Tummy Troubles

I will not be able to address all the facets of this topic completely, but I must touch on them in some way because nothing is more difficult to navigate than the presence of both identifiable symptoms due to food intake and an anxiety disorder.


Allergy, intolerance and sensitivity are often identified by those with eating disorders as reasons for not being able to reintroduce a broad array of foods back into the diet.

Now of course we all know that sometimes the patient explains her reasons for avoiding food as being due to an allergy or intolerance but there is no clinical allergy or intolerance present. In some cases, the patient is fully aware she does not have an allergy or intolerance but it is a convenient way to avoid any discussion about eating disorders with others.

But when it comes to this blog post, I am actually going to address the more insidious form of self-identified food allergy, intolerance and sensitivity that actually arise because the patient experiences symptoms when eating certain kinds of foods. In other words, she avoids foods that cause a reaction. The reaction is usually gastrointestinal, but may also involve rashes, headaches or foggy-headedness.

Those kinds of symptoms do not usually denote an allergic reaction of any kind, but what is a patient supposed to do if she needs to recover from an eating disorder and yet cannot eat a broad array of foods because they worsen physical symptoms?


There are two definitive and undisputed kinds of responses to foods: allergies and intolerances.

Immunoglobulin E (IgE) is the antibody that mounts the response leading to allergy and it is a reaction to the protein found within the offending food.

An IgE (immunoglobulin E) response will occur usually within five to ten minutes of eating the offending food. The symptoms are: extreme itching, hives, angioedema, wheezing, difficulty breathing and of course this can progress to anaphylactic shock. The only exception to the immediacy of the response is delayed food-dependent exercise-induced anaphylaxis where both food intake and exercise mean a severe reaction perhaps up to 4-5 hours after either exercise then food, or food then exercise is involved. The most common food associated with exercise-induced anaphylaxis is wheat. And the symptoms are still: extreme itching, hives, wheezing, difficulty breathing and swelling.

For those with food allergies, the only treatment is complete avoidance of the food.

It is possible to develop food allergies later in life if you have a history of tree-pollen allergies (hay fever-related symptoms). This kind of food allergy is also IgE-mediated and involves the same symptoms as listed above, but the offending food will be related to cross-reactivity of similar proteins found in both the tree-pollen and foods in question.

An example of cross-reactive food allergies of this kind would be allergic response to raw apples and a pre-existing allergy to birch tree pollen. Again, the only treatment is the avoidance of the food in question.

There are two exceptions here when it comes to complete avoidance of foods that actually cause allergic reactions:

  1. If you are in your teens, it is more likely than not you will outgrow many food allergies that have been present in childhood
  2. Improved health can allow a patient who formerly had to avoid a food allergen to reintroduce the food into his or her diet without any subsequent reaction to the food because (you guessed it) there are accompanying improvements in the gut’s microbiotic makeup and function. 1,2

Absolutely, never, ever reintroduce any known food allergen into your diet without the express involvement of your immunologist or allergist.

Food allergens that may be responsive to reintroduction with improved overall health status are those that are classified as the cross-reactive food allergies and often heating them changes the protein structure sufficiently that the immune system does not respond. Again, these are not areas in which you ever experiment without guidance and advice from medical experts on the topic.


Lactose intolerance is the most common example of food intolerance: the inability to produce lactase to breakdown lactose causes gastrointestinal symptoms within 30-60 minutes of consuming lactose-based foods.

Intolerance does not involve an immune response. There is primary and secondary lactose intolerance in populations.

Primary lactose intolerance occurs for many humans at around age four and their bodies stop producing lactase, the enzyme that digests lactose. That switching off of lactase production coincides with an age at which prehistoric humans would have been weaned.

However, many people have a mutation that allows for lactase to be produced throughout their entire lives. If you are of European descent, then it is very unlikely you have primary lactose intolerance; whereas if you are of Southeast Asian descent, the likelihood is high.

People often wrongly assume that lactose is present in all dairy products. However, lactose is not present in almost all cheeses and most lactose-intolerant individuals are not impacted by yogurt at all either as lactase is there within the product itself.

Secondary lactose intolerance happens for many with chronic illness, including eating disorders. Their bodies are so energy compromised that they cannot produce enough lactase to digest lactose. However, when they recover, they can produce the lactase again. Using a product such as Lactaid (lactase enzyme) can support the body until it can make its own lactase when the individual is well again.

An intolerance to a food item will mean that the body is unable to produce enough digestive enzymes to handle the food breakdown effectively and the result will be various gastrointestinal symptoms: gas, bloating, pain, sometimes acid reflux, possibly diarrhea and/or constipation, and occasionally skin rashes as well.

When food intolerances appear and the patient has an eating disorder, then the primary reason for failing to tolerate these foods will be too little energy within the body available to produce adequate amounts of digestive enzymes.

It’s a catch-22: you have to eat to provide enough energy for the digestive system to get back up to speed, but the digestive system is how you transform food into energy and it’s not yet up to speed. I’ll get into some more detail on how you might navigate this dilemma further on in the this post.

Celiac Disease

Gluten intolerance is a confusing term because in fact gluten sensitive enteropathy, or celiac disease, does involve an immune system response (meaning it is not technically an “intolerance”), but not with IgE. The specific antibody that attacks gluten in those with celiac disease is IgA.

