Cobbers on the Brain

What’s the best way to understand Addiction?

Although virtually everyone either has struggled or knows someone who has struggled with addiction, actually defining what addiction is can be tricky. To hopefully clear some things up, I will briefly contrast two competing definitions of addition: the dominant disease model and an alternative developmental cascade model. I argue that the developmental cascade model is a more compelling model because it more closely aligns with contemporary neuroscience (re: neuroplasticity) and offers less stigma/more agency for those struggling with addiction.

What is the disease model of addiction?

The National Institute on Drug Abuse defines addiction as a “chronic, relapsing brain disorder characterized by compulsive drug seeking and use despite adverse consequences”. The following sentence talks about how similar addiction is to other diseases, like heart disease…but does the brain science support this view?

Most researchers and medical professionals take the disease definition at face value, arguing that it is more accurate and helpful than unscientific views of addiction which portrayed addicts as “weak-willed” or “immoral”. The disease model of addiction also focuses on pharmaceutical treatments to solve addiction, much like cancer or heart disease. However, not everyone agrees with this view on addiction.

A close look at the disease model of addiction shows that it largely rests on two pillars, 1) There are distinct, significant changes in the brain associated with addiction, and 2) these changes are pathological because they can be extremely harmful to the drug-addicted individual.

What happens in the brain (The disease model interpretation)?

All drugs of abuse ultimately produce the same effect: they increase the amount of dopamine that flows from the VTA to the nucleus accumbuns (the reward circuit). Repeated use of these drugs can lead to changes in which the size and strength of synapses, how genes are regulated, and reduced connections between the reward circuit and other parts of the brain, like the pre-frontal cortex. Over time these neurological changes become stable, the act of drug-seeking changes from impulsive to compulsive, and harmful consequences occur more frequently and more severely.

Clearly, there are long-lasting changes in the brain involved with addiction, and these changes can be extremely harmful/deadly to those suffering from addiction, but does that make it a disease?

Why is the disease model wrong?

First, to the claim that addiction changes the brain. Yes, addiction absolutely changes the brain, but here’s the thing—so does literally everything we do! Change is the constant of the brain. Neuroplasticity, neural change through experience, is foundational for learning, without a changeable brain you couldn’t read this post!

How the brain changes in substance use disorders (alcohol, heroin, other typical “drugs”) are very similar to brain changes in behavioral addictions (gambling, internet, sex, binge-eating, etc) where there is no molecular drug that crosses the blood-brain-barrier to “hijack” our reward system.

Even more shocking is how human behaviors most people think are “healthy”, like falling in love, also produce significant changes in the reward system! At the molecular level, the types of cellular/molecular changes (cellular memory) at play in addiction are also seen in non-problematic behaviors/habits. In other words, when someone says addiction changes the brain, they’re not necessarily saying a whole lot because everything changes the brain.

Secondly, just because the consequences of addiction can be incredibly harmful, both to the individual and to those around them, does not make addiction a disease. Bullying, domestic violence, and racism are all deeply harmful and destructive human traits, but they’re learned behaviors, not diseases.

What all these examples hopefully show is that a different mechanism might be at play in addiction. Just because something changes the brain in no way necessarily means that change is caused by a disease.

What could be a more accurate picture of addiction?

In contrast, the learned behavior/developmental cascade model of addiction defines addiction as “motivated repetition that leads to deep learning”. The concept of “desire” comes in handy here. Desire, the longing feeling(s) of wanting something, is how the brain motivates us to repeatedly pursue goals. Dopamine is a key neurotransmitter involved in focusing attention on what to desire, regardless of the type of reward (food, euphoria, comfort, etc). As desirability increases so does the amount of VTA-nucleus accumbuns dopamine signaling. Therefore, addiction can be seen as a difference in degree, not kind, compared to gambling, falling in love, or cheering on a favorite sports team.

To be clear, rejecting the disease model does not mean reverting back to the moral failing model. Instead, by focusing on neuroplasticity the habit model provides agency for those afflicted by addiction and avoids stigmatizing them with either helplessness or shame. Most people recover from addiction, and surprisingly most recovered addicts do so without traditional treatment. Another blow to the disease model (I don’t think most cancer patients spontaneously recover), this fact shows that providing resources and support for addicts to change in their own time might be a more effective way to help.

