Eating Disorders And Gut-Brain Connection: 8 Research-Backed Links

Eating disorders and gut health go hand-in-hand thanks to a little thing called: “the gut brain axis.”

The Gut-Brain Connection Basics

The “gut brain axis” is exactly what it sounds like.

Your gut is connected to your brain, and your brain is connected to your gut. The brain-gut connection is established by the vagus nerve—your 10th cranial nerve that runs directly from your brain to your heart and gut.

Your vagus nerve is often called body’s “information highway” that delivers messages throughout your body—in fact 80% of information comes directly from your gut to your brain! The vagus nerve is also responsible for operating your body’s autonomic nervous system—the system that controls all natural body functions, especially digestion. The vagus nerve also greatly influences your personal stress levels by regulating your  “sympathetic” (fight or flight) and “parasympathetic” (rest and digest) responses.

eating disorder - woman looking at fher phone not interested with the food

For example, if a bear is chasing you in the wild, your vagus nerve signals your “sympathetic” (fight or flight) response to kick into high gear and help you escape—increasing your heart rate, breath rate and firing up adrenaline to help your run faster.

On the flip side, if you are doing a meditation or yoga class, your vagus nerve signals your “parasympathetic” (rest and digest) response to help you relax. Your vagus slows your breath rate, increases cellular and tissue healing and slows your heart beat to a relaxed state.

Your vagus is really great at turning up or turning down the volume to help your body deal with stress unless…your vagus nerve is overworked or overly stressed. If that bear keeps chasing your, for example, then the vagus eventually poops out and you become bear meat!

How Eating Disorders Affect Brain Health & Gut Health

Chronic dieting and eating disorders wreak havoc on your gut-brain connection.

Your body and brain can only take so many binge eating episodes, head-in-the-toilet-bowl experiences, under-eating dieting and over-training sessions before the vagus nerve and the gut-brain connection gets disrupted. (Hello constipation, bloating, nausea, gastroparesis and beyond!).

Not only does mental stress you feel in your brain impact your gut health, but bad gut health from the eating disorder behaviors also impact your brain health—keeping you stuck in a seemingly never-ending loop.

Some key ways that eating disorder behaviors affect your gut health include:

Suppressed stomach acid and digestive enzymes from overtraining, food restriction, binging, purging or chronic stress

Decreased healthy gut bacteria from lack of diet variety & eating the same things

A congested and sluggish gallbladder from low-fat diets or high fat processed food diets, laxative abuse, alcohol or substances

Poor liver health from too much cortisol (stress hormones), long-term use of SSRI’s or birth control pills, processed and packaged diet foods

Leaky gut from eating inflammatory foods you’re told are “healthy” for you (diet bars and shakes), overtraining, under-eating or binging.

—Just to name a few.

The moral of the story?  If you have an eating disorder, the gut-brain connection plays a huge role in how you think, feel and also can greatly impact your eating disorder recovery outcomes—for the better or the worse.

The good news? When you understand the gut-brain connect, you can use your knew knowledge about the importance of good gut health to help you (and your brain) heal from your eating disorder—not just manage it.

(Hint: Eating disorder recovery goes far beyond just following a meal plan, taking a pill or talk therapy. Although these may be helpful at certain times, if you are not addressing the gut-brain axis, then eating disorder recovery can be much more complicated). 

8 Research Backed Links: Eating Disorders & Gut-Brain Connection

eating disorders - woman lying on the sofa trying to eat

Here are 8 researched backed links between eating disorders and gut health.