Celiac disease is a genetic predisposition that can be activated by infection, stress, or hormonal changes. Sometimes patients with eating disorders who have this genetic predisposition find that the stress and hormonal changes associated with the eating disorder activate gluten intolerance. Gluten intolerance is celiac disease, otherwise known as gluten sensitive enteropathy.

Those with celiac disease have a body that mounts an immune response to the presence of gluten and the results are progressive destruction of the villi (the small hair-like protrusions throughout the gut that move the food forward and allow for proper absorption of nutrients).

There is no cure, but 100% gluten-free diet (replacing wheat, barley and rye in the diet with gluten-free grains) will ensure the patient does not develop further serious medical complications down the line.

For celiac disease testing, the various kits screen for the presence of IgA and IgG. They cross reference the levels of IgG because some patients have a mutation where they produce unnaturally low levels of IgA and that can lead to a false negative. These tests are not fabulously accurate (90%) and that is why it is still considered necessary to have a biopsy confirmation for the presence of celiac disease if a blood test comes back positive. For a whole host of reasons I won't get into, the biopsy is far from definitive too but we have not much else as a way to confirm the presence of the condition at this time.

First-degree relatives in your family with celiac disease or Crohn’s disease, or family members with hemochromatosis (excess iron production in the blood) would suggest that screening for celiac disease, assuming identifiable symptoms, is wise.

Naturopaths and Tests

Naturopaths often requisition various tests for what is called “sensitivity” to certain foods; but it may very well be that the results do not indicate sensitivity at all.

The blood test used by naturopaths to identify food sensitivities is based on the premise that high circulating levels of IgG (yet another distinct antibody of our immune systems) will correlate with clinical symptoms. The test itself involves coating a petri dish with food antigens and adding your blood sample to look for antibody interaction. Physicians, allergists and immunologists also use IgG screening, but the interpretation of the results will be different.

The big problem with IgG blood testing is that there is no clinical evidence as yet that the presence of high circulating IgG actually correlates with specific food sensitivities.

Many allergy and immunology associations have come out with position statements reinforcing that these tests are not definitive. IgG appears to be present in response to all foods and there is a competing theory that IgG may in fact act as a blocking mechanism (i.e. reducing immune responses to food intake).

"IgG molecules mediate interactions of cells with different cellular and humoral mechanisms. IgG antibodies signify exposure to products— not allergy. IgG may actually be a marker for food tolerance, not intolerance, some research suggests.” 3

There is one randomized controlled trial suggesting that IgG testing for food sensitivity and the subsequent removal of those foods from the diet resulted in the improvements of irritable bowel syndrome (IBS) symptoms. 4 However, both the method of blinding and the very weak outcomes have been criticized. Most notably the involvement of the company who creates the IgG test and their financial support of the trial was also identified as further confirmation that this trial is far from definitive. 5 For an excellent science-based overview of this entire issue, please check out: Science-based Medicine.org.

What is also completely off radar, and yet very likely critical for patients recovering from restrictive eating behaviors, is the fact that the symbiotic (friendly) and commensal (presumably neutral) bacteria in the large intestine are highly involved in the modulation of our immune responses to food. These colonies are decimated during bouts of restriction and excessive energy expenditures.

Quorum Sensing

Both bacteria and fungi have an ability that has been recently studied and identified called quorum sensing. The research in this area dates back to the 1960s with bioluminescent bacteria. It was discovered that these animals only emitted light when there was a particular number of them in the petri dish.

Quorum sensing, through chemical release and reception, allow individual bacterium to “sense” when there are enough of them present to do what it is they are there to do.

If we take Streptococci group A, a group of bacterial strains responsible for strep throat, as an example – 12% of all children carry these strains with no symptoms. Those asymptomatic children have immune systems that ensure the number of Streptococcus never reaches a quorum. Should one of those children become immunocompromised in a mild way (lack of sleep, a viral infection) then the Streptococci in her throat may multiply to reach a quorum and cause a sore throat (strep throat). She may require antibiotics to return the bacteria to its sub-quorum levels, or (more likely) her immune system will do it for her.

Quorum sensing is also relevant for all the good bacteria in the large intestines. When you restrict food intake, those colonies drop below quorum sensing levels and then they are unable to modulate all whole host of things on your behalf: proper reabsorption of water, immune responses to eradicate the presence of unwanted pathogens, supporting the mucosal lining’s ability to allow the right nutrients through to the blood stream and make sure the wrong things do head out the back door so to speak.

Disparate gastrointestinal symptoms (e.g. bloating, distention, flatulence, gas, diarrhea, loose stools, poorly digested foods, constipation, burping…) tend to flare up significantly as you enter a recovery process and that is because not only does your body have to bring back online proper digestive enzyme production and release, but the bacterial colonies have to multiply and start modulating the digestion and immune responses in the ways that they are meant to do as well.

Sometimes taking digestive enzyme supplements can help in the early phases of recovery. Yogurts with active cultures of Lactobacillus bulgaricus and Streptococcus thermophiles are known to help those recovering from eating disorders—clinically supporting normalization of gut function and even easing anxiety and the desire to restrict. 6 Saccharomyces boulardii (over-the-counter product Florastor) also aids in supporting the re-colonization of good bacteria and easing some of the gastrointestinal distress common in recovery. 7,8 It bears repeating that you should discuss the use of such supplements with your doctor before you embark on taking them.

