I utilize my own shared recovery experience to provide compassionate recovery care and empower clients to a life of health and wellness.
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Eating disorders are complex illnesses that are comprised of genetic vulnerability. So some people are just born with certain genetic variants that make them at a higher risk, and then that is usually coupled with some sort of environmental stressor. Dieting and food restriction are probably the most famous, but there is a long list of things that we know can trigger eating disorders: trauma, endurance, exercise, medical illnesses, and especially anything that can cause a negative energy balance.
Most of the available treatments currently focus on the nutrition and the psychological parts because we know the most about what caused those, and then we intercede first by addressing nutritional status, interrupting bingeing or purging behaviors, restoring weight if necessary, and then addressing psychological issues. But, historically, we have not been able to do anything on the biological side, the genetic side, because we didn’t know what those genetic mutations were that were increasing the risk of developing an eating disorder.
So that’s what I’ve been working on in my career since 2008 or so. It took me a long time, over a decade, but we finally were able to get to the point where we could start to identify some of those genetic factors. So I did a lot of that as pure research. It wasn’t around patient care but I did it for many years just trying to find the variance. And then I left research and just did full-time clinical care in 2016.
And then around 2019/2020, I was able to start offering some of those services to patients that we could only do before in a research setting. So we could actually start looking at their DNA, seeing what mutations they had, and then seeing if there was anything in there we could use to help improve their treatment. So, I don’t typically recommend it as a first-line option. It’s more something that we can have as an option down the road if people don’t respond well to traditional treatments, something that might be able to give us some new insights or some new treatment options.
For some people, it can be incredibly helpful. Sometimes we can’t find anything, and then sometimes we find things that we just can’t do anything about. The feedback I get from a lot of people is that there is a lot of guilt and shame associated with eating disorders. So what I hear from a lot of people is that just seeing it on paper and seeing what the variants are makes them feel less shame and less guilt, and more engaged in treatment.
Well, it’s a very flattering question. I was one of the first people doing it, I’m not the only one. There are lots of research groups that have looked at it. There’s a whole range of mutations. There are hundreds, probably thousands, tens of thousands of mutations, and there’s just a lot of variability of how much risk, some mutations give a very tiny amount of risk, like .1 percent risk.
And then some of them are very damaging. I tend to look at the ones that are more damaging, the ones that tend to run in families. Based on my training, those are a little easier for me to find. So I focus on these which are called rare highly damaging mutations. So mutations that dramatically increase the risk of getting an eating disorder.
This is one of the beautiful things about genetics. It’s what I call an unbiased approach. I’m literally sequencing all of your genes, that’s over twenty thousand pairs of genes, which is forty thousand total genes. So we’re sequencing everything. We make no assumptions at all of what could be causing it. We simply just look at all the mutations that people have and then we try to find genes that are more likely to be mutated in people with an eating disorder versus people without an eating disorder.
And you have no idea what you’re going to get coming out of it. It’s just completely unbiased. It’s like pulling out a fingerprint from a crime scene and running it through a database. Whatever you find is going to be interesting. You’re going to find somebody that was at the scene of the crime. So whether or not they were the actual killer or just a witness, you’re going to find something interesting.
So I was shocked by this. What I have found consistently over and over again is that people with restricted type eating disorders, such as anorexic restricting type and ARFID, tend to have mutations and genes related to metabolizing macronutrients. So fat is the most common. There are about twenty genes related to fat metabolism that are more likely to be mutated in people with anorexia or ARFID. Amino acids come from proteins.
So when you eat protein, you break that down into amino acids that can also be used as energy or can also be used to make proteins in your body. I think there are about fourteen genes in amino acid pathways, and then there are also ones related to vitamin D, carbohydrates, and B vitamins. So, B vitamins are very important for metabolism, your body uses B vitamins to help these chemical reactions that convert food into energy.
So B1 is thiamine, B2 is riboflavin, B3 is niacin, B7 is biotin, B9 is folate, B12 is cyanocobalamin, and then, pyridoxine is B6. So all of those are B vitamins that your body needs in order to help convert food and energy, these chemical reactions. And those also tend to be more likely to have mutations in them in the general public. Some people have these clusters of mutations and pathways related to metabolizing food for energy.
