.

It is for sponsor, sponsee and family as well as medical professionals to contribute to the debate on continued medication.

My lasting concern, however is the 70% figure cited in this blog. It does not tally with my experience of recovery.

Another part of the AA pamphlet cited also warns,

“Experience suggests that while some prescribed medications may be safe for most nonalcoholics when taken according to a doctor’s instructions, it is possible that they may affect the alcoholic in a different way…”

Again this seems to be alerting us to the question when is medicating actually self medicating?

 

 

This has been my main experience with medication, that those taking them do not always look completely sober.

In order to recovery fully perhaps we have to be fully sober first?

I will continue this discussion in Part 2 of this blog when I discuss also whether considering alcoholism purely as a “spiritual malady” complicates this argument.

In the DSM manual 75% of the disorders contained therein have emotion dysregulation at the centre of their condition. I believe alcoholism and addiction also have although not acknowledged.

Insted DSM states the emotional dysfunction seen in addiction is the result of some of co-morbidites mentioned above. I disagree.

Is it not about time we got our heads together and agreed on what the hell we suffer from?

Isn’t addition an emotional disorder in it’s own right compounded by other co-occurring conditions?

Then we will be in a position to discuss how the 12 steps can treat this condition and related conditions of emotion dysregulation?

The main issue for the blog addressed, is that the author, and many others, cannot understand how a spiritual malady has anything to do with their other conditions, when, in reality, alcoholism is another type of disorder, similar to that with which it often co-occurs .

More on this later…

 

 

 

 

 

 

 

Why we need to be more accurate in diagnosing co-morbidity.

In this blog we have repeatedly queried whether the co-occurrence of so-called co-morbidities with substance use disorders (SUDs) is as high as reported in many studies (1).

In a blog from yesterday Are most co-morbidities really substance-induced disorders?  that diagnosis is often flawed in many studies and that the so-called diagnosis of co-morbidity is not borne out long term with many presumed co-morbid disorders disappearing in time.

In an recurring example given, the author uses the high prevalence of so-called comorbidity with mood disorders to illustrate how alcoholics and addicts appear to have a similar range of mood disorders as that of a normal population sample, i.e. as normally in society, around 15%.

This is in keeping with our ancedotal evidence of attending numerous AA meetings over a number of years has shown that in the vast majority of individuals the symptoms of a supposedly co-morbid disorder such as General Anxiety Disorder (GAD) or major depression (MD) appear to dissipate after some weeks.

This either means that there 12 step program of recovery outlined in mutual support groups like AA can provide profound therapeutic effect on other disorders (which they very well may do) or that the co-morbidities highlighted in many studies is greatly exaggerated.

This exaggeration has two major consequences. The study of and research into SUDs is hampered by relegating affective dimensions to that of co-morbidity while not exploring the specific emotional dysregulation at the heart of SUDs ( in particular dyscontrol over subcortical/amgydaloid emotional responding appears at the heart of most of these psychopathologies so they have common neural substrates and mechanisms but they may not manifest in the same behavioural responses – in other words there may be common emotional dysregulatory mechanisms but different pathomechanisms)

Burden of Addiction Graph

 

That is not to say that co-occuring disorders can not exaggerate the trajectory of a SUDs as disorders such as post traumatic stress disorders may, for example, add to distress based responding and may also require further and more specific treatment in addition to that for a SUD.

Also research needs to not only to predict behaviour e.g. in the case of addiction, relapse, but also to help prevent conditions arising. Thus it is imperative that research more fully informs prevention and intervention in children and adolescents at risk from later SUDs.

Thus the specific aspects of emotional dysregulation specific to a SUD such as, for example, a tendency to act rashly or impulsively under distress may be addressed by considering whether this is also the function of emotional processing deficits which mean emotions are “avoided” rather than processed by cortical areas, resulting in more reactive sub-cortical responding which has consequence for a decision making profile which is more based on alleviating this distress state, this unpleasant feeling state, than it does the recruiting via effective emotional processing and regulation of more cortical areas of the brain. All of which has ramifications for a more accurate study of the aetiology of addiction per se and it’s prevention.