Breath Testing for SIBO

Testing for small intestine bacterial overgrowth (SIBO) using a breath test (glucose or lactulose hydrogen) involves accuracy concerns as well as a questionable value of treating SIBO related to IBS as well.

To refresh everyone’s memory, IBS is a marker of having identifiable symptoms in the absence of any definitive diagnosis. IBS is not a disease state.

The correlations between SIBO, small bowel motility and IBS using these breath tests are weak and unreliable. 9,10,11,12,13

Even if the correlations were strong (and they are not), correlation is not causation. Therefore the presence of the gasses produced by these bacteria may suggest “bacterial overgrowth” but the causes for this overgrowth and whether said overgrowth should be treated or merely viewed as a symptom of another underlying cause that should be addressed, is beyond the scope of these screening tests in any case.

Between 30-62% of healthy subjects produce methane (or more correctly their natural gut flora do so). 14 Given that both hydrogen and methane release occurs in healthy and diseased subjects, there is little consensus as to what ranges might indicate disease. Healthy volunteers had fructose absorption capacity that varied from 5g to more than 50 g in one study with no subjective or objective symptoms of malabsorption either way. 15

We also know that the interoceptive awareness of those with IBS compared to non-IBS controls when a balloon is inflated in the colon (to simulate bloating and gas) involves the subjective experience of much more discomfort and pain for the IBS group compared to the non-IBS group. 16,17 I’ll get into more detail on interoception and why that might be relevant later on in the post.

What all of this means is the diagnosis of SIBO using breath testing does not have any evidence-based links to suggest the presence of the gases it identifies confirm that there is bacterial overgrowth, or that the presumed overgrowth could explain either IBS symptoms or gut motility issues either.

Furthermore, while treatment using a diet to eradicate the consumption of fermentable oligo-, di-, and mono- disaccharides and polyls (FODMAP) does correlate to the reduction of symptoms identified as IBS, it does not eradicate symptoms, nor does it resolve what may be any underlying, and as yet unknown, causative agent(s).

Most critically within the research community at present, researchers are concerned that the diet has no long term efficacy and is damaging to health overall. Randomized controlled trials suggest a lower bifidobacteria count as a result of removing these foods from the diet. 18,19

For a brief look at why lower bifidobacteria counts are of concern, the following meta-analytic review offers up these highlights:

Bifidobacteria are able to prevent or alleviate infectious diarrhoea through their effects on the immune system and resistance to colonization by pathogens. There is some experimental evidence that certain bifidobacteria may actually protect the host from carcinogenic activity of intestinal flora. Bifidobacteria may exert protective intestinal actions through various mechanisms, and represent promising advances in the fields of prophylaxis and therapy.” 20

Fancy Pants Stool Testing

When you are done with exhaustive scratch tests, skin tests, breath tests, saliva tests and the like, well you may end up at the other end of the system offering up samples of your own excrement for review by various medical and alternative practitioners.

Medical stool testing will have three main areas of investigation: 1) the detection of occult blood, 2) the presence of fat, bile, various enzyme levels, white blood cells, and 3) the presence of ovum and parasites (O&P).

Alternative practitioners offer many specialized stool tests to detect bacterium and fungi that are not considered parasitic and therefore not isolated within medically requisitioned stool tests. If you choose to undergo these tests, the results do not provide any causative relationship to your gastrointestinal symptoms. Here is a common species of fungi that can show up in these tests...

Candida Species

The Candida genus is a group of yeasts that are primarily either commensal (non-harming neutral presence) or symbiotic (helpful) in their relationship to humans and the human GI tract. Severe compromise of the immune system is a pre-determinant for the development of any systemic Candidiasis.

The most common Candida species responsible for what we call thrush (infection of the throat by the fungus) and vaginal yeast infections is C. albicans.

Candida species became the presumed source of numerous chronic conditions with the publication of The Yeast Connection, by Dr. William Crook. 21

As a result, many of you may have heard of a condition called Candida hypersensitivity syndrome.

Candida albicans infection has been proposed to cause a chronic hypersensitivity syndrome characterized by fatigue, premenstrual tension, gastrointestinal symptoms, and depression.” 22

In the above quoted randomized controlled trial for treatment confirmed that long-term antifungal treatment performed no better than placebo in alleviating the above listed symptoms or accompanying psychological distress.

And a thorough meta-analysis suggests there is no evidence to date for the existence of Candida syndrome, or Candida hypersensitivity syndrome in humans. 23

For severely immunocompromised patients (those with AIDS are the patient communities most commonly studied regarding these kinds of infections), C. albicans can cause systemic disease. There is a Candida species known to generate sepsis in wounds: C. parapsilosis. C. tropicalis closely related to C. albicans and is yet another pathogen (harmful agent) in severely immunocompromised patients as well. And finally there is C. dubliniensis also isolated primarily from AIDS patients.

There are three other species that are sometimes isolated with specialized O&P stool testing: C. krusei, C. glabrata and C. lusitaniae along with, of course, C. albicans as the most common. How an “overgrowth” may be identified from a stool or blood test is questionable. Most of us have these Candida species in our guts and, unless we are severely immunocompromised, they are never particularly invasive or opportunistic organisms for us.