#1. Over 90% of Eating Disorder Patients Have Functional Gut Disorders

#2. You Have Over 500 Million Neurons in Your Gut (that Influence How You Think About Food)

#3. 95% of Your Serotonin is Produced in the Gut

#4. Gut Bacteria Tell You What to Crave & Eat

#5. Weight & Metabolism is a Reflection of Your Gut Microbiome

#6. Purging & Restriction Signals “Satiety” to the Brain

#7. Eating Disorder Patients Have 2x Risk of Getting an Autoimmune Disease (a Byproduct of Poor Gut Health)

#8. Binge Eating Often Happens from Hypoglycemia & Poor Nutrient Absorption  

#1. Over 90% of Eating Disorder Patients Have Functional Gut Disorders

In an observational study (1) of nearly 300 eating disorder patients in an eating disorder treatment unit, researchers found that over 90% of the patients had a functional gut disorder. Functional gastrointestinal disorders (FGIDs) or “functional gut disorders” are common disorders that are characterized by persistent and recurring GI symptoms as a result of abnormal functioning of the GI tract (like low stomach acid or digestive enzymes, dysbiosis or bacterial overgrowth). They are not caused by structural or biochemical abnormalities, like an enlarged colon or intestinal blockage.  The most common and best researched FGID is Irritable Bowel Syndrome (IBS) – abdominal pain associated with altered bowel habits of diarrhea, constipation or alternating between both. Other common FGIDs include functional dyspepsia (pain or discomfort in the upper abdominal area, feeling of fullness, bloating or nausea), functional vomiting, functional abdominal pain, and functional constipation or diarrhea. Although it’s estimated that 1 in 4 people nationwide have a functional gut disorder, in those with a history of ED (and impaired mental health), that number spikes up to be more than 3 in 4!

#2. You Have Over 500 Million Neurons in Your Gut (that Influence How You Think About Food)

There are approximately 500 to 600 million neurons (brain cells) in your gut, also known as your “enteric nervous system” (gut nervous system)—that’s more neurons in your gut than any other organ and about the same amount as your spinal cord.

These neurons (brain cells) are sensitive to changes, shifts and inflammation in your gut, explaining perhaps why 1 in 2 people with IBS also have psychiatric conditions, like anxiety and eating disorders.

Additionally, many of the peptides in our body that regulate food intake are also found in the enteric (gut) nervous system. For example, a peptide called OXA that influences leptin (fullness hormone) is housed in the gut. If the gut microbiome is thrown out of whack, then OXA gets thrown out of whack—and so do your hunger signals (2).

Similarly, gut sensations (like bloating, slowed motility and constipation, decreased stomach acid and enzymes, or gut bacteria that crave certain foods) also fire signals to your brain from the gastric and intestinal nerve receptors in your enteric (gut) nervous system. Your physical gut feelings tell you things like “stop eating,” “turn to laxatives or purging,” or “binge on plantain chips” (2).

And ghrelin (your “hunger hormone”, that says “feed me” to your brain), works directly on the enteric (gut) nervous system. This is why when you feel hungry, you may feel a pit or hollowness in your stomach.

eating disorders-woman eating pizza

Have you ever wondered why women with anorexia can subsist on 500 calories per day, but not feel hungry? Although ghrelin levels (hunger cues) are increased in women with anorexia (because they are physically  starving!), their enteric (gut) nervous system replaces their sensations of hunger with feelings of bloating, constipation and fullness when they do eat thanks to stress. As the need for more food and more calories is consistently not met in women with anorexia, their enteric (gut) nervous system sends signals of “stress” and “starvation” to their brain, which, in turn, sends “stress” signals right back to the gut! The result? Women with anorexia become even less desiring of food (even though their body is hungry) as the body’s survival, defense mechanism to deal with stress of not getting enough food (3).

#3. 95% of Your Serotonin is Produced in the Gut

The majority of serotonin (95%)—your feel good brain chemical—is produced in your gut (4).

In short: if your gut health is off, then your brain health is off.

Alterations in serotonin have long been believed to contribute to diverse aspects of eating disorders, including binge eating, over-training, dieting, perfectionism, impulsivity, anxiety and mood-regulation problems.

