Addiction in Reverse: The Link Between Anorexia and Reward Deficiency

What if food restriction fuels the cycle, not breaks it?

Imagine a netball carnival buzzing with teenage energy – a kaleidoscope of team colours and high-fives. Beneath the surface of this vibrant scene, a silent disease persists, one measured not in coughs and sniffles, but in barely touched lunches and secretly discarded snacks. This is the hidden world of teenage eating disorders, where food avoidance can mask a complex neurological struggle.

We’re used to thinking of addiction as a state of excess – the insatiable craving for more drugs, more alcohol, more stimulation. But what if anorexia nervosa represents a chilling flipside? What if the relentless restriction we see in some teens is fueled by a reward system chronically deprived of even the smallest pleasures? This theory, known as the inverse addiction hypothesis, proposes that a chronically under-stimulated reward system can fuel the restrictive behaviours seen in anorexia nervosa. 

The Inverse Addiction Hypothesis

Could a starved reward system drive anorexia nervosa?  This theory suggests that restricting food intake for prolonged periods may have profound effects on the brain’s reward pathways, making it difficult to find satisfaction in eating.

The Starved Brain

In the world of addiction, a protein called DeltaFosB plays a crucial role. It accumulates in the brain’s reward system with repeated exposure to pleasurable stimulation, often triggered by dopamine spikes. Over time, this buildup of DeltaFosB leads to tolerance: we need a bigger hit to achieve the same level of pleasure, reinforcing compulsive behaviours in a quest for that initial feeling. But what happens when the stimulation is absent?

Some researchers theorise that prolonged food restriction, regardless of the cause, may lead to abnormally low levels of DeltaFosB. While research is ongoing, this offers a possible explanation: with chronic undernourishment, the brain might decrease DeltaFosB production. This decrease could then trigger a vicious cycle of further restriction. Because DeltaFosB levels are low, the brain misinterprets even small amounts of dopamine, released in response to any eating, as a signal of fullness.  This leads the individual to restrict their intake even further, but this only worsens the problem. With continued restriction, DeltaFosB levels are likely to decline even further, perpetuating the cycle until the sufferer cannot consume any food at all.

The Testosterone Factor and Dopamine

Testosterone, a hormone much more prevalent in males, is a dopamine stimulant. This means that adolescent boys, who generally have access to levels of testosterone hundreds of times higher than adolescent girls, have higher baseline levels of both dopamine and DeltaFosB. This may offer some protection against the inverse addiction cycle of anorexia nervosa.

This biological difference could be a contributing factor to the significantly higher rates of anorexia nervosa in adolescent girls compared to boys (often a tenfold difference). Girls, with much lower baseline testosterone levels and therefore potentially less dopamine stimulation, might be more susceptible to the development of the reward system dysfunction seen in anorexia.

Beyond the Surface

It’s important to note that unlike traditional addictions, anorexia nervosa does not appear to be increasing in incidence. It remains a relatively rare disorder, affecting a small minority of people (approximately 0.1% to 0.2%) with a significant gender disparity – the overwhelming majority of sufferers are female. This pattern of rarity and stable incidence strongly suggests that predisposition plays a crucial role, with biology influencing who is most likely to develop the condition.

And not everyone is equally susceptible to reward system dysfunction. Emerging research offers a fascinating glimpse into factors that might influence a teen’s predisposition to different eating disorders. Think of your index finger and ring finger: the difference in their lengths (the 2D:4D ratio) may reflect how much testosterone and oestrogen a foetus was exposed to. Some studies suggest that girls with lower 2D:4D ratios (meaning, likely higher prenatal testosterone) might have a higher susceptibility to anorexia, potentially due to a hypersensitive reward system. Those with higher 2D:4D ratios might be more likely to develop bulimia, perhaps linked to a blunted reward response, making them more attracted to food.

The Path Forward

Acknowledging the potential biological underpinnings of anorexia doesn’t mean excusing it or minimising the psychological struggle. Eating disorders are complex, influenced by genetics, environment, and individual experiences. But if the inverse addiction hypothesis proves true, it could revolutionise how we approach these conditions:

• Reframe Our Understanding: Instead of seeing anorexia as purely about willpower or body image, we might focus on a brain being satisfied way before the body actually is.
• Compassionate Treatment: By understanding the neurological factors, we can reduce stigma and tailor treatments to rebalance the starved reward system– potentially including therapies that directly target these reward system deficiencies.
• Early Intervention: Research into prenatal influences may help identify at-risk teens, offering preventative support.

The adolescent meticulously restricting their food deserves our empathy, not our judgement. The answers to eating disorders may lie in the hidden workings of the teenage brain, and a better understanding might pave the way for healing.