For example, teaching at risk children how to identify, label, and verbalise their emotions at an early age will help them learn how to process and regulation them; to then use these feeling states to guide goal-directed adaptive behaviour rather than and  recruiting more subcortical emotive-motor parts of the brain to flee these distress states resulting in more reactive  decision making and emotional management. It would also help with reducing the effect that initial alcohol use has on adolescents as  emotional dysregulation potentiates reward, so distress/stress make the rewarding effects of drugs and alcohol heightened. It may also mean heart rate variability is also higher so that the smoothing, calming effects of alcohol are not as exaggerated. It would help put some neural brakes on increasingly out of control behaviour.

It would help tackle the premorbid distress at the heart of vulnerability to later addiction at its source, its manifestation as emotional reactivity.

It would return us to a theoretical conception of addicts as suffering human beings not neurobiological machines, which can be tweeked by this neurochemical or that!

This leads me onto the second short point. If we relegate the anxiety, impulsivity mood  and affective dimensions of a SUD to co-morbidity we limit our understanding of the overlapping and interlinked roles of emotional processing and regulation deficits on reward processing for example.

There is a tendency in some researchers to see addiction purely in terms of neurbiological processes, usually dopaminergic, equating addiction to the effects that a drug or alcohol has on the neurobiology and neuro-anatomy of the brain, and not to see how these deficits may not be simply drug induced but also linked to stress dysregulation which itself is linked profound and pre-existing impairments in emotion processing and regulation.

A chronic addict is emotionally distressed most of the time, who do dopaminergic models explain this emotional response or the fact that most relapse is stress or emotional distress based and prompted.

Or the effects of maltreatment or abusive childhoods, or economic deprivation or deviant peers. Observing addiction as a inherited emotional regulation and processing deficit, exaggerated by sometimes dysfunctional  parenting  (especially if the parents are also addicts and alcoholics) and persistent stress allows us to observe how genes in certain individuals are influenced by environment and manifest in behavioural undercontrol, emotion lability and reactivity and impaired, impulsive decision making in those at risk from later addiction. It may be important to study what is impaired before the neurotoxic effects of chronic drug and alcohol use profoundly aggravate these “pre-morbid”  impairments.

To conclude, there is “overlap of the biological substrates and the neurophysiology of addictive processes and psychiatric symptoms associated with addiction”

Pani et al suggest the “inclusion of specific mood, anxiety, and impulse-control dimensions in the psychopathology of addictive processes.”

We suggest these can be accommodated under the umbrella of emotional regulation and processing deficits as the above and additional deficits seen in alcoholics and addicts are more satisfactorily covered by this nosology.

We agree with Pani et al, that “addiction reaches beyond the mere result of drug-elicited effects on the brain and cannot be peremptorily equated only with the use of drugs despite the adverse consequences produced.”

We infer that emotional dysregulation is at the “very core of both the origins and clinical manifestations of addiction and should be incorporated into the nosology of the same, emphasising how addiction is a relapsing chronic condition in which psychiatric manifestations play a crucial role.”

We agree that “addictionology cannot be severed from its psychopathological connotations, in view of the undeniable presence of symptoms, of their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.”

References

Pani, P. P., Maremmani, I., Trogu, E., Gessa, G. L., Ruiz, P., & Akiskal, H. S. (2010). Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?. Journal of affective disorders, 122(3), 185-197.

Are most co-morbidities really substance-induced disorders?

Are most co-morbidities really substance-induced disorders?

a Guest Blog from Inside the Alcoholic Brain

In this blog we re-emphasize the need for accurate diagnosis of co-morbidity with a substance use disorder. It appears form the article cited here (1) that diagnosis is often flawed in many studies and that the so-called diagnosis of co-morbidity is not borne out long term with many presumed co-morbid disorders disappearing in time.