For example, human studies show that overstimulation in serotonin production (too much serotonin) from eating disorder behaviors such as over-training, increased consumption of tryptophan foods (like chicken, soy, fat free dairy and turkey, common in women with anorexia and orthorexia), bright light (like staying up late to read Dr. Google articles on your phone screen) and reward-chasing (“earning your food” and dieting apps) lead to further restrictive eating behaviors. On the other hand, reduced serotonin levels overall leads to compulsive or binge eating in efforts to try to raise them from rewarding food as well (5).

However, up until recently, most researchers and medical textbooks believed serotonin levels were all in your head. (This is why SSRI drugs (selective serotonin reuptake inhibitors) like Prozac or Zoloft are so popular in the treatment of eating disorders—aimed at helping patients establish the “just right” amount of serotonin in their brain to feel good and no longer need the rewards of their eating disorder).

Buzz! Serotonin is produced by gut bacteria in your gut.

While SSRI drugs can be a helpful adjunctive brain boosters for some folks, if you don’t address the real underlying mechanisms behind serotonin imbalances (the reasons why serotonin levels are “off”), then you will continue to need drugs, serotonin stimulation or suppression tactics (eating disorder behaviors) to try to modulate your own serotonin levels.

#4. Gut Bacteria Tell You What to Crave & Eat

eating disorders-woman craving for cake

Our gut bugs influence our cravings and food choices.

Specific types of gut flora help a host animal detect which nutrients are missing in food and then finely titrate how much of those nutrients the host really needs to eat.

Here’s why: The vagus nerve, responsible for decision-making and digestion, connects the brain’s frontal lobe to the gut. Add to that the fact that the gut is home to feel-good chemicals—serotonin and dopamine—and it’s no surprise that gut microbes affect our mood, behavior, and food cravings.

In the case of unhealthy gut bacteria, pathogenic or overgrown microbes often crave foods that keep them alive. Since the nutrients in certain inflammatory foods are often favored by pathogenic bacteria, these bacteria try to get us to consume foods that may taste good, but don’t always make us feel great.

This can also happen with the foods we hate or avoid. Detest broccoli or Brussels sprouts? Supertasters—folks who can’t stand such vegetables, especially kids—have been shown to have a completely different gut bacteria profile that tells them not to eat bitter foods such as crucifers (6).

Ever wonder why cheese is so addicting? Cheese is one of the most common food cravings in the Western diet, despite a widespread lactose intolerance in America (about 60% of people do not have enough lactase enzymes to properly digest lactose in dairy). Although cheese itself is not innately bad, for those who truly don’t feel well or tolerate cheese, it can still prove almost irresistible. Cheese contains the protein casein, as well as casein fragments called casomorphins. These are naturally occurring morphine-like compounds. When consumed, they attach to the same brain receptors that other morphine-like compounds, such as heroin, attach to, stimulating the brain’s reward center by releasing dopamine, one of those feel-good chemicals. Party in your mouth—and cravings for more cheese (even if you experience bloating, constipation, allergies, skin breakouts, stuffy nose, poor immunity, low energy).

If you have low bacterial diversity or low amounts of healthy bacteria, your gut bacteria may also tell you to eat the same foods every day. On the other hand, a diverse, healthy biome thrives on a diverse diet.  A study (7) on this phenomena involved observations for three groups of fruit flies with different gut bacteria and diets. Scientists fed one group of flies a sucrose solution containing all the necessary amino acids (proteins). Another group got a mix that had some of the amino acids needed to make protein but lacked essential amino acids that the hosts couldn’t synthesize by themselves. For the third group, the scientists removed essential amino acids from the food one by one to determine which was being detected by the microbiome.