This would have been about the last thing I would have ever guessed going into this book. What I find over and over again is that people with restrictive-type eating disorders just tend to be metabolically less flexible. They’re less able to switch between different macronutrients or energy, which might be why they develop aversions to food or very restricted diets.
The body somehow knows which foods are harder to metabolize and tends to create aversions to those types of foods. For instance, people with difficulty breaking down amino acids, oftentimes, I find are vegan. They tend to not like heavy protein diets.
Obviously, with anorexia, there’s a very classic association with fear of fat. They don’t like to eat really fatty foods, red meat, oily or greasy foods, fried foods, or certain types of oils. If you look at the composition of those foods, they tend to be very high in the types of fat that they have a hard time metabolizing or breaking down. So the brain is amazing. The body somehow knows exactly what it can and cannot use as nutrients and then relays that back to the brain to kind of shape eating.
Yeah. It’s really striking sometimes, I’ll know the genetic results and so ahead of time without telling them, I’ll ask, “What foods do you really not like?”
In my mind, I’ll be like, oh my gosh. You know, those are all high in long-chain fatty acids.”
It’s been a very humbling experience because I’ve trained all these research hospitals and clinical treatment centers. I really thought I knew everything and we used to push all these foods and exposures and think patients were just afraid. And now I’m looking back, I was at the University of Iowa.
They were very proud of the fact that every Wednesday, they got bacon. Every Wednesday morning, they had to eat bacon. And looking back down, I’m like, oh, that probably was not the best idea. These patients, a lot of them probably just can’t metabolize these foods. And, they eat them and they feel very sick and they don’t like them, but they don’t know why. So what do they do? They see diet culture messages and weight loss messages and all this, and I think they attribute it to that, but my theory is there is an underlying biological process that’s driving a lot of these food aversions.
A lot of this is still preliminary. There are ways that you can measure a lot of these products. You can measure amino acids or breakdown products, amino acids, or fats. And it is very clear that they are elevated in people with restrictive types of eating disorders.
If you look at binge eating and bulimia, it’s pretty clear that there are four clusters of genes that are more likely to be mutated in people who binge eat. Those are all related to hormones or neurotransmitters related to regulating food intake and appetite. So in the response of eating, there’s a series of signals that get sent back to the brain to tell you to eat or not. If you’re fasting or going into starvation, a lot of appetite hormones get turned on or turned off.
And these are very well-established systems. You can go into mice and genetically delete these, and you can see effects on appetite and hunger. Those pathways tend to be more likely to be mutated in people with binge eating.
So that’s probably less surprising, a lot of people probably would have guessed that those pathways were involved.
I don’t recommend it for everyone, especially because it’s not covered by insurance, so it’s an out-of-pocket cost right now. I typically recommend it to people who have not responded well to the direct traditional approaches. If there’s a strong family history, so if you have multiple family members who have similar eating issues, we’re much more likely to find it in that case, and really unusual cases.
Or if people have really unusual symptoms where you think maybe there’s a medical condition that’s underlying the eating issues. It’s not like a traditional eating disorder. Those are the cases.
For some people, they have mutations that are really damaging and give them a very high risk of getting an eating disorder. Sometimes up to eighty-ninety percent of patients with a specific mutation will have an eating disorder, which is huge. For some patients, I’ll hardly find anything. So there is a a spectrum of genetic risk.
And oftentimes, the people who have fewer genetic mutations will have more trauma and more psychosocial stressors in their lives. Whereas people who have more of the genetic factor, they will develop it very young, eight, nine, ten.
We do know that first-degree relatives of patients with eating disorders are about five to ten times more likely. But, you only have about a one percent chance anyway. So even if you take the top end of that and you say your family member is ten times more likely to have an eating disorder, you’re still at only ten percent. And genetic testing at this point is not to the point where it can predict if somebody’s going to get an eating disorder or not.
I don’t typically recommend that. The most common thing I see in anorexia is a mutation that you call B-box one, which is kind of fun to say, but it makes this compound called carnitine. And carnitine is important for a number of metabolic reactions including burning long-chain fatty acids.