The blood test that is usually performed checks for levels of IgG, IgA and IgM in the presence of the antigen (in this case Candida). However, the presence of IgG for identifying any intolerance is questionable as there is evidence this particular immunoglobulin may act as a modulator and not an excitor, as mentioned above. The presence of IgA in this situation merely indicates a mucosal response and will likely suggest the presence of a vaginal or throat yeast infection.

And finally, IgM antibodies respond to agents in the absence of ever having identified them as antigens prior to first exposure. IgM is often called our natural immunization response because it arrives at the scene to a possible invader whether the immune system has had prior knowledge of the antigen or not. In other words, an IgM response does not pre-suppose that you are already experiencing a Candida infection, but rather you have a healthy immune response to something that is not meant to be in your blood stream in the first place.

As for O&P stool testing, the presence of symbiotic and commensal strains of Candida is expected and the concept of “overgrowth” is undefined.

Alternative medicine presupposes that systemic Candida infections can exist in human beings at essentially sub-clinical severity. However, there is no good trial evidence to suggest that Candida floats about all over our bodies causing all manner of unpleasant but non-life threatening conditions (anything from hay fever to flatulence).

Medically, systemic Candida infections are pretty deadly and severe. That’s why they are only seen in severely immunocompromised patients. And while many, many chronic conditions are complex and largely not understood by medicine, infectious agents happen to be a knowledge area of extreme superiority largely because infection has been the paradigm under which the entire medical research community has been working since the time of Louis Pasteur.


Dysbiosis is not easily measured with stool samples, blood or breath tests etc. The inter-relationship and relative colony sizes of all your symbiotic, commensal and opportunistic bacteria and fungi in the gut simply cannot be identified and counted. We have to rely on symptomatic evidence and then we have no clue how to definitively rectify any imbalance of these populations in relation to each other. And one person’s imbalance might be another person’s healthy asymptomatic balance as well.

To make matters more complicated we have all but just begun to amass evidence that all these fabulous creatures are modulating our immune systems in wondrous and helpful ways and therefore any gut flora imbalance won’t necessarily involve only gut-limited symptoms.

And of course, the study of dysbiosis within the medical community predominately involves acute and not chronic conditions.

Dysbiosis can be readily achieved through the use of broad-spectrum antibiotics. Because broad-spectrum antibiotics are indiscriminant in their killing abilities, the relative presence of symbiotic to commensal to opportunistic microorganisms in your gut can end up off kilter.

There are promising data in the area of applying fecal bacteriotherapy for those with severe (and often fatal) cases of dysbiosis that are usually the result of other serious diseases. 24

When it comes to milder forms of dysbiosis associated with eating disorders, most cases require absolutely no intervention to return to an optimal balance of gut flora. However, it takes time— perhaps two to four years after weight restoration.

A note on why skin rashes occur with gastrointestinal dysbiosis: because your gut’s microbiota are intimately involved in keeping the mucosal lining of the gut healthy and capable of allowing the right substances pass into the blood stream, when the microbiota are decimated by starvation, then the wrong kinds of substances pass into the blood stream. When that happens, then the immune system mounts a response. A common marker of that response will be skin rashes, headaches, generalized inflammation and the like.

Eating Into the Pain

What follows is my suggested approach to the resolution of IBS and dysbiosis that occur due to eating disorders. I offer this up as an approach that may not be suitable for everyone, but is often suitable for more people than not.

Absolutely, never, ever drastically increase your food intake when you have an active eating disorder without the express involvement of your medical practitioner.

When a patient has any major surgery, returning to normal food intake and mobility is encouraged within mere hours of a post-operative return to consciousness.

Our gastrointestinal system is the fulcrum of our energy intake, waste outflow and immune system function. It is not healed through easing up on its use (through less intake, delayed intake, spacing out intake every few hours, removing macronutrients from the diet, etc. etc.).

While symptoms and inflammation can be eased by avoiding the use of this basic life-sustaining system, that does not equal a cure or a resolution of the underlying problems that are triggering the symptoms in the first place.

And attempting to support your body’s desperate need for more energy while maintaining a restrictive diet of any kind is problematic to say the least.

I approach eating disorders through the discipline of triage. Eating disorders are deadly; IBS is not. That is not to say that the symptoms associated with IBS are not phenomenally unpleasant and painful, they are. But there is no question in my mind that re-energizing an energy-depleted body must take precedence over squelching non-life threatening symptoms, to the maximum level to which the patient can manage the impact.

Furthermore, there is plenty of evidence that much of the gastrointestinal distress that is monstrously present for those with active eating disorders, actually resolves with aggressive re-feeding tactics. 25,26,27,28,29

If you think about it in a mechanical way, what would likely (in the absence of obstructions or inflammatory conditions such as Crohn’s or ulcerative colitis) resolve constipation, gastroparesis, anorectal dysfunction and colonic inertia? Enough energy needs to be available to the body for it to manage repairs to the enteric (gut) nervous system and restore the gut’s microbiotic balance.

If a patient has been bed ridden for some time due to severe illness, the muscles may not even support her swinging her legs to the side of the bed. Resolving muscle atrophy is not achieved by avoiding use of those muscles and the same holds true for gastrointestinal atrophy as well.