After 72 hours on the different diets, flies in the all three groups were then fed a buffet offering their usual sugary solution along with protein-rich yeast (a pathogenic food). The researchers found that flies in the two groups whose diet lacked any single essential amino acid exhibited a strong craving for yeast to make up for the missing nutrients. But when scientists increased five different types of bacteria found in the flies’ digestive tracts—Lactobacillus plantarum, L. brevis, Acetobacter pomorum, Commensalibacter intestini, and Enterococcus faecalis—the flies completely lost the urge to eat more protein-rich yeast. In other words: When the flies had enough healthy bacteria in their gut, they no longer wanted the food that fed an unhealthy microbiome.

Although this study was only in fruit flies, researchers concluded that it added a new perspective on the coevolution of gut bacteria and the hosts they feed (us). Our gut bacteria influence what we eat more than we give them credit for.

In human studies, gastric-bypass patients and pregnant women offer great insight on cravings (8). After bypass surgery, the gut biome undergoes some major changes—including a big change in cravings. People who once grazed through a bag of chips in one setting or ate handfuls of candy suddenly stop craving sweets. They lose their taste for fatty foods. Research suggests this is because of changes in the biome’s cravings, not the decrease in stomach volume.

Pregnancy also creates major shifts in the mom’s biome, mainly due to major hormonal shifts that occur throughout each trimester. Vaginal microbes begin favoring lactobacillus species and different, sometimes odd cravings take center stage—pickles and ice cream, pimento cheese sandwiches on rye bread, saltine crackers and ginger ale, Mac and cheese. Anything goes.

#5. Weight & Metabolism in Eating Disorders is a Reflection of What’s Happening in the Gut Microbiome

Weight loss and weight gain are common in eating disorders and other psychological-related conditions for that matter. For some people stress causes weight loss, suppressed appetite, missed meals and an overactive metabolism; for others, stress causes weight gain, poor food choices, binge episodes and a sluggish metabolism. It can vary from person to person. A key differentiator for both extremes? Once again, the gut biome.

We absorb more or less energy depending on the types of bacteria in our gut and specific types of gut bacteria harvest calories differently from others.

Simply put: The healthier your gut bacteria, the better your metabolism. Your gut bacteria produce metabolites that aid your metabolism in breaking down the fats, carbs, and proteins you eat, in order to deliver nutrients for all your body system functions (9). Dysbiosis causes malfunction for otherwise normal bodily processes.

Similar foods are metabolized differently, depending on our gut health. One study in  over 800 fit and overweight people found markedly different blood-sugar responses to exactly the same foods. Overweight subjects eating low-glycemic-index snacks exhibited very large blood sugar spikes, whereas the leaner subjects exhibited lower blood sugar spikes. The researchers concluded that gut bacteria have a significant impact on blood-sugar response from person to person (10).

Identical twins with the same DNA (genes), but different gut bacteria have different metabolisms. A person who is an identical twin with less bacterial diversity and unhealthy gut microbiota is more prone to obesity and metabolic disease, whereas an identical twin with more gut bacteria diversity is prone to a lean body type and better metabolic function (11).

Multiple clinical trials in subjects with overt metabolic disease (for example, obesity or diabetes), as well as those prone to binge eating show significant reductions in inflammatory markers such as cholesterol, high blood pressure, and Interleukin-6; improved insulin sensitivity and cravings; and BMI and waist circumference with the alteration of the gut microbiota through probiotics, short-chain fatty acids and prebiotics alone (12).

On the opposite end of the spectrum, women in recovery from anorexia as well as those who struggle to gain weight benefit from probiotics, short-chain fatty acids, and prebiotics in foods and supplements in order to attain a healthy weight. Low bacterial diversity causes a hyper-metabolism—a common experience for those in eating-disorder recovery from anorexia, during which dietitians may prescribe upwards of 4,000 to 5,000 calories per day for patients to maintain if not regain one to two pounds per week. Studies in mice with gut bacteria similar to those with long-term histories of anorexia found that the mice not only had less body fat, but also had to eat 30% more daily calories to maintain normal growth, compared with conventionally raised rodents. They were also more constipated and had slower digestion (13).

