What is addiction? Understanding the life-process learning disorder model.
What is addiction? Is it a disease? If so, are we experiencing a pathological disease process when we become “addicted” to the naturally-rewarding endorphin release that comes with exercise? Are our addictions to the internet and coffee attributable to a ‘disease’ process too, or are those just habits, despite one (caffeine) having a basis on an actual, physical, chemical dependency?
When does a habit become an addiction — or an addiction become a disease — and how, exactly? Do various chemicals and drugs, themselves, cause a disease process in only THOSE specific addictions? Is gambling addiction a disease, even though there are no drugs involved? Does that make it a disorder as opposed to a disease? What’s the difference? Habit, addiction, disorder, disease — what do each of these words mean, and, more importantly, what do they look like in the brain?
As a result of the ongoing global pandemic, rates of alcohol and drug use, both pharmaceutical and otherwise, are skyrocketing, along with obesity. Against a backdrop of stress, fear, isolation, and actual or potential economic scarcity, more and more of us are developing maladaptive coping mechanisms like binge eating, binge drinking, and compulsive use of technology — even when we know that these actions will have adverse effects on our physical and mental health.
On top of these issues, many of us are succumbing to the depression and anxiety that so commonly co-occur with addictive disorders, and we might find that our bad habits accelerate and gain strength as our mental health deteriorates. Why is this so? What are the TRUE neural underpinnings of these experiences, divorced from any bought-and-sold biases? How can we use this knowledge to strengthen us?
It has never been more important for all of us to come to a collective understanding of exactly what addiction is, what is isn’t, how it happens, how we free ourselves from it, and how we can avoid it in the future or use our natural addictive tendencies to our advantage. Addiction exacts an almost incalculably high financial and human toll on us here in the United States, as the total economic cost to society is greater than all types of diabetes and all cancers combined. That’s a lot.
As our life situations complicate and our problems are exacerbated, we might feel that our survivability is at risk. The rampant stressors of 2020 have triggered emotions that are primordial valuation signals. Emotions are e-motive; they come from a Latin root that means ‘causing movement’. Our emotions are motivational. Emotions are evolutionary signals that are designed by nature to get us to assess how we fare on the daily road of survival and moderate our behavior accordingly. Fear is a primal emotion that is designed to get us to do something, NOW — but what can we really do right now?
As a result of evolution, we mammals are subconsciously wired on an extremely basic level to avoid the negative emotional stressors that often led to pain and death in our ancestors and seek the comforts and pleasures we intrinsically associate with survival. As a result of these ancient emotional valuation systems, stressors are a known trigger for comfort-seeking behavior. Hence, we are all at greater risk of falling into the kinds of impulsive, ritualized, and isolated routines of comfort-seeking despite negative consequences that define addictive disorders — which includes the binge eating that often leads to obesity, as Nora Volkow, the director of the National Institute on Drug Abuse, has so beautifully illustrated with her work.
The emotionally-driven, binge-style eating that has caused an average of 10–15 pounds of weight gain for Americans during the pandemic looks remarkably similar to drug addiction in the brain. Given the current obesity crisis in America, where the adult obesity rate stands at 42.4 percent, it is clear that our understanding of addiction, in every shape and form, is highly relevant to the health and lives of us all.
I will be referring to addiction through the lens of the life-process learning disorder model. I’m borrowing the term ‘life-process’ from the thinking and treatments of psychotherapist Stanton Peele, PhD. I’m borrowing the concept of addictive disorders as essentially disorders of learning from the idea that, of all the brain systems implicated in addictive disorders, the impact on the learning and memory functions seem to be the most far-reaching, longest-lasting, and most consequential. The idea that addictive disorders are best understood as disorders of learning are attributable to addiction specialist and author Maia Szalavitz and the incredible neuroscientist Marc Lewis, PhD.
The works of ‘affective neuroscience’ pioneer and revolutionary genius Jaak Panksepp, PhD are heavily influential in the life-process learning disorder model, as well. Emotions are crucial to understand clearly if we are to understand and best treat addictive disorders as well as the other mental disorders that co-occur with them. Understanding emotional dysregulation is as key to understanding addiction as the learning and memory processes of the brain, and they are deeply, deeply linked. Nobody has done deeper work into mammalian emotional processes than Jaak Panksepp, PhD, yet perhaps nobody has had their work more marginalized by the neuroscientific community.