Redefining addiction as a deeply learned behavior does not mean the addict is at fault, or that they just need to “get over it”. Addiction changes the brain. What we do have is the power to influence how our own brains change, given the right tools and a supportive environment. Since addiction is learned via neuroplasticity, the same way brains learn everything, and since addiction is maintained by reduced neuroplasticity, recovery can focus on returning that neuroplasticity the toolbox is the same! Helping people (re)discover interests beyond their specific addiction and educating them on neuroplasticity might be fruitful ways to help addicts who are ready to grow out of addiction. What is needed is empathy and support, not shame or stigma.

A recent study found that rats equally prefer Oreos and cocaine over control substances (rice cakes and saline). Not only that—the same brain regions are activated when both Oreos and cocaine are consumed, and are even more strongly activated by Oreos. Does this mean that Oreos are more addictive than cocaine? How does food addiction work on a neurochemical level? Why don’t we have “Oreo junkies” running around the streets? Read on as we “unwrap” food addiction.

Addiction On The Brain

First we need some background on what being addicted to a drug of abuse does to the brain. Drug addiction has several behavioral trademarks. People experiencing addiction tend to experience a loss of control regarding behavior and consumption of a drug, they become dependent on the drug, and they can easily relapse if they try to stop using the drug.

On the molecular level, being addicted to a drug causes physical changes in the brain. Long-term consumption of a drug resulting in addiction can even change the way that our genes are expressed, meaning the way proteins are made based off our DNA.

These changes involve reward and learning pathways of the brain. Drugs elicit a positive “reward” response because they make us feel good. The brain learns that consuming the drug = having good feelings, so we turn to the drug with increasing frequency to feel good. The brain even becomes tolerant to the drug as it learns to expect a dose, having a less intense reaction when the same amount is consumed. The number of receptors for certain neurotransmitters that make us feel good, like dopamine, increases as drug addiction sets in. The amount of dopamine that our brain naturally produces decreases, especially in a certain brain region known as the nucleus accumbens. This means the brain requires a dose of the drug just to reach its normal level of dopamine, and then requires larger and larger doses to chase the “high” or good feelings—and if we stop taking the drug entirely, our brain is so accustomed to it that we can experience dangerous symptoms of withdrawal.

Is Food Addiction a Thing?

Experts have debated whether or not “food addiction” is a valid form of addiction. One argument against this classification is that food can’t be considered a drug since it is necessary for human life. However, there is a compelling argument that food addiction is valid, which we will focus on here—and whether it fits the bill of an ‘addiction’ or not in the long run, it is certain that food addiction is detrimentally affecting the lives of thousands of people daily.

Symptoms of food addiction are similar to drug addiction: losing control of what, when, and how much food is consumed and becoming dependent on food when experiencing stress or negative emotions. For people who try to break out of food addiction through diets and even medical procedures, relapsing into disordered eating habits is very likely.

The neurochemical similarities of food addiction and drug addiction are striking. The same reward circuit is activated when high-calorie, high-sugar food is consumed as when a drug is consumed. In the nucleus accumbens, dopamine levels decrease over time so the brain becomes reliant on food consumption to stimulate good feelings, like in drug addiction.

Are Oreos Really More Addictive Than Cocaine?

After getting some neurochemical background, now we can look at the “Oreos and cocaine” study. The study found that rats show an equal preference for Oreos over rice cakes as they do cocaine over saline. The researchers looked at the nucleus accumbens (the brain’s reward center discussed earlier) and found that Oreos stimulated even more reward neurons than cocaine or morphine.

Now, does this mean that Oreos are more addictive than cocaine, or that they’re even addictive in the first place? Not necessarily. Our brains do show a strong positive “reward” impulse when consuming high-calorie, high-fat, and high-sugar foods like Oreos, but this doesn’t necessarily mean we are forming addictive habits. First, everyone living eats food, and very few people become addicted. Additionally, food addictions don’t appear to be food-specific; people who are addicted to food don’t necessarily having a craving that can only be sated with Oreos, any calorie-fat-sugar blast tends to do the trick.

Although the study’s findings have interesting implications in relating neurochemical effects of food addiction to effects of drug abuse, we don’t have to worry about becoming Oreo junkies just yet.