To address this, current nutritional rehabilitation practices for eating disorders, particularly anorexia, is pointing more towards a focus on gut microbiota restoration through a balanced diet, including plenty of gut-enriching fibers, polyphenols, and monounsaturated fats, with less focus on the high-fat, low in non-digestible carbohydrate recommendations found in traditional nutritional models, which lead to further alterations and exacerbations of the gut microbiota—particularly in the Firmicutes species, associated with greater metabolic damage when present in abundance (14).

Regardless of which end of the spectrum you fall on—weight loss and metabolic disease or easy weight loss and catabolism—long-term restrictive eating characterized by low nutrient intake and diminished gut bacteria lead to the final metabolic mayhem disruptor—hormone imbalances.

#6. Purging & Restriction Signals “Satiety” to the Brain

eating disorders-woman holding an apple and smelling a chocolate bar

Food intake and the addictive-like nature of eating disorders are greatly influenced by motivation and reward loops that are signaled from the gut to the brain.

Alterations in dopamine (DA), acetylcholine (ACh) and opioid systems—all reward-related areas in the brain—occur in response to eating disorder behaviors that alter the gut (such as binge eating palatable foods; restrictive eating; overtraining; or purging). Interestingly, like serotonin, the vast majority of your dopamine and acetylcholine are also produced in the gut (15, 16, 17).

Although it may seem far-fetched for outsiders to see how sticking your head in a toilet, skipping lunch or running 10 miles most days of the week can feel rewarding, studies show that purging behaviors can increase the release of acetylcholine (ACh) and feelings of satiety, and restrictive dieting in anorexia increases dopamine–feeling better about oneself for deprivation (18).

#7. Eating Disorder Patients Have 2x Risk of Getting an Autoimmune Disease (a Byproduct of Poor Gut Health)

A study comparing the prevalence of 30 autoimmune diseases in patients with a history eating disorders compared to normal controls found the ED patients had nearly twice the chance of getting an autoimmune disease over the 15 year evaluation period (19). Even more, the majority of these patients were likely to develop symptoms of autoimmunity within the first four years of their eating disorder diagnosis.

Significant stress in the body and mind from a disordered eating lifestyle is the greatest precursor to autoimmune disorders. Stress sets off the release of catecholamines and corticoids (stress hormones), which then alter immune T-cells and stir up a cytokine storm to spark an autoimmune response, which results in a self-tissue attack.

Chronic dieting also has a substantial impact on the gut—the place where 70 to 80% of your immune system is produced and activated, specifically in the GALT (gut associated lymphatic tissue). From diminished microbial diversity, to digestive enzyme deficiencies, impaired immune cell activity and a leaky gut, all of these may underlie low-grade inflammation and increased risk of autoimmune diseases (20).

For example, just one year of restrictive dieting, eating 70% of their optimal calories—for example, 1400 calories if 2000 calories was your optimal diet—results in significantly reduced microbial diversity, dendritic cell dysfunction and increased autoimmunity (21).  Dendritic cells  are your first-responder immune cells that regulate tolerance to food antigens, limit reactivity to the gut microbiota, and are required for optimal response to intestinal pathogens.

A leaky gut, characterized by a gut that looks like Swiss cheese, also allows antigens (food proteins, foreign particles, toxins, and chemicals) to cross the intestinal wall when stress is present, and has been noted in those with anorexia. Even in healthy individuals, relatively brief situations of acute stress, such as what happens with public speaking, are followed by an increase in intestinal permeability, specifically in those who also respond with elevated cortisol levels (22).

Some women with histories of anorexia and bulimia end up developing autoimmune reactions that make it harder for them to regulate food intake and their body weight due to metabolic endotoxemia—the translocation of gut bacteria itself—across the intestinal wall. This causes cross-reactive antibodies to form, which then bind to hunger and satiety hormones such as ghrelin. This in turn alters food intake and weight regulation (23, 24). Moreover, increased levels of antibodies for a large number of hunger and satiety hormones—including leptin, ghrelin, orexin, and alpha-MSH—have been found in patients with eating disorders, including patients with anorexia, and some of the antibodies also correlated with eating-disorder symptom severity (19).