The life-process learning disorder model proposes that addictive disorders be understood as occurring on the spectrum upon which they are diagnosed by medical professionals, which is of chief importance. There is a huge difference between mild cannabis use disorder, moderate problem gaming disorder, severe binge-eating disorder, and severe cocaine use disorder, and they should be viewed differently based on social-emotional life context and therefore treated on an individualized basis. The life-process learning disorder model, or LPLD for short, is based upon the idea that our addictions are deeply-learned habitual responses and sources of gratification and security that can be best understood in the context of our deepest and most emotional experiences, our social relationships, and the personal, subjective experiences that define our humanity.
Basically, it says that there are personal reasons for our addictive behavior that go beyond the simplified, impersonal explanation that the addiction-related behaviors are merely impersonal symptoms caused by the brain disorder that is observable when a person is in an addicted state — no matter what that person is addicted to. The LPLD model brings about much-needed reconciliation between the undeniable disorder-causing brain changes that occur in the cases of ALL addictions, including non-drug behavioral addictions, and the fact that the addicted person is a human being with a deeply nuanced and personal social-emotional background, which provides the invaluable context of life experience to their addiction(s).
To simplify addiction down to mere neurochemical processes gone awry, which we do by saying addiction is just the result of an impersonal ‘disease process’ is no longer sufficient given the accumulating recent, relevant, and revelatory neurological findings. Current paradigms of addiction, which focus on impersonal brains that we imagine to be interfaced like a computer, devalue life experience and social-emotional context, which is just as important — if not more important — than understanding the temporary underlying state of brain disorder that can be observed in brain scans.
In order to understand and address the temporary, impulsive or compulsive reward-seeking state that the disordered person becomes stuck in, we must understand that person and their social upbringing and what they’ve experienced in their lives and how that has affected them and stuck with them on an emotional level. At the same time, the LPLD model has room for the notion of relapsing chronicity and other ideas that come from what we currently call the ‘disease’ model of addiction, reserved for when severe addictive disorders overlap with each other and co-occur with other mental disorders.
Though outdated, I believe the concepts put forth by the disease model still have value, and I believe there’s some room for overlap. I also don’t want to do a disservice to the recovery community by zealously degrading the disease model, the 12 steps, or the total-abstinence approach that comes with them; it is very important to me that I pay respect and homage to the recovery community and the 12-steppers who have transformed their lives despite living without the deep and detailed scientific knowledge that we have now.
Despite being continuously prosecuted, misunderstood, ostracized, and discriminated against, many of those who have found understanding in the disease model and the peace that comes with personal recovery through the 12 steps have become anchors for their communities. They’ve also inevitably stumbled upon some deep and fascinating neuroscientific truths, which I will certainly post later on.
I propose that some of the ideas put forth in the disease model do fit with Bill Wilson’s original idea of a ‘spiritual malady’, that our new confirmed understanding of dopamine as being associated with ‘wanting’ rather than ‘liking’ provides a valuable perspective on severe addictions that incorporates the essence of the severe addiction as being beyond the temporary pleasures of the brain and instead existing in the deepest, most emotional, inextinguishable desires of the human mind or spirit. I also propose that the 12 steps are a solution of group spirit-power/willpower that can be explained in neuroscientific language when successful.
Before we go any further, though, we must answer the question: why do humans use drugs, in the first place, let alone get addicted? Can we stop people from using drugs, or has drug prohibition been doomed to fail from the start, just like alcohol prohibition?
The idea of severe addictions and alcoholism as being a disease is an ancient one, and one that can be traced back thousands of years and across oceans and societies. Humans have been self-medicating with the various plant medicines we have isolated, reduced into chemicals, and now call ‘drugs’ for thousands of years — since before we were even humans.
Humans share 98.8% of our DNA with chimpanzees, and chimpanzees are known to self-medicate for intestinal parasites by eating the Aspilia root, which they have been observed seeking out and consuming in nature when necessary. Otzi, a human whose frozen body was recovered near the alps in 1991, lived approx. 3000 years BC and carried in his pouch a travel pharmacy that included a polypore fungus with antibacterial and hemostatic properties, presumably for self-medication.
Indeed, humans, monkeys, elephants, mongoose, ants — so many species of animal life have been known to self-medicate — including with intoxicants — that entire books have been written about it, and medical professionals have a word for it: zoopharmacognosy, which comes from the greek roots “animal-medicine-knowing”. We know when we need medicine, and we medicate ourselves when we feel the need — or, these days, we call a doctor with the expectation of a filled prescription. To read more about this fascinating phenomenon, check out ‘Intoxication’ by Ronald K. Siegel, PhD.
