Eating Disorders, Oxytocin, and Vasopressin

February 21-27 is National Eating Disorders Awareness Week.  I have a history of some pretty disordered eating which landed me in the hospital a few years back, but it’s not something that I’m extremely comfortable talking about.  In the spirit of “awareness,” I’ve decided that it’s something I should talk about more.  In my personal life, this will mean that I’ll have to be a little more open with my friends.  Here on this blog, I’d like to share a little bit of the interesting information I’ve found in my search to understand my relationship with food a little more clearly.

I decided one day that I could either be a scientist or an anorexic for a living.  The energy I was spending counting calories and weighing my food and planning my next meal was a full-time job, and at the end of the day, I didn’t have any time left over for studying or reading or writing.  I carefully weighed the two options and decided that I should go with scientist- it has a slightly higher paycheck.  So I thought I’d start my endeavor by trying to understand why food can be such an all-consuming enterprise.  I had just learned about the little monogamous prairie voles, and thought that perhaps the “addiction” that those guys get to each other is similar to the “addiction” that some people have to chocolate, and that maybe in myself, that reward pathway had been broken or usurped by something else.  So I looked to oxytocin and vasopressin for answers.

It’s well-established that hormones and neurotransmitters are intrinsically linked with food intake, satiety, and metabolism.  Leptin, for instance, has been shown to act as a long-term regulator of appetite.  It is released by fat tissue and is able to cross the blood/brain barrier  to interact with receptors in a specific area of the hypothalamus.  Once there, leptin binds to another peptide called Neuropeptide Y and together they reduce the activity of the neurons in this area of the brain.  This tells the rest of the body that you are full.  Some research suggests that people can become “leptin resistant” in the same way that you can develop insulin resistance.

I spoke earlier of my “relationship” with food- and lots of people describe food this way, which is funny.  You can love food, but it’ll never love you back!  So why do we feel this emotional connection to a specific combination of apples, butter, and cinnamon that you have every year at Thanksgiving?  Or to fried green tomatoes like grandma used to make?  Or to those little fried potato sticks that used to be a staple of your elementary school lunches?  (Excuse me as I wipe a wistful tear from my eye…)

There’s no doubt that certain combinations of foods trigger responses in the neuroendocrine system, so it’s not unreasonable to say that those emotional connections to food are caused by neurotransmitters.  However, it is impossible to point to one peptide and say, “this is what is causing your craving for chocolate.”  The neuroendocrine system is highly interrelated, so we have to look not only at a specific peptide, but also to its relationship to other peptides.  As it turns out, oxytocin and vasopressin are no different.

Oxytocin and vasopressin are very similar to each other.  Both are only nine amino acids long, and between the two peptides, only two of the amino acids are different. They both act in both the peripheral and central nervous systems.  In the peripheral nervous system, oxytocin is one of the hormones responsible for inducing uterine contractions during birth,  release of milk into the collecting ducts in new mothers, and is elevated during orgasm in both men and women.  Vasopressin is important for kidney function and blood pressure regulation.  It helps to regulate how much water is released from the body as urine, and can increase blood pressure.  In the Central Nervous System, oxytocin has been shown to have very important functions related to memory, mother-infant bonding, pair bonding, and trust.  Vasopressin also plays a role in memory and partner preference, as well as aggression and circadian rhythm.  In many cases, oxytocin and vasopressin seem to be reciprocal to one another:  Oxytocin disrupts memory, while vasopressin enhances it.

In people with anorexia nervosa, the concentration of oxytocin in the brain is reduced, and peripheral nervous system responses are reduced or impaired.  Vasopressin, on the other hand, is elevated.  In patients with bulimia, oxytocin levels are normal, but vasopressin is elevated.  These reduced and elevated hormonal profiles are most likely to be the result of restricted eating and starvation rather than the cause of them.  But the elevated levels of vasopressin may play a role in recovery.  If vasopressin is important during the formation and retrieval of memories, it could be contributing to the difficulty many patients have in changing their old routines of restriction.

I said earlier that I simply “decided one day” to stop having an eating disorder, but it really didn’t work that way.  I’ve committed to memory the approximate caloric value of most foods that I eat regularly, so it’s a rare day that I don’t have a running tally going on in my head of how much I’ve eaten that day.  Is an elevated level of vasopressin influencing that behavior?  Maybe.  Is it the sole cause of it?  Probably not.   But I think it’s helpful to remember that recovery is not a simple act of willpower.  Willpower and empowerment play an important part, but there are all sorts of reasons why it’s harder than it seems like it should be, and we’ve only just begun to scratch the surface when it comes to this kind of research.

Bailer, U., & Kaye, W. (2003). A Review of Neuropeptide and Neuroendocrine Dysregulation in Anorexia and Bulimia Nervosa Current Drug Targets-CNS & Neurological Disorders, 2 (1), 53-59 DOI: 10.2174/1568007033338689
Frank, G. (2000). CSF oxytocin and vasopressin levels after recovery from bulimia nervosa and anorexia nervosa, bulimic subtype Biological Psychiatry, 48 (4), 315-318 DOI: 10.1016/S0006-3223(00)00243-2
Kaye, W. (1996). Neuropeptide abnormalities in anorexia nervosa Psychiatry Research, 62 (1), 65-74 DOI: 10.1016/0165-1781(96)02985-X

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