Some researchers speculate that restrictive diets from disordered eating and the Standard American Diet—used for re-nutrition in some eating-disorder recovery treatments—may negatively alter the gut microbiome and support the growth of bacteria capable of triggering gut-immune inflammation during post-recovery recovery (22).  Notably, the administration of Lactobacillus and Bifidobacteria probiotics have been shown to decrease circulating corticoid hormone levels, further emphasizing the essential role of the microbiome in stress regulation. This might suggest a useful therapeutic option for autoimmunity.

#8. Binging and Odd Food Preferences Often Happen from Hypoglycemia in the Gut (& Stress Signals to the Brain)

eating disorders-woman craving for sugar

The “hypoglycemic binge” is exactly what it sounds like—hypoglycemia (a dip in blood sugar) that triggers a binge. Blood sugar is the amount of energy in your cells and blood at any given time. Ideally you want “balanced blood sugar” for a feeling of peace, balance and stability throughout the day.

When your blood sugar is low, you think more about food, may feel hungry or like you have a hollow pit in your stomach, and may even become hangry, lightheaded, dizzy or shaky. Low blood sugar also drives cortisol levels (stress hormones) up—making you think about food and survival even more.

In turn, your body tells your brain, “feed me!” Innately, you respond by turning to foods that naturally spike blood sugar quickly (often carbohydrate-based foods like pizza or pasta, sugar, fruits, or snack-type foods). For women with more anorexia-like and restrictive dieting behaviors, they may not turn to pizza, but they turn to artificial sweeteners, diet soda, air popped popcorn, chocolatey protein powders, fat free ice cream, carrot sticks or fruit to curb their hypoglycemic response.

Common reasons why hypoglycemia happens include not eating enough (especially earlier in the day); low protein, low fat or low carb dieting (extremes of any sort); overtraining; sleep deprivation; dehydration, impaired nutrient absorption from bad digestion, such as decreased stomach acid or low digestive enzymes and dysbiosis (an altered gut microbiome).

Studies show that when you decrease unhealthy bacteria in your gut and increase beneficial species, glucose metabolism (blood sugar) dramatically improves and satiety levels increase.

For example, a big reason why the medication metformin may “work” as an insulin management and appetite-modulating solution in patients with Type 2 Diabetes is not because it magically balances blood sugar, but because it modifies the gut microbiota composition by inducing the growth of several healthy bacteria, especially Akkermansia muciniphilafurther pointing to the the gut-brain connection as patients with diabetes no longer crave sweets like they once did when they feel more balanced (25).

Another double-blind randomized clinical trial study of 14 overweight to obese men showed that after consuming of a high-fat milkshake containing the prebiotic inulin (a fiber that feeds healthy gut bacteria), the study subjects experienced lower post-meal blood sugar and insulin levels compared with the group receiving the high-fat milkshake with sugar alone (no pre-biotic) (26).

Start In Your Gut

Health (including improved brain health) is an inside job, starting in your gut. Unfortunately, the gut microbiome is still not a common therapeutic focus of eating disorder treatment, despite rapidly evolving research pointing to its influence on eating disorder thoughts and behaviors. However, at Heal Your Root, my online virtual functional medicine and disordered eating recovery clinic, we are changing that.

If you’re looking to write a new story for your health, body and mind in your eating disorder recovery, contact my online clinic today to schedule an Initial Intake Appointment where we will build you a Custom Blueprint—your personal nutrition, lifestyle, lab testing, supplement recommendations and ongoing therapy and coaching support “game plan” to help you heal your gut and kick ED thoughts to the curb!

