The human body, which of course encompasses the brain, is an incredible and very complex machine. As humans we have evolved over thousands of years to become the highly intelligent, sophisticated and curious beings we are today.
Having spent time learning about the brain and how it works in conjunction with the body, I am endlessly struck by just how much, even with the modern science and research that we have now, we still don’t know about how the brain and body connect and function because it is so intricate, finely balanced and really very complicated!!
Due to my background with an eating disorder and my work today with others who have eating disorders, I developed a curiosity into the neuroscience of hunger, eating and satiety. What is it that drives us to eat (or not) and what mechanisms are at play? Is anything happening any differently in a person with an eating disorder?
Many of us have been guided to believe that we eat calories (food), we expend calories through movement or resting energy expenditure and as the calories out become more than the calories we put in, our brain realises that we need more food and so tells us we are hungry and to go eat.
Well… when you start to dig into the science behind hunger and eating, then you realise that all the processes regulating hunger and satiety are a lot more complicated than this.
But despite the neuroscience-biology of hunger and satiety processes not being overly simple, I do think it is useful to understand some of the mechanisms involved in hunger because when you have an eating disorder and your ‘normal’ biology is altered, knowing a bit of the science could help in your pursuit for health.
So, if you have your brain in gear for a bit of science then let us begin…
Brain Based Structures Responsible for Hunger
One of the main brain regions controlling hunger is within the hypothalamus of the brain and is called the arcuate nucleus (please don’t worry too much about the names I provide!).
Within the arcuate nucleus are two types of neurons (fancy name for brain cells) – one called the orexigenic neurons (responsible for circuits promoting feeding behaviours) and the other are the anorexigenic neurons (responsible for circuits that inhibit (stop) feeding behaviours).
From the arcuate nucleus, these neurons project to three other brain regions with signals that can then drive energy balancing responses within the body.
These are:
The paraventricular nucleus which influences body systems which promote the breakdown of larger energy molecules to smaller ones for use. These systems include the thyroid gland, cortisol and oxytocin pathways.
The ventro-medial hypothalamus which suppresses feeding behaviour by releasing a chemical called brain-derived neurotrophic factor (BDNF).
The lateral hypothalamus which can send signals to the body, stimulating the search for calorie dense food and promotes movement by releasing a few other hormones.
I hope I have not lost you already. Please don’t get scared off by the names of the structures or this bit of science... This section is merely to give an initial overview and demonstrate that eating behaviour is far from simple!
Hormones Controlling Hunger Levels
There are also two key hormones that help control the hunger and satiety levels within the body.
LEPTIN – Produced in adipose (fatty) tissue and acts on receptors in the arcuate nucleus to promote feelings of satiety (fullness) and stimulate heat production. If there are insufficient or decreasing fat stores in a person, leptin levels will be low, triggering a person to feel uncontrollable hunger and urges to eat, as well as making them feel colder than they should. Leptin helps to explain why 'normal' people who diet will rarely sustain their diet beyond an initial amount of weight loss as when they lose some fat stores and their leptin levels decrease, they feel overpowering urges to eat which are impossible for them to resist.
GHRELIN – Produced in the gastro-intestinal (G.I.) tract, sending signals to the brain to increase hunger and reduce energy expenditure. Ghrelin is responsible for stimulating the brain to give the increased thoughts of food we have when we are hungry as a means to drive us to seek food and eat! Ghrelin is also linked to increase cortisol release.
Cortisol is the main stress hormone and in acute stress it serves to provide the body with enough glucose for instant energy to deal with the stressful situation (by promoting the breakdown of larger energy molecules to smaller ones). However, when cortisol levels are elevated over longer periods of time, they can cause a blunted response of the brain to leptin so feelings of satiety are reduced and people experience a higher desire for sugary foods, also causing the body to store more abdominal fat (for instant access as the body deems it will be needed in this chronically stressful situation).
In people without eating disorders but who are experiencing ongoing stress, this rise in cortisol might explain why they are driven to eat more highly palatable foods when they are stressed than they would usually.
For somebody with an eating disorder, where the eating disorder will give rise to chronically elevated cortisol levels, this again can also help to explain why, in recovery, people are driven initially to seek sugary and highly palatable foods and also why initial weight gain in recovery is often stored as fat around the abdomen.... When this happens, recognise it as an expected and necessary physiological process and trust that it will all balance out with ongoing healing if you keep eating and stay in recovery.
LEPTIN RESISTANCE – Research has demonstrated that some people can develop some form of leptin resistance. This means that their brain does not respond to leptin release in an appropriate way, which leads to reduced feelings of satiety and a drive to keep eating. Leptin resistance can be genetically linked and can explain why some people do have naturally much bigger bodies.
Please note - if you have an eating disorder and strong ongoing hunger despite having eaten a lot of food (i.e. extreme hunger), this is being caused, not by leptin resistance, but by a body that is not yet producing enough leptin due to your ongoing energy deficit and lower fat stores than your body needs. When you come out of that energy deficit and gain sufficient fat stores, your leptin levels will normalise, and the satiety signals stabilise with it. Your body knows what it is doing and is just grateful you are now giving it the energy it needs to heal!