Reintroducing all the foods that are currently absent from the diet as well as upping the calorie intake and eating constantly is the best prescription for the myriad gastrointestinal symptoms that appear and persist with chronic energy deficiencies.

Please note all the necessary caveats to that re-feeding effort: that you do not have diagnosed inflammatory conditions such as Crohn’s or ulcerative colitis; neuropathic or myopathic disease; biopsy-confirmed celiac disease; any food allergy that suggests severity that may lead to anaphylactic shock; any obstruction, or risk of obstruction in the GI tract; and/or any other diagnosed medical condition that might increase your risk of mortality should you begin to reintroduce macronutrients that are currently off limits.

If you and your medical professionals are comfortable that there is nothing life threatening at hand to reintroduce foods, then work to reintroduce everything in rotation and keep a food/symptom journal. But, critically, rate the symptom severity as well.

Honestly, this approach is not about comfort. It is about weighing up short-term discomfort against long-term quality (and length) of life benefits.

When a patient is encouraged to get up out of bed immediately after knee surgery, it is no comfortable thing— nor are the rehabilitation and physiotherapy treatments either.

The same is true for a patient going through exposure and response prevention therapy to deal with a phobia of flying. The patient is encouraged to rate her anxiety one through ten and most will absolutely feel at a “15” as they try to approach rather than avoid their identified threat (in this case flying).

Being bloated, constipated, exhausted and in pain is just plain miserable. And all those symptoms are part and parcel of the recovery process – reintroducing foods, eating more food and eating constantly.

Recovery is rehabilitation and it is not an asymptomatic ride that’s for sure.

Interoception, Pain & Recovery

At this point you might be thinking: “Really? Seriously? Your suggestion is to just ‘lean into that pain’?” That might even be followed by some choice expletives directed my way as well actually.

So here is how to navigate your pain and your recovery that is respectful of your reality:

The above pain scale is from Hyperbole and a Half and it is my favorite pain scale.

Here is the accompanying explanation for each pain grade:

0:  Hi.  I am not experiencing any pain at all.  I don't know why I'm even here.

1:  I am completely unsure whether I am experiencing pain or itching or maybe I just have a bad taste in my mouth.

2:  I probably just need a Band Aid.

3:  This is distressing.  I don't want this to be happening to me at all.

4:  My pain is not fucking around.

5:Why is this happening to me?

6:Ow.  Okay, my pain is super legit now.

7:  I see Jesus coming for me and I'm scared.   

8:  I am experiencing a disturbing amount of pain.  I might actually be dying.  Please help.

9:  I am almost definitely dying.

10:  I am actively being mauled by a bear.

11: Blood is going to explode out of my face at any moment.

Isn’t Allie Brosh brilliant? We can never know another person’s pain. I am only practiced in my own pain levels and so if you tell me you are at “11”, then you are.

As a general guide, to move yourself through recovery when you face pain, try to persist unless and until you are beyond a “6”. Then retreat.

Let’s get into how you persist and how you retreat.

Interoception Volume Knob

You likely know this but we actually have many more senses than the five we are taught in school: sight, taste, touch, smell and hearing. Here are all the additional senses:

Our body in 3-dimensional space – you know where your hands are without having to look at them (proprioception).

Pain (nociception).

Temperature (thermoception).

Satiation/Hunger (I presume this might be called homeoception, as a nod to homeostasis).

Itchiness (pruritoception)

Verticality in space – whether you are upright (equilibrioception)

Passing of time (chronoception)

Navigation – it appears to be a very weak sense in humans (magnetoception)

Chemical levels – breathing rate (oxygen blood levels), hormone transmission…  (chemoception)

Physiologic condition of the body – sense of internal organs (interoception).

Various neural conditions, traumas to the brain or lesions can really mess with any or all of these senses.

These senses are just a bunch of nerve stimulation, and it is the brain that interprets those electrical signals. If the brain has anomalous ways of interpreting the raw data, then our sense of things is going to deviate from the norm. Autistic children are notorious for being more highly sensitive to sights, tastes, touch, smell and hearing. The sensitivity resides in how the brain is interpreting the raw electrical signals.

Nociception, our perception of pain, is a complex sense that is heightened by emotional salience. The misapplied phrase of “it’s all in your head” is technically correct. You experience pain in two ways: the physical identification of damage or excitation of the nervous system, and the interpretation of that sense within the emotional and conscious areas of your brain.

Dr. VS Ramachandran has done some amazing work with phantom limb pain that re-wires what might be considered a completely locked-in sense of pain stimuli that reside entirely in the brain and not the (now absent) limb. In other words, the pain experienced resides entirely within the central nervous system and is without its originating, localized nerve damage or excitation.

Many pain management treatment programs and protocols are designed to try to help a patient reframe the emotional and conscious connections he or she might have to physical pain. There are also some fascinating programs that endeavor to intercede between the peripheral and the central nervous system communication so that the kindling of the pain perception loop is severed.

For any of you who have ever been prescribed opioids you are probably familiar with the fact that this class of drug is capable of emotionally distancing you from the pain, but that it doesn’t really take the pain away. We shorthand that experience by saying it “dulls” the pain. In fact, it dulls your connection to that pain— and pretty much the connection to everything else in your life as well.