If self-medication with plant and therefore chemical medicines is completely natural in all animal life, from an ant to an elephant, the question bears asking: when does self-medication, which is totally natural, become pathological or ‘diseased’? Roman physician Celsus claimed that physical dependence on intoxicating drink was a disease way back in approximately 200 A.D and was perhaps one of the first to delineate between natural self-medication and pathological physical dependence.
Dipsomania seems to be the first medical term we used for the idea of an addictive disease of addiction, which was coined in the 1800’s. Dipsomania, or ‘thirst-mania’, is characterized by uncontrollable cravings for alcohol and periodic, compulsive binges on alcohol. A dipsomaniac might abstain from alcohol for a while without too much trouble, but as soon as that innate desire for self-medication kicked in, an anti-reward stressor triggered a subconscious reward-seeking response, or the dipsomaniac tasted alcohol again, there seemed to be some kind of internal reaction that was different from that of a ‘normal’ person: uncontrollable cravings and compulsive use would again manifest themselves. Dipsomania was thought to be a chronic, lifelong, cyclical condition based essentially in uncontrollable cravings and alcohol-related compulsions that were unique to the dipsomaniac.
Nora Volkow is considered the pioneer of the current disease model of addiction, which includes these centuries-old fundamental criteria: uncontrollable cravings, compulsive addiction-related behaviors, and lifelong chronicity. The disease model, which 80% of addiction treatment centers in America use as their dominant paradigm, is based on the dopamine hypothesis, which is based on the idea that all addictions stem from a ‘hijacking’ of the mesolimbic dopaminergic ‘reward system,’ which is a fancy way of saying that all drug addictions are thought to share the same basic biochemical basis and characteristics, which include the progressive development of an initially-pleasurable habit into an addiction that manifests as a behavioral compulsiveness that is simply beyond conscious control and applies to all drugs. That made sense to me for a long time — these exchanges of dopamine occur deep in extremely primitive parts of the brain that are thought to be all but completely beyond our conscious control.
The disease model that we, as a society, subscribe to in the 21st century, brings with it these ancient ideas of compulsive use, uncontrollable craving, and lifelong chronicity: ‘once an addict, ALWAYS an addict’ is a harmful stereotype in the eyes of some formerly-addicted people but a helpful daily mantra for others. Again, this illustrates the desperate need for reconciliation between life-process and choice-related models of addiction with the disease model. If addiction is a disease, we cannot ignore the incredible rates of ‘spontaneous remission’. We cannot ignore the fact that statistics have shown that an addicted person has the same chance of recovering on their own as they do if they receive treatment, and we cannot ignore the simple fact that the single greatest predictor of relapse is belief in the disease model, itself (Lewis, 2016). These are statistical facts — they are controversial, but they are statistical facts that are easily confirmable with a google search.
One of the problems with the dopamine hypothesis is that it posits that addiction is a brain disease on a molecular basis yet offers no molecular confirmation, like a blood test that could confirm that one person has the brain disease while another doesn’t. Biomarkers that we might use to confirm the presence of a drug-induced addictive pathogen, like DeltaFosB, occur in the cases of ALL addictions — even behavioral addictions — and only confound us further.
The dopamine hypothesis postulates a disease process that looks something like this: initial use of a drug causes sensations of pleasure which feel different to a person that is genetically predisposed to ‘the disease of addiction’. Increased subjective experiences of pleasure, which might better be understood as ‘hyper-euphoria’ in those that are genetically predisposed, lead to repeated use of the drug, which leads to the loss of control that characterizes addiction. As we continue to use drugs, our addiction worsens. At some point, we have contracted a brain disease.
We call this a brain ‘hijack’ because the constant seeking of survival-related rewards like social connections and food are superseded by the ever-increasing drive to use drugs, which work on a neurochemical level to cause feelings of pleasure that are incomparably more euphoric than anything ‘natural’. The dopamine hypothesis for the disease model of addiction is based on the old idea that dopamine is directly and causally associated with pleasure. We now know that this isn’t the case; dopamine is more associated with feelings of ‘wanting’ than the more typical feelings of ‘liking’ that we used to associate with dopamine (Berridge et al, 2016).
Since the disease model is based on an outdated and disproven theory about the role of dopamine in the brain, it is obvious that the disease model — and, as an extension of this, our understanding of addiction as a whole — is in desperate need of a serious update. To start, calling the dopaminergic system the ‘reward system’ is based in a misunderstanding that dates back to the 1950’s.
To read about the tenets of ‘affective neuroscience’ and how the affective neuroscience approach differs from traditional cognitive-behavioral views of addictive disorders, click the link to read the next article in the series.