It is also important to be aware that there are a number of other hormones and chemicals that come into play in the complicated processes of promoting or inhibiting appetite and those mentioned here are just some of the key players! The roles of ghrelin and leptin are also described in relatively simple terms.
Pleasure Systems Driving the Desire to Eat
In addition to some of the biochemical structures and hormones that drive appetite levels, the other key factor in considering eating behaviours are the pleasure and emotional systems found within the brain.
In healthy people, eating is a pleasurable experience and so it overlaps with the brain’s reward circuits which drive pleasure seeking behaviours, reward learning and motivation.
Dopamine is a chemical most people have heard of and attribute to feelings of pleasure and reward and dopamine circuits in the brain are known to promote feelings of reward from eating foods as well as driving people to seek pleasure in food.
As the brain is really quite smart, the brain's reward, structural and hormonal circuits closely intertwine so that when the brain senses a need for more energy, it can activate all these processes to drive the person to find food and eat, hence increasing the likelihood of food intake and so, very importantly, survival!
In eating disorders, some of the reward and pleasure systems from eating becomes slightly wonky and that is now worth considering.
What Goes Wrong in Eating Disorders?
Firstly, let me start this section by saying that, as I said above, with everything to do with the body and the brain there is SO much we just don’t know. Research is only just beginning to learn much of the information provided above about normal hunger, let alone what happens in an eating disorder.
However, there is more science emerging now (happily).
In people with restrictive eating disorders, researchers have found that there are elevated levels of ghrelin and cortisol and reduced levels of leptin (as might be expected).
When someone has a restrictive eating disorder and so is not eating enough for the body’s needs, the brain identifies this as a stressful situation and so it will elevate cortisol levels to release immediate energy to seek food. The increased cortisol therefore also causes the typical hyperactivity many people with eating disorders experience. Ghrelin is simultaneously released which reduces unnecessary energy expenditure by reducing the metabolism and creates an increase in thoughts of food.
The hyperactivity caused by the raised cortisol in someone not eating enough can become a vicious cycle as this then results in further energy deficit, which the brain identifies as more stress and so releases even more cortisol!
Therefore, in cases of restrictive eating disorders, it is thought that cortisol is chronically elevated but that this is tied to a reward system that is not working as it should.
Within eating disorders, it is well documented and understood that there is a strong fear and anxiety-based reaction that develops to food and eating.
This can be seen within people with eating disorders, who have dopamine reward pathways that are less activated in response to food seeking and eating (as they are found to be in healthy people) but are activated in response to restriction and movement.
Over time, therefore, avoidant behaviours of food become stronger and the restrictive and hyperactivity behaviours become more rewarding, to the point that they can even become addictive and strongly habitual.
It is now recognised that people with restrictive eating disorders have the same hunger processes and can feel hunger in the same way as a ‘healthy person’ (as anyone with an eating disorder can testify to) but the reward from eating is negated by the fear and anxiety generated from the eating process and this overrides the drive to eat sufficient amounts.
In addition to all of the above, brain science also tells us that when it comes to compensatory behaviours within eating disorders, the strong impulses to compensate for eating are seemingly coming from reduced inhibitory control mechanisms that are seen in the pre-frontal cortex region of the brain (the part of the brain responsible for higher function).
Therefore, in eating disorders, the ability to override hunger and the behaviours typically seen within the illness appear to be stemming from a combination of elevated cortisol levels with a reduced reward response to eating and elevated reward response to food aversion and movement, tied into a reduced ability to stop oneself carrying out compensatory behaviours.
What Can YOU Do With This Information In Your Recovery?
Firstly, reducing your cortisol is going to be key, so reducing stress wherever possible in recovery is crucial. This is both emotional and life stress but also the stress created through movement, exercise and hunger!
Then, recognising that you are hungry and listening to those signals your body IS sending you while knowing that the fear response to food and the sense of reward from restriction is not appropriate and needs addressing. Finally, recognise that while underweight (that is, underweight for your body), your hormone levels, particularly leptin which usually provides feelings of satiety, will be low but with recovery they will normalise and the hunger cues that might feel a bit whacky now will become stable too.
I appreciate that this has been a long post and it is quite scientific, but I also know my readers are highly intelligent and that knowing the science can help.
Understanding and being able to explain to others the neuroscience behind why people might be seen to ‘over or under eat’ can also help reduce stigma of these illnesses that have been traditionally seen as a lack of will power, about 'control' or being deliberately difficult.
Science today is demonstrating more than ever that eating disorders and ‘obesity’ are not people without will power but this is biology gone awry and chemical processes that are producing symptoms and behaviours for which the only blame lies on their cells and DNA!!
Bibliography
Kinasz, K. R., Ross, D. A., & Cooper, J. J. (2017). Eat to Live or Live to Eat? The Neurobiology of Appetite Regulation. Biological psychiatry, 81(9), e73–e75. https://doi.org/10.1016/j.biopsych.2017.02.1177
**This post is a transcript of a podcast episode on my series,
'Feck it, Fun, Fabulous and Free in Eating Disorder Recovery',
which you can access for free here or wherever you usually listen to podcasts!**