Most diagnoses in medicine are based on a combination of symptoms, their time-course and a threshold beyond which the syndrome is felt to be clinically relevant [1].

No single indicator is likely to be sufficient to establish a diagnosis because these are rarely unique to one syndrome.

Potential problems with the diagnostic process increase almost exponentially when substance use disorders  (SUDs) and psychiatric syndromes occur together.

First, combinations of SUDs and psychiatric disorders may represent two or more independent conditions, each of which is likely to run the distinct clinical course relatively unique to that disorder. Here, both conditions must be treated comprehensively.

Secondly, the first disorder could influence the development of the second condition in a such manner that the additional disorder  then runs an independent course. For example, the frequent use of high doses of substance could unmask a latent predisposition toward a psychiatric disorder.

Similarly, a psychiatric disorder (e.g. mania) could increase the risk for heavy use of substances, an SUD that might continue even when the pre-existing psychiatric condition is treated or remits.

A third relationship could be seen if the second condition developed through an effort of the patient to diminish problems associated with the first
syndrome. Here, for example, a person might escalate the use of substances and develop an SUD in an attempt to alleviate feelings of depression, or to decrease side-effects of psychiatric medications. Here, while the substance
use disorders might become a long-term problem, the excessive use of alcohol or an illicit drug might disappear when the pre-existing clinical syndrome is addressed appropriately.

This review focuses the high prevalence of psychiatric comorbidities
seen in individuals with SUDs and syndromes which may be
temporary psychiatric conditions.  The distinction between the types of comorbidities, each of which are likely to operate in some patients, has
important implications [8,9]. The etiologies may be different  (a factor of importance for research), as these “substance-induced disorders” are likely to have distinct clinical courses and responses to treatment.

comorbid02

METHODOLOGICAL ISSUES THAT AFFECT RESULTS

Different definitions of comorbidity
Comorbidity has been defined in a variety of ways. Some studies place an emphasis on ‘pure psychiatric diagnoses’, defined as a psychiatric condition observed in the absence of any other major diagnosis during the same year.

Multiple diagnoses have been placed into a primary versus secondary
approach where the first condition to develop is labeled as ‘primary’.

The independent versus substance-induced distinction  is an extension of the primary/secondary approach.
It was developed in recognition that a psychiatric syndrome (e.g. a major depressive episode) might also be identified during periods of abstinence.

Problems with making a diagnosis – One major  issue is whether the diagnosis
is required to be associated with great distress or impairment  or if a simple endorsement of the symptoms by a respondent is enough to make a diagnosis.

A similar problem can occur if the criteria did not include the need for some problems to have occurred repeatedly (an issue relevant to many of the criterion items for SUDs), or did not determine if the items clustered together during the relevant period. Studies also vary regarding their emphasis on syndromes occurring in the last year versus during the life-time. Differences across studies on any one of these items are likely to have a large impact on the results regarding the incidence, time course, and optimal treatment of comorbidities.
An additional and very important research issue relates to the types of interviewers employed and their level of supervision.  Many  studies
require large numbers of non-clinician interviewers who can have difficulty interpreting the relevance of some complaints (e.g. mania), and demonstrate problems determining whether the symptoms were relatively mild and transitory (e.g. for some simple phobias) versus those relevant to a diagnosis. The need for so many interviewers also means that the problems reported by subjects are less likely to be reviewed by clinicians.

Other problems reflect the approach used to deal with what appear to be multiple diagnoses in the same person. This occurs, for example, when a subject endorses depressive symptoms, reports panic attacks and describes discomfort in social situations. In some studies these are listed as three separate diagnoses, but others establish a hierarchy, searching for one overarching diagnosis (e.g. major depression) that might explain the other complaints (e.g. temporary panic attacks and feelings of social discomfort).

