Theories of Addiction Explained

What are the different theories of addiction?

We've got the reward deficit theory, which basically says individuals

with hypodopaminergic states will seek out substances.

There is the impulsivity theory that says it's actually the opposite,

where there is excessive activity of the brain's reward

system

that moves the individuals towards seeking.

There is the incentive sensitization theory, which

posits that drug addiction,

it's the excessive amplification

specifically of psychological wanting

triggered by cues

without amplification of liking.

So this is a really important concept.

Sensitization is where initially what would have been liking

is now reduced liking with amplification of wanting.

And we'll see

the fourth one, which really brings all of it together,

known as the habit learning

theory. The evolution of addiction is linked

to the transition from liking a substance to wanting

and eventually seeking it compulsively,

reflecting a shift from conscious reward-driven behaviors to

automatic habits. When we think about humans, we are

very-- we know that our systems are brilliant at

moving from goal-direct action to habits.

So therefore,

when primed, when with certain circumstances,

any of us with the right

vulnerabilities

with substances can move from here, this

exact sort of

goal-directed action to ha-habit forming aspects.

We have the wiring for it. We can move from liking to wanting to

seeking.

Okay. In fact, the basis of psychodynamic

psychotherapy also is about automatized predictions.

Solms, Mark Solms calls it automatized

predictions, which is

nothing but the habits that we all have.

Some are not ever accessible to the

conscious, and that's why they are the true unconscious.

They are only seen in patterns of behavior.

And in order for those to change, we've got to write-- we've got to

bring them up to the conscious, to the consciousness, so

that we can actually

change it, which is exactly the same

neurobiologically.

Remember, what we're trying to do is to strengthen the frontal,

prefrontal striatal circuits, i.e.

strengthen cognition, because ultimately it's cortical drive

that

controls the subcortical aspects.

So often I find that the languages and psychodynamic aspects

are different. The methods that we use are different, but the principles

remain the same.

So reward deficit syndrome is a really interesting concept because

it's

transdiagnostic. Essentially what it says

is individuals lie on a

spectrum, and there are genes, there are neurobiological

aspects, and cognitive processes, so endophenotypes.

And RDS, you can-- this paper is, you know,

uh, the paper describes it as

an octopus.

Eating disorders, substance use, ADHD, post-traumatic

stress disorder, OCD, impulse dysregulation disorders are

all part of this octopus

where, uh, underpinned by reward deficit state.

You can see all of us lie on a spectrum.

You'll see ventral to dorsal shift.

You see, in the early phases, there are goal-directed

behaviors, which basically means that the prefrontal cortex

is still having some control over this

system. It's still goal-directed.

But it's this shift

from the dorsomedial striatum to the dorsolateral

striatum, the habit part, i.e. from the goal-directed

to the habit, that really starts creating the issues.

Because remember how our

structures have evolved. They've evolved to move

everything from goal-directed to habit.

The-- what's happening here is the substances move along

exactly the same way because that's how we've evolved.

We've evolved to move from goal-directed to habit.

They're taking the substance behavior along with it.

So what we've got here is this happens in the late phase.

So what's known as impulsivity to compulsivity

happens in eating disorder. That's why it's more resistant to treat,

because the

prefrontal cortex

starts losing its battle,

and the individual starts operating

on a compulsive mode, on a habit mode, on a primitive mode.

Let's recap the cascade towards addiction.

Starts off with reward learning, correct?

The exposure to substance, the

unexpected signal, because it's the first time you've used

it, you've

never been exposed to the substance ever before, there is a

surprise signal generated, right?

Now, in some individuals, that surprise signal will

lead to escalating drug use with the belief that we can

control it.

The issue here

is that we know what we think we can do is often quite

different from our behavior.

We know that the allostatic load through this escalating drug use has

started.

It's having its effect on the brain reward

pathways.

So therefore, we have allostatic load with incentive

sensitization. So you remember the incentive

sensitization

is the process where liking is going down

and wanting is going up.

Essentially, we're moving towards the process of normal

reward learning, where the substance is being associated with the cues,

right? Whilst the actual reward is not giving us what we

experienced at the start,

and number of cues will start being associated.

Then as it continues,

the prefrontal cortex will start gradually weakening or losing its

battle, simply because it's learnt

and it's moved towards the habit area.

That's known as the ventral to dorsal shift.

Then comes what's known as the dark side.

I'll touch on this dark side

a bit later.

This then moves towards a learned association,

because this dark side is where negative responses

are removed by the drug. Therefore, there's a learned association that

this drug helps me, or it removes the

negative aspects.

Then we move towards cues and seeking, cues

and relapse, and then cue generalization.

Lots of other cues will start getting added on, and you

can see how this process

can continue.