Eating Disorders and Nociception

As an eating disorder is inherently an anxiety disorder anchored in a specific misidentification of food as a threat, heightened emotional salience pertaining to the physical sensation of eating and digesting food would seem an expected outcome of having the condition.

There are much research data available on the fact that restriction of food intake lowers nociception, the perception of pain, in patients with eating disorders. 30,31,32 Conversely, healthy controls deprived of food show a marked increase in nociception. 33 One small study of bulimic patients who were classified as recovered for one year appeared to maintain an increased tolerance to pain when compared to healthy control. 34

And while it is difficult to come by, some limited research actually shows that re-feeding and unrestricted eating status increases the perception of pain. 35

What this means is that you may become increasingly aware of your physical symptoms and that this awareness will cycle through the emotional centers of your brain to generate increasing levels of anxiety. And anxiety tends to drive us to act without thinking – great for real survival maneuvers but really damaging when the original panic button should not have been pressed in the first place.

In a study of patients who had been assigned the IBS classification where each subject had a balloon inserted up from the rectum to the large intestine and then inflated while in place, those with IBS described significantly more pain and discomfort associated with the experiment than healthy controls. 36 What does that mean? It could mean a whole bunch of things. The researcher suggests it indicates a biopsychosocial model might be more appropriate regarding the onset of the cluster of symptoms that have no underlying identifiable disease (namely IBS):

With the Crohn's disease example, the clinical expression of the disorder is not explained by the degree of disease activity. Rather, the symptoms and impaired quality of life relate to preexisting psychosocial determinants. The observed association of stress with disease activation in Crohn's disease is explained by stress-related alterations in psychoimmunological function via the hypothalamic-pituitary-adrenal axis.” 37

Additionally, an fMRI study showed marked differences in neural responses for those with IBS vs. those without with these kinds of pain stimuli. 38

I am a great believer in “kindling”. The model, when used in a neurological sense, is actually applied to the expression of epilepsy. Repeated stimulation lowers the threshold for more seizures to occur once an initial seizure has occurred.

The kindling model can also easily be applied to all our senses, particularly both interoception and nociception.

Nociception, or pain perception, has a mechanical side and an interpretation side (as do all the other senses for that matter). The mechanical side is the various electrical signals traveling from the peripheral or enteric nervous systems to the central nervous system indicating damage and distress of some kind or other.

It is the central nervous system (CNS) that interprets the raw data. And the interpretation is inextricably linked to the emotional centers of our brain. We feel pain. And within those areas of the brain, we can also experience a loop that makes the pain perception more salient (important to us) and therefore more “painful”. The very identification of pain can generate more pain. It’s a positive feedback loop in those circumstances – kindling instead of dampening.

Here are two videos on the topic: Elliot Krane and Vilayanur Ramachandran.

As you know, neurons that fire together wire together (ground zero of kindling). If smells, noises and certain lighting all trigger nausea and food aversion, then the next time these stimuli appear it takes lower amounts of the stimuli to create an equal or stronger reaction.

And if you have found you are bloated, in pain, and dealing with acid reflux when you eat cheese, then the same type of kindling loop could be occurring for you as well.

That’s where all the mindfulness, meditation, relaxation techniques, yoga and unplugging come in—finding ways to allow for physical pain without allowing emotional salience to generate more feeling of the pain than is present.

There was a quote that whipped by me recently – can’t remember the author. It was something along the lines of: “It is imperative I practice meditation a half hour a day, except when it gets really busy. Then it has to be an hour a day.” [edited to add: site member Persephone has kindly informed me that the originator of this quote is Jon Kabatt-Zin, author of Full Catastrophe Living.]

I do not suggest that any of these techniques eradicate the physical discomfort; they only shift the emotional relationship with those physical symptoms. Often pursuing pain or symptom management with these techniques is misconstrued as suggesting that the entire experience is somehow “made up” or “just drama”. Nothing could be further from the truth, as I know full well.

IBS is specifically nomenclature used in medicine to denote that identifiable and often measurable symptoms are most certainly present, but that no underlying disease can be detected as the cause of those symptoms. It is not a “mental illness”. But our emotional relationship to any chronic condition can radically change our experience of the condition itself.

Approach Retreat Repeat

Because anxiety, which is the foundation of an eating disorder, is all about triggering avoidance, it is important to create a framework to ensure that you do not retreat from pain and then just keep going because it reinforces restriction.

When the pain, in your estimation, hits “6”, then commit to self-compassion and self-care for 20 to 30 minutes. Examples of this might be to go sit or lie down with a heating pad while sipping on some tea; or sitting with your cat on your lap (if he or she will oblige) – stroking your pet can ease your emotional connection to the pain; or watching a few funny YouTube videos for distraction might work as well.

Reassess at that point whether the pain is now “5” or lower. If it is, then you return to eating. If it is not, then go back to the various self-compassion and self-care options but this time also include sipping on a calorie-dense drink that is easily digested for you (if it has to be Fortisip or Ensure that’s fine, or perhaps banana/chocolate smoothie with full-fat yogurt). Or if liquids don’t appeal, then go for nibbling on nuts or seeds.

The important part of the equation is to recognize that the emotional salience of your pain can quickly be leveraged towards avoidance of food. You want to be respectful of not pushing through untenable levels of pain while also reinforcing that you must keep approaching and eating food.

