Recovery from Severe Substance Addiction: Understanding different models and interventions in supporting the recovery journey.

In this conversation, we are asking, what are the particular considerations in discussing recovery from severe substance addiction, such as alcohol and opiates. And specifically the role of medical and pharmacological interventions in supporting the recovery journey.

Additionally, to bring into view the ‘Learning Model of Addiction': ‘while the brain has the capacity for addiction, it also has the capacity for behaviour change, shifting the emphasis to recovery.’

About Substance Dependence

The presence of substance dependence increases the risk for potential ‘years lived with disability’, reflected in the DSM-5 diagnostic criteria for diagnosing and classifying substance use disorders. The impact on quality of life and years lived with disability before it can be resolved is high, or else the potential of death. Hence why this discussion is so important. But what do we mean by addiction?

Prominent addiction theories characterise addiction as a transition from controlled to “compulsive” drug-seeking and drug-taking behaviours. There are different definitions for ‘compulsivity’, reflecting the complex nature of addiction. Here is one definition:

“Risky substance use refers to quantity/frequency indicators of consumption; Substance Use Disorder (SUD) refers to individuals who meet criteria for a DSM-5 diagnosis (mild, moderate, or severe); and addiction refers to individuals who exhibit persistent difficulties with self-regulation of drug consumption [despite harmful consequences]. Among high-risk individuals, a subgroup will meet the criteria for SUD and, among those who have an SUD, a further subgroup would be considered to be addicted to a substance. However, the boundary for addiction is intentionally blurred to reflect that the dividing line for defining addiction within the category of SUD remains an open empirical question” (Heilig et al, 2021).

Moral Model and Learning Model of Addiction

The ‘moral model of addiction’ discusses recovery through shame and humiliation, which reflects a poor societal response and is the opposite of the Learning Model of Addiction' which argues that ‘while the brain has the capacity for addiction, it also has the capacity for behaviour change. Shifting the emphasis to recovery(Heilig et al, 2021). One that accounts for the changes in the brain, without removing hope in the possibility of flourishing after addiction, through supported recovery.

There is much work needed, and being done, in the area of ‘recovery-oriented approaches and drug treatment interventions’, including therapeutic and also medicalised treatment methods and objectives (NIDA) (Drug Strategy, 2010) (Wangensteen and Hystad, 2021). Read on to find out more.

Neurobiological basis of Substance Addiction

In this discussion, we will be focusing on the neurobiological basis of substance dependence or the ‘brain disease model of substance addiction characterised by compulsive drug seeking. Suggesting addiction to be a chronic relapsing and remitting illness that some people suffer from and others will not. Before this, a ‘moral model of substance addiction’ presided up to the 1980’s suggesting addiction to be a choice, and so this stigmatised users in society.

Made worse by challenging stereotypes of laziness and affliction, which is often still portrayed today in this moral model. Both models emphasise a deterministic view of the compulsive/impulsive dimensions of addiction, where the sufferer is powerless, and so reliant on interventions, including pharmacological.

The efforts of researchers evidencing the neurobiological basis of substance addiction in the brain disease model consider that addiction may have components of genetic and developmental risk. They found clear evidence that brain changes do occur in the use of addictive substances, particularly in the reward centre of the brain and frontal lobes or pre-frontal cortex, changing the way that a person thinks, makes judgements, and is motivated to do things when under the influence, for example.

The brain disease model of substance addiction, however, fails to factor in heterogeneity or individual differences in the population in remission and recovery. Environmental, social and socioeconomic processes implicate and influence relapse, and treatment compliance also seems to be ignored.

Treatments and Interventions

Being addicted to opiates results in acute withdrawal symptoms if a user stops. Opiate substitution treatment (OST), such as methadone, has been proven through several studies and anecdotally, as an effective treatment in providing stability and safety, while adapting to the recovery journey.

And in its application, Drug Strategy (2010) describes the adoption of what is termed ‘low threshold prescribing’ where the objective is not stopping someone from using heroin long-term, but with the idea of substituting OST over time, to reduce harm.