Unless closely supervised lay interviewers may have difficulties distinguishing periods of situational excitement or substance-related irritability from mania?  Epidemiological interviewer-based instruments might exaggerate the rates of psychiatric disorders and SUDs by reporting conditions that might not meet a full and clinically relevant
syndrome. These interviews might not be optimal for exploring more complex questions such as comorbid conditions, especially with regard to substance-induced disorders.

No one study or single group of subjects can give the ‘true answer’ regarding the prevalence and patterns of psychiatric and SUDs.

The timing of the evaluation is also important. For example, rates of comorbid psychiatric syndromes are likely to be temporarily elevated if substance-dependent subjects are interviewed during intoxication, withdrawal or the first several weeks of abstinence. These are times of highest prevalence of substance-induced disorders.

It is also important to gather additional sources of data about subjects whenever possible. These include clinician reviews of all available information on a patient using additional informants (e.g. a spouse).

These can be key in determine  whether, for example, depressive symptoms reported in a follow-up were truly independent of substance use.

DO SUBSTANCE-INDUCED DISORDERS  EXIST?

Evidence supporting substance-induced mood disorders

download (7)

Temporary depressive symptoms have been reported in the context of intoxication or withdrawal for nicotine, cannabinoids, opioids, hallucinogens and other drugs of abuse.

Interviews with clinician review of diagnoses have documented that >40% of alcoholics have ever fulfilled criteria for major depressive-like syndromes, with almost 70% of these being substance-induced disorders. However, a large national epidemiological study using the AUDADIS diagnostic  and lay interviewers without clinical supervision reported high rates of depression in alcoholics, but noted that few were substance-induced. These divergent results probably reflect different methods across studies as described above.

Additional support for the relevance of substance induced mood disorders comes from prospective studies that suggest that heavy drinking at time 1 is likely to predict depressive symptoms at time 2. A 6-year follow up of 176 subjects reported that drinking predicted an increased number of subsequent transitions from functioning well to periods of depression (perhaps reflecting substance-induced mood disorders), while individuals with prior (but not currently active) alcoholism had no increased number of transitions to depression over time.

Another prospective study reported that heavier drinking during month 2 predicted depressive symptoms during month 3

In addition, 3- and 12-month follow-ups of almost 200 alcoholics
revealed that only those who had returned to drinking were likely to demonstrate depressions.  Finally, a follow-up of young subjects found no relationship between earlier heavy drinking and later AUDs, unless the individuals continued heavy drinking.

Prospective studies of populations at high risk for depression or alcoholism also generally support the existence of substance-induced mood disorders.

Results also indicate that independent major depressions tend to run a true course, and are not usually associated with later alcoholism unless, perhaps, there are alcohol-dependent relatives as well.

Some studies have  noted no increased risk for alcohol use disorders (AUDs) in children of depressed individuals. One study, an evaluation of ∼1000 16–25-year-old subjects in New Zealand, showed  earlier drinking patterns were predictors of alcohol-related outcomes but not of depressive disorders.

A prospective evaluation of two generations of 453 families of alcoholics and controls noted that an orders, but not independent major depressive episodes
alcoholic relative predicted higher rates of alcohol use disorders, but not independent major depressive episodes

When substance-induced mood disorders are identified, they are likely to disappear soon after abstinence, a situation not seen with independent depressive episodes.

Thus, overall continued abstinence in alcoholics is likely to be associated with a decrease in depressive symptoms.

For example, follow-up of alcoholics with substance-induced mood disorders reported that the proportion with marked depressive symptoms decreased from 42% to 6% with 1 month of abstinence [67]. A separate study of unmedicated male alcoholics documented that, for those with induced depressions, an average Hamilton Depressive score of 16 after 1 week of abstinence decreased to a score of six after 4 weeks dry, while similar
decreases are not seen for subjects initially identified as having independent major mood disorders.

Similarly, in another investigation the proportion of alcoholics with major depressive-like symptoms decreased from 67% to 13% over a month, without antidepressant treatment,  findings supported by several other clinical
observations.  In addition, 85% of those with alcohol-induced mood disorders ran the course predicted regarding the temporary nature of the symptoms.