Keeping a log of pain levels may seem counter-productive: “Why would I reinforce my experience of pain by measuring it and jotting it down?” In fact this approach tends to help you apply your cognitive functions so that you can develop more flexibility in relationship to your pain. You can become more curious about its expression; register what circumstances make the pain more or less noticeable to you; and provide opportunities to identify your success at shifting your interactions with your pain.

Any Doubt? Then Don’t Second Guess It

The odds are always in favor of a recovery process that will involve a lot of gastrointestinal distress but that it will signify nothing ominous or life threatening. And it will ease as your recovery progresses.

But (there is always a “but”), there are most certainly cases where the pain indicates that something has gone awry and that medical intervention is absolutely necessary.

My first-hand experience has been that such complications are very rare, but they can be serious. If the pain you are experiencing is beyond a “6”, or the pain is unrelenting, or the pain has changed in its nature/duration/type, or the pain has persisted and doesn’t seem to be trending downwards despite continued rest and re-feeding, then do not second guess yourself and seek medical attention.

And all the cute gif imagery at the start of this blog post aside, there is nothing cute about pain. So please do not interpret my suggestions regarding pain management as always applicable or to be interpreted as dismissing the intensity and seriousness of your particular circumstance.

1. Tang, Mimi LK. "Probiotics and prebiotics: immunological and clinical effects in allergic disease." In Microbial Host-Interaction: Tolerance versus Allergy, vol. 64, pp. 219-238. Karger Publishers, 2009.

2. Özdemir, Ö. "Various effects of different probiotic strains in allergic disorders: an update from laboratory and clinical data." Clinical & Experimental Immunology 160, no. 3 (2010): 295-304.

3. Gavura, S. "IgG Food Intolerance Tests: What does the science say." Science-based Medicine Blog (2012).

4. Atkinson, W., T. A. Sheldon, N. Shaath, and P. J. Whorwell. "Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial." Gut 53, no. 10 (2004): 1459-1464.

5. Hunter, J. O. "Food elimination in IBS: the case for IgG testing remains doubtful." Gut 54, no. 8 (2005): 1203-1203.

6. Nova, Esther, Olga Toro, Pilar Varela, Irene López-Vidriero, Gonzalo Morandé, and Ascensión Marcos. "Effects of a nutritional intervention with yogurt on lymphocyte subsets and cytokine production capacity in anorexia nervosa patients." European journal of nutrition 45, no. 4 (2006): 225-233.

7. Lochs, H. "Interaction between nutrition, intestinal flora and the gastrointestinal immune system." In Home Care Enteral Feeding, vol. 10, pp. 179-188. Karger Publishers, 2005.

8. Kelesidis, Theodoros, and Charalabos Pothoulakis. "Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders." Therapeutic advances in gastroenterology 5, no. 2 (2012): 111-125.

9. Posserud, Iris, Per-Ove Stotzer, Einar S. Björnsson, Hasse Abrahamsson, and Magnus Simrén. "Small intestinal bacterial overgrowth in patients with irritable bowel syndrome." Gut 56, no. 6 (2007): 802-808.

10. Simrén, Magnus, and Per-Ove Stotzer. "Use and abuse of hydrogen breath tests." Gut 55, no. 3 (2006): 297-303.

11. Bratten, Jason, Stewart Spies, and Michael P. Jones. "W1338 Preliminary Observations of Simultaneous Lactulose Breath Testing (LBT) and Scintigraphy in Controls: SIBO Is Not SIBO." Gastroenterology 134, no. 4 (2008): A-683.

12. Vanner, Stephen. "The lactulose breath test for diagnosing SIBO in IBS patients: another nail in the coffin." The American journal of gastroenterology 103, no. 4 (2008): 964-965.

13. Ford, Alexander C., Brennan MR Spiegel, Nicholas J. Talley, and Paul Moayyedi. "Small intestinal bacterial overgrowth in irritable bowel syndrome: systematic review and meta-analysis." Clinical Gastroenterology and Hepatology 7, no. 12 (2009): 1279-1286.

14. Sahakian, Ara B., Sam-Ryong Jee, and Mark Pimentel. "Methane and the gastrointestinal tract." Digestive diseases and sciences 55, no. 8 (2010): 2135-2143.

15. Rumessen, J. J., and E. Gudmand-Høyer. "Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides." Gut 27, no. 10 (1986): 1161-1168.

16. Bradette, M., M. Delvaux, G. Staumont, J. Fioramonti, L. Bueno, and J. Frexinos. "Evaluation of colonic sensory thresholds in IBS patients using a barostat." Digestive diseases and sciences 39, no. 3 (1994): 449-457.

17. Bouin, M., M. Boivin, V. Plourde, M. Riberdy Poitras, F. Lupien, M. Lanagiere, P. Verrier, and P. Poitras. "Rectal distension testing for diagnosis of IBS: sensitivity, specificity of pain sensory thresholds." Gastroenterology 122 (2002): 1771-1777.

18. Khan, Muhammad Ali, Salman Nusrat, Muhammad Imran Khan, Ali Nawras, and Klaus Bielefeldt. "Low-FODMAP diet for irritable bowel syndrome: is it ready for prime time?." Digestive diseases and sciences 60, no. 5 (2015): 1169-1177.