Eventually, this may involve progressively coming off OST and leaving the structured treatment plan altogether. Although, exiting the use of OST earlier can cause harm, especially if it leads to relapse. These are important indicators of an individual’s recovery progress that must be factored in.

Recovery is therefore seen as a broader and more complex process as aforementioned. OST is just one option, that includes working closely with a relevant support team. Incorporating support through increasing motivation, reducing risk-taking behaviour, helping overcome dependence, and improving general brain-physical-mental health in the personal wish for recovery - which is a voluntary choice.

Referring back to the history of drug misuse is an important concept in understanding who might actually need medical treatment considering the question - are all addictions curable? Some problematic substance users may in fact continue to use without too many problems; so-called ‘high-functioning’ addicts.

That is, they are able to hold down a job or run a business and perform well. But behind closed doors, alternating between heavy usage, abstinence and a return to using. Some may even stop on their own, known as ‘spontaneous recovery’ led by life events, such as getting married or starting a new job.

Being ‘ready’ to take up treatment may improve outcomes too, related to the concept of ‘hitting rock bottom’. Rock bottom is a narrative that comes from users themselves implying that treatment educates people; learning through the treatment journey, which includes putting support systems in place to make changes in real-life, or choosing to stop using altogether.

Self-detoxification in the case of opiates and alcohol is a common example. In this context, working closely with the relevant support team in obtaining medicalised treatment. Naltrexone, for example, treats alcohol addiction by reducing cravings. Naltrexone is in fact an opioid receptor antagonist or a substance that binds to a relevant receptor inside cells or on the cell’s surface, causing the same action as the innate endogenous opioids that would normally bind to opioid receptors in the cells. So, Naltrexone ‘mimics’ this. It is also used in the management of opioid addiction by blocking the harmful effects of opioids and therefore reducing cravings.

Recent advances in the fields of molecular biology, behavioural neuropharmacology and Neuroscience, including brain imaging, have changed our understanding of the addictive processes in the brain, and why relapse can occur. Especially in the face of adverse consequences or life events.

The role of applied neuroscience in understanding the complex interactions between repeated exposure to drugs, and the biological (i.e., genetic and developmental), and environmental factors (i.e., drug availability, drug cues, social, and economic/education variables) are helping to unravel the complexities of addiction, sometimes referred to as an unpredictable illness.

This unpredictability means it is difficult to say what the tipping point is for user dependence, and how addictive states are likely to develop in determining a treatment plan, including medicalised treatment. The available research, and as reflected in Psychiatric clinical care (DSM-5), concludes addiction to be on a continuum. That is a continuous sequence, where the extremes can be quite distinct, rather than binary (‘you are addicted or not’?). So, you are more or less addicted, depending on where you are on the continuum, and also depending on severity level.

Do interventions need to be tailored to individuals and contexts, therefore? Examples include alcohol addiction and the mentioned use of Naltrexone. However, the particular withdrawal syndrome for alcoholics can be dangerous, with the potential to cause seizures. In opiate addiction, ‘take-home’ naltrexone can be used by families and friends for users to ‘rescue’ from overdose or worse, to buy precious time to reach out for medical assistance.

Drug users, especially those injecting, are offered Hepatitis B vaccination, in order to prevent blood-borne viruses. In the context of club drugs, where psychological dependence may also feature, alongside physical dependence, interventions could include the potential of providing medical help onsite in clubs.

The concept of treatment penetration is a final point, in that the treatment system may not necessarily engage everyone in treatment. Individuals have agency as to whether they want to take part or not. The bad news is more than 80% of addicted individuals do not seek treatment and this may reflect a lack of recognition of the severity of the disorder by individuals, and a historical bias by the medical fraternity led by societal stigma (Goldstein et al, 2009).

The content presented in this blog incorporates factual information along with perspectives and opinions. It is designed to stimulate discussions and exploration of emerging research. However, it does not represent official advice or exhaustive factual claims. Readers of course consider multiple sources when forming a viewpoint. Alternative viewpoints are highly encouraged and welcomed at Blindspot.

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