A tendency toward diminution or disappearance of depressive symptoms
with abstinence has also been reported for patient in care for  stimulant or opioid dependence.

To summarise, it appears that  substance-induced disturbances are more likely than independent disorders to diminish and disappear with time alone.

images (27)

While the acute phase of withdrawal from alcohol lasts 4 days or so, this is likely to be followed by a protracted abstinence syndrome that can last several months or more . Here, while the alcoholic is not depressed all day every day (i.e. does not fulfill criteria for a major depressive episode), they are likely to experience insomnia, problems concentrating and irritability that improve with increasing time of abstinence.

These are not, however, independent major depressive episodes. It is also worth noting that as many as 15% of any group of individuals (including alcoholics) are likely to show major depressive episodes as a reflection of the usual prevalence of these mood disorders.

Therefore, in summary, most studies document substantial proportions of alcoholics and stimulant-dependent subjects have substance-induced conditions.

The symptoms of most substance induced conditions resemble closely those of the relevant independent psychiatric disorders. However, 85% or more of substance-induced syndromes improve rapidly with abstinence,  distinct from what would be expected with, for example, independent schizophrenia
and major depressive episodes.

 

References

Schuckit, M. A. (2006). Comorbidity between substance use disorders and psychiatric conditions. Addiction, 101(s1), 76-88.

Measuring the so-called “Alcoholic Personality”.

Measuring the So-called “Alcoholic Personality”?

Guest Blog

by Paul Henry

We recently came across an article which satisified some of our curiosity with regards to two important theoretical and research considerations in relation to both the accurate definition of  the so-called “addictive or alcoholic personality “, which has falling out of fashion in terms of recent research but which still intrigues some researchers, while also addressing, in passing, an issue of so-called co-morbidity which is reported to be high in alcoholics, particularly generalized anxiety disorder (GAD).

We have written in the past about co-morbidities and whether the prevalence of co-occurring conditions or psychiatric disorders such as GAD are as prevalent as many researchers suggest.

We will discuss difficulties with measuring co-morbidities in later blogs. The study we cite here appears to be reporting that  so-called anxiety reported here in this participant pool of alcoholic dependent people were  transient. This tallies with our own ancedotal evidence of anxiety disappearing as recovery proceeds or in the words of this study “high state anxiety unlike those with anxiety neurosis, who have a high trait anxiety. This indicates that anxiety in alcohol-dependent individuals is transitory, varies in intensity and fluctuates over time, and can be easily modified.”

This type of finding outlines difficulties in diagnosing GAD in alcoholics and supports the idea that anxiety is transient. In fact we suggest that the symptoms of anxiety often expressed in alcoholics may be the result of escalating chronic stress and emotional dysregulation in the addiction cycle and which appears to lessen or disappear in recovery or be provoked by situations.

Potential alcoholics tend to be emotionally immature, expect a great deal of the world, require an inordinate amount of praise and appreciation, react to failure with marked feelings of hurt and inferiority, have a low frustration tolerance, and feel inadequate and unsure of their abilities to fulfil expected male or female roles.1

This study (1) found significantly higher scores on extroversion which indicates that alcohol-dependent subjects are characterized by traits such as being more assertive, dominant, sociable, carefree and venturesome as compared to non-dependent people. This finding is in agreement with that of Mathew and Baby13

Alcohol-dependent patients also obtained significantly higher scores on the neuroticism dimension. This indicates that they are significantly more emotional, frequently anxious and/or depressed, moody and tense. Similar results were reported in earlier studies.12,15