19. Halmos, Emma P., Claus T. Christophersen, Anthony R. Bird, Susan J. Shepherd, Peter R. Gibson, and Jane G. Muir. "Diets that differ in their FODMAP content alter the colonic luminal microenvironment." Gut (2014): gutjnl-2014.

20. Picard, C., J. Fioramonti, A. Francois, T. Robinson, F. Neant, and C. Matuchansky. "Review article: bifidobacteria as probiotic agents–physiological effects and clinical benefits." Alimentary pharmacology & therapeutics 22, no. 6 (2005): 495-512.

21. Crook, William G. The yeast connection: a medical breakthrough. Vintage, 2010.

22. Dismukes, William E., J. Scott Wade, Jeannette Y. Lee, Bonita K. Dockery, and Jack D. Hain. "A randomized, double-blind trial of nystatin therapy for the candidiasis hypersensitivity syndrome." New England Journal of Medicine 323, no. 25 (1990): 1717-1723.

23. Zunder, Thomas, Roman Huber, Anna Sander, Franz Daschner, and Uwe Frank. "The pathogenetic significance of intestinal Candida colonization–a systematic review from an interdisciplinary and environmental medical point of view." International journal of hygiene and environmental health 205, no. 4 (2002): 257-268.

24. Gough, Ethan, Henna Shaikh, and Amee R. Manges. "Systematic review of intestinal microbiota transplantation (fecal bacteriotherapy) for recurrent Clostridium difficile infection." Clinical infectious diseases 53, no. 10 (2011): 994-1002.

25. Mehler, Philip S., Amy B. Winkelman, Debbie M. Andersen, and Jennifer L. Gaudiani. "Nutritional rehabilitation: practical guidelines for refeeding the anorectic patient." Journal of nutrition and metabolism 2010 (2010).

26. Buchman, Alan L., Marvin E. Ament, Marvin Weiner, Anatoly Kodner, and Emeran A. Mayer. "Reversal of megaduodenum and duodenal dysmotility associated with improvement in nutritional status in primary anorexia nervosa." Digestive diseases and sciences 39, no. 2 (1994): 433-440.

27. Brown, Jeffrey M., Philip S. Mehler, and R. Hill Harris. "Medical complications occurring in adolescents with anorexia nervosa." Western Journal of Medicine 172, no. 3 (2000): 189.

28. Chial, Heather J., Donald E. McAlpine, and Michael Camilleri. "Anorexia nervosa: manifestations and management for the gastroenterologist." The American journal of gastroenterology 97, no. 2 (2002): 255-269.

29. Sharp, C. W., and C. P. Freeman. "The medical complications of anorexia nervosa." The British Journal of Psychiatry 162, no. 4 (1993): 452-462.

30. Lautenbacher, Stefan, Andrejs Michaels Pauls, Friedrich Strian, Karl-Martin Pirke, and Jürgen-Christian Krieg. "Pain sensitivity in anorexia nervosa and bulimia nervosa." Biological Psychiatry 29, no. 11 (1991): 1073-1078.

31. Papežová, H., A. Yamamotova, and R. Uher. "Elevated pain threshold in eating disorders: Physiological and psychological factors." Journal of psychiatric research 39, no. 4 (2005): 431-438.

32. Bär, Karl-Jürgen, Silke Boettger, Gerd Wagner, Christine Wilsdorf, Uwe Jens Gerhard, Michael K. Boettger, Bernhard Blanz, and Heinrich Sauer. "Changes of pain perception, autonomic function, and endocrine parameters during treatment of anorectic adolescents." Journal of the American Academy of Child & Adolescent Psychiatry 45, no. 9 (2006): 1068-1076.

33. Pollatos, Olga, Beate M. Herbert, Jürgen Füstös, Katja Weimer, Paul Enck, and Stephan Zipfel. "Food deprivation sensitizes pain perception." Journal of Psychophysiology (2012).

34. Stein, Daniel, Walter H. Kaye, Hisato Matsunaga, Daniel Myers, Israel Orbach, Dov HarEven, Guido Frank, and Rhadika Rao. "Pain perception in recovered bulimia nervosa patients." International Journal of Eating Disorders 34, no. 3 (2003): 331-336.

35. Krieg, Jürgen-Christian, Stephan Roscher, Friedrich Strian, Karl-Martin Pirke, and Stefan Lautenbacher. "Pain sensitivity in recovered anorexics, restrained and unrestrained eaters." Journal of psychosomatic research 37, no. 6 (1993): 595-601.

36. Drossman, Douglas A., F. H. Creed, K. W. Olden, J. Svedlund, B. B. Toner, and William E. Whitehead. "Psychosocial aspects of the functional gastrointestinal disorders." Gut 45, no. suppl 2 (1999): II25-II30.

37. Drossman, Douglas A., F. H. Creed, K. W. Olden, J. Svedlund, B. B. Toner, and William E. Whitehead. "Psychosocial aspects of the functional gastrointestinal disorders." Gut 45, no. suppl 2 (1999): II25-II30.

38. Bonaz, B., M. Baciu, E. Papillon, R. Bost, N. Gueddah, J-F. Le Bas, J. Fournet, and C. Segebarth. "Central processing of rectal pain in patients with irritable bowel syndrome: an fMRI study." The American journal of gastroenterology 97, no. 3 (2002): 654-661.