Resources

1.) Wang, X., Luscombe, G. M., Boyd, C., Kellow, J., & Abraham, S. (2014). Functional gastrointestinal disorders in eating disorder patients: altered distribution and predictors using ROME III compared to ROME II criteria. World journal of gastroenterology, 20(43), 16293–16299. https://doi.org/10.3748/wjg.v20.i43.16293. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239520/
2.) Näslund, E., & Hellström, P. M. (2007). Appetite signaling: From gut peptides and enteric nerves to brain. Physiology & Behavior, 92(1), 256–262. https://doi-org.uws.idm.oclc.org/10.1016/j.physbeh.2007.05.017
3.) Peeters T. L. (2005). Ghrelin: a new player in the control of gastrointestinal functions. Gut, 54(11), 1638–1649. https://doi.org/10.1136/gut.2004.062604
4.) Camilleri M. (2009). Serotonin in the gastrointestinal tract. Current opinion in endocrinology, diabetes, and obesity, 16(1), 53–59. https://doi.org/10.1097/med.0b013e32831e9c8e
5.) Steiger H. (2004). Eating disorders and the serotonin connection: state, trait and developmental effects. Journal of psychiatry & neuroscience : JPN, 29(1), 20–29.
6.) Turner, A., Veysey, M., Keely, S., Scarlett, C., Lucock, M., & Beckett, E. L. (2018). Interactions between Bitter Taste, Diet and Dysbiosis: Consequences for Appetite and Obesity. Nutrients, 10(10), 1336. https://doi.org/10.3390/nu10101336
7.) Leitão-Gonçalves R, Carvalho-Santos Z, Francisco AP, et al. Commensal bacteria and essential amino acids control food choice behavior and reproduction. PLoS Biol. 2017;15(4):e2000862. Published 2017 Apr 25. doi:10.1371/journal.pbio.2000862
8.) Behary, Preeshila, and Alexander D. Miras. “Food Preferences and Underlying Mechanisms after Bariatric Surgery.” The Proceedings of the Nutrition Society 74, no. 4 (November 2015): 419–25.
9.) Rastelli, M., Knauf, C., & Cani, P. D. (2018). Gut Microbes and Health: A Focus on the Mechanisms Linking Microbes, Obesity, and Related Disorders. Obesity (Silver Spring, Md.), 26(5), 792-800.
10.) David Zeevi, Tal Korem, Niv Zmora, David Israeli, Daphna Rothschild, Adina Weinberger, Orly Ben-Yacov, Dar Lador, Tali Avnit-Sagi, Maya Lotan-Pompan, Jotham Suez, Jemal Ali Mahdi, Elad Matot, Gal Malka, Noa Kosower, Michal Rein, Gili Zilberman-Schapira, Lenka Dohnalová, Meirav Pevsner-Fischer, Rony Bikovsky, Zamir Halpern, Eran Elinav, Eran Segal. Personalized Nutrition by Prediction of Glycemic Responses. Cell, 2015; 163 (5): 1079 DOI: 10.1016/j.cell.2015.11.001
11.) Tomiyama, A. J., Mann, T., Vinas, D., Hunger, J. M., Dejager, J., & Taylor, S. E. (2010). Low calorie dieting increases cortisol. Psychosomatic medicine, 72(4), 357–364. https://doi.org/10.1097/PSY.0b013e3181d9523c
12.) Xavier-Santos, Douglas & Bedani, Raquel & Lima, Egidio & Saad, Susana. (2019). Impact of probiotics and prebiotics targeting metabolic syndrome. Journal of Functional Foods. 64. 103666. 10.1016/j.jff.2019.103666.
13.) Bäckhed, F., Ding, H., Wang, T., Hooper, L. V., Koh, G. Y., Nagy, A., Semenkovich, C. F., & Gordon, J. I. (2004). The gut microbiota as an environmental factor that regulates fat storage. Proceedings of the National Academy of Sciences of the United States of America, 101(44), 15718–15723. https://doi.org/10.1073/pnas.0407076101