So, I have a lot of patients who have mutations in this B-box one gene, and that might be a case where it could make sense if you had a mother that had that mutation and had anorexia because it’s very easy to replace. You just give a supplement to get back to carnitine.
You could do the genetic testing and see if anybody in the family might benefit from getting a supplement of carnitine. That might be a case. I guess you could also just measure the carnitine levels in the child. That might be a case where you could rationalize doing the testing if it is something that is easily treatable.
We touched on this a little bit earlier. We published our original findings in 2017. That was the last study I ever published out of my lab, and we’d sequenced the DNA of I think it was, thirty-nine people with bulimia and seventeen with binge eating. So we had like fifty-six people that they had us group together as a binge eating group. And then just last week, I just released a second analysis of of my own patients that I’ve been seeing for the last few years.
And it largely confirms what we initially saw, that there are what are called these peptide neurotransmitters. They are these neurotransmitters that are made out of proteins, so they’re encoded in your genes. A lot of neurotransmitters are not encoded in your genes. Like, there’s no gene for dopamine, and there’s no gene for serotonin or norepinephrine. Those are all molecules that your body has to make. But there are genes for certain hormones and neurotransmitters.
Insulin is one. Ghrelin is one. Ghrelin is a hunger hormone or an appetite-signaling hormone. So there are dozens of these peptide neurotransmitters, and they’re involved in lots of what we call physiological processes regulating appetite, body weight, metabolism, sleep, reproduction, and things like that. So those certain molecules in that group are more likely to be mutated in patients with eating disorders. Some of these are around appetite, stimulating hunger. Others are around what I would call satiety, so turning off appetite after a meal.
The one thing I would take away is to really listen to people with the illness. So many of our patients just get dismissed. They get dismissed by family members, medical providers, or even experts like myself. For years, I now realize I was giving the wrong advice. And if we just sit and listen to people, they’ve really been telling us what was wrong the entire time.
We have all of these people saying, “I don’t like fat. I don’t want to eat fat. Having body fat makes me really uncomfortable.” And the whole time, we’re just dismissing them and saying, “Oh, that’s just your diet culture. You want to be thin and society is telling you that. Don’t believe that.”
And, obviously diet culture is huge and it does lead people to engage in behaviors that put them at risk for developing eating disorders. But our patients also have been telling us the whole time that there is something wrong and I just haven’t been listening to them.
So many of our patients say that they have GI pain. They have bloating and distress and things like that. And we’re all just like, “Okay, deep breathing. It’s just anxiety. it’s all in your head.”
One of the most common things I found is mutations in these genes called SCN7A and SCN9A. And they are they’re called ion channels. So they regulate the excitability of nerves, especially nerves in the part of the spinal cord that relays pain information from the extremities and from the gut. And people with these mutations tend to just be hypersensitive to pain and physical reactions.
So, I’ve got fifteen people with 7A mutations and then 19 with 9A. This is out of probably two hundred patients. so probably fifteen percent of my patients have mutations in these pathways that really are sensitive to sensory information from the intestine.
They probably are very sensitive to bloating and abdominal distension and all this stuff. And there are treatments. There are certain medications we can use to help normalize those pain signals. And, again, we’re just like, “Oh, it’s all in your head.”
We talk about patients wanting a sense of control, using this because they don’t feel in control of their lives. Now I’m wondering, are we just creating this lack of sense of control in these patients? Because for years, we’ve just been telling them not to believe their own experience. We’re just saying, “Oh, there’s nothing wrong. It’s just anxiety.”
I can see how that would create this really strong lack of agency, that they don’t feel in control of their own life because we’ve been telling them not to believe their own experience.
So, just listen to people and really try to be thoughtful. And if you just keep asking questions, I find a lot of times patients will really tell you what’s going on. They might not know it themselves, but they’re able to give you the information that you really need to figure out how to help them.
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Published by Merrit Elizabeth on April 20, 2024.
Merrit Elizabeth is an Eating Disorder Recovery Coach certified by The Carolyn Costin Institute. She holds a master’s degree in Health Promotion Management and has years of experience working with women with eating disorders.
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