Among the personality traits studied in alcohol-dependent individuals, antisocial personality has been looked into most often.1 In this study alcohol-dependent subjects obtained significantly higher scores which is in agreement with the findings of Neeliyara et al.16 A longitudinal study of men older than 40 years also revealed that antisocial behaviour in adolescence is the sole individual predictor of alcoholism.17  However, it must be pointed out here that the high Pd scores in alcohol-dependent patients indicate a transitory state, which may be amenable to change with treatment. Our finding that alcohol-dependent patients showed disturbances in the depression, mania, schizophrenia, psychopathic deviance and anxiety scales is consistent with previous research that the emotional disturbance in people with substance abuse is broad-based, variable and non-specific.18

Alcohol-dependent individuals also obtained significantly higher trait and state anxiety scores.  These findings support those of a few earlier studies.14,16

This aspect may be aetiologically significant in alcohol dependence. Anxiety has been suggested to be an important factor in the initial development and subsequent maintenance of alcohol abuse and dependence. Some patients use alcohol as a medication for the treatment of anxiety. Unfortunately, an accurate diagnosis of anxiety disorders is difficult to make, since current anxiety symptoms may be secondary to alcohol withdrawal rather than reflecting underlying anxiety disorders.19 The findings of this study also reveal that alcohol-dependent individuals are different from those with anxiety neurosis, since they have a high state anxiety unlike those with anxiety neurosis, who have a high trait anxiety. This indicates that anxiety in alcohol-dependent individuals is transitory, varies in intensity and fluctuates over time, and can be easily modified.

Low_Self_Esteem_by_scarybuttfreezer

 

One of the sources of anxiety is a low level of self-esteem, fear of disapproval from significant people, loss of position, prestige, stature or self-esteem.16 Thus, these findings also support our finding that alcoholics have low self-esteem.

Patients with alcohol dependence experience significantly more stressful life events in the past year and over their lifetime. These findings are in line with previous reports.13,14,20.

Men who are lifelong abstainers experience fewer life events than problem drinkers. Alcoholics may offset stress-induced emotional distress by resorting to drink which, in turn, might lead to a further increase in negative life events.

A person’s self-structure is an important aspect of his personality. A healthy personality is manifested when an individual has a positive attitude towards him/herself. Studies in this area have shown that psychiatric patients have unhealthy self-structures by way of poor self-concept. In this view, alcohol-dependent individuals suffer from lowered feelings of self-esteem, pervasive feelings of inferiority and powerlessness, coupled with unusually strong inhibitions against the expression of hostile or aggressive impulses. In the present study, alcohol-dependent individuals had significantly lower self-esteem as compared with normal subjects. This finding is in agreement with that of Neeliyara et al.16 This indicates that alcohol-dependent individuals have less positive self-feelings and more feelings of alienation and isolation.

Higher numbers of alcohol-dependent subjects were identified to have alexithymia. This finding is congruent with earlier work.15,21 

In recently sober alcoholics the alexithymic cognitive dimension—an inability to identify feelings and to distinguish them from bodily sensations—is related to depressive symptoms and suicidal ideation.

Finally this study concluded that alcohol-dependent individuals show significantly high neuroticism, extroversion, anxiety, depression, psychopathic deviation and significantly low self-esteem as compared to normal control subjects. Significantly more alcoholics were found to be alexithymic.

So what does this study tell us? It is useful in illustrating the transient nature of some co-called co-morbid disorders such as GAD. It more importantly does highlight   certain personality characteristics which we believe, based on extensive ancedotal evidence of a number of years in recovery, are relevant and pertinent to alcohol-dependent people. In fact in recovery, new comers to recovery are often warned against the very variables highlighted here such as not isolating from others in recovery.

Ultimately, however, we believe that the personality characteristics mentioned in this study come under a wider definitional umbrella of emotional regulation and processing deficits which manifest as these personality characteristics and explain not only these characteristics but also the sometimes situationally specific trait anxieties and perhaps other co-morbidities.

References

1. Chaudhury, S.K. Das, B. Ukil,  Psychological assessment of alcoholism in males Indian J Psychiatry. 2006 Apr-Jun; 48(2): 114–117. doi: 10.4103/0019-5545.31602