14.) Ruusunen, A., Rocks, T., Jacka, F. et al. The gut microbiome in anorexia nervosa: relevance for nutritional rehabilitation. Psychopharmacology 236, 1545–1558 (2019). https://doi.org/10.1007/s00213-018-5159-2
15.) Galland L. (2014). The gut microbiome and the brain. Journal of medicinal food, 17(12), 1261–1272. https://doi.org/10.1089/jmf.2014.7000
16.) Nezami, B. G., & Srinivasan, S. (2010). Enteric nervous system in the small intestine: pathophysiology and clinical implications. Current gastroenterology reports, 12(5), 358–365. https://doi.org/10.1007/s11894-010-0129-9
17.) Xue R, Zhang H, Pan J, Du Z, Zhou W, Zhang Z, Tian Z, Zhou R, Bai L. Peripheral Dopamine Controlled by Gut Microbes Inhibits Invariant Natural Killer T Cell-Mediated Hepatitis. Front Immunol. 2018 Oct 17;9:2398. doi: 10.3389/fimmu.2018.02398. PMID: 30386344; PMCID: PMC6199378.
18.) Avena, N. M., & Bocarsly, M. E. (2012). Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa. Neuropharmacology, 63(1), 87–96. https://doi.org/10.1016/j.neuropharm.2011.11.010
19.) Anu Raevuori, Jari Haukka, Outi Vaarala, Jaana M. Suvisaari, Mika Gissler, Marjut Grainger, Milla S. Linna, Jaana T. Suokas. The Increased Risk for Autoimmune Diseases in Patients with Eating Disorders. PLoS ONE, 2014; 9 (8): e104845 DOI: 10.1371/journal.pone.0104845
20.) Seitz J, Belheouane M, Schulz N, Dempfle A, Baines JF, Herpertz-Dahlmann B. The Impact of Starvation on the Microbiome and Gut-Brain Interaction in Anorexia Nervosa. Front Endocrinol (Lausanne). 2019;10:41. Published 2019 Feb 12. doi:10.3389/fendo.2019.00041
21.) Niiya T, Akbar SM, Yoshida O, et al. Impaired dendritic cell function resulting from chronic undernutrition disrupts the antigen-specific immune response in mice. J Nutr. 2007;137(3):671-675. doi:10.1093/jn/137.3.671
22.) Herpertz-Dahlmann, B., Seitz, J., & Baines, J. (2017). Food matters: how the microbiome and gut-brain interaction might impact the development and course of anorexia nervosa. European Child & Adolescent Psychiatry, 26(9), 1031–1041. https://doi-org.uws.idm.oclc.org/10.1007/s00787-017-0945-7
23.) Bergh, C., Brodin, U., Lindberg, G., & Södersten, P. (2002). Randomized controlled trial of a treatment for anorexia and bulimia nervosa. Proceedings of the National Academy of Sciences of the United States of America, 99(14), 9486–9491. https://doi.org/10.1073/pnas.142284799
24.) Fetissov, S. O., Lucas, N., & Legrand, R. (2017). Ghrelin-Reactive Immunoglobulins in Conditions of Altered Appetite and Energy Balance. Frontiers in endocrinology, 8, 10. https://doi.org/10.3389/fendo.2017.00010
25.) Gérard, C., & Vidal, H. (2019). Impact of Gut Microbiota on Host Glycemic Control. Frontiers in endocrinology, 10, 29. https://doi.org/10.3389/fendo.2019.00029
26.) van der Beek CM, Canfora EE, Kip AM, Gorissen SHM, Olde Damink SWM, van Eijk HM, et al. . The prebiotic inulin improves substrate metabolism and promotes short-chain fatty acid production in overweight to obese men. Metabolism (2018) 87:25–35. 10.1016/j.metabol.2018.06.009

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