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The Low-FODMAP Diet for IBD: Everything You Need to Know

Alyssa Luck · Mar 14, 2022 · Leave a Comment

Summary: The low-FODMAP diet originated in 2005 out of a hypothesis about IBD pathogenesis, but quickly became a go-to treatment for IBS. For IBD, the diet has found its niche as an intervention for addressing lingering functional gastrointestinal symptoms in patients whose IBD is in remission. For this purpose, the diet has demonstrated successful symptom reduction in clinical trials, but no evidence yet indicates that it is helpful for quelling inflammation. The biggest risk associated with a low-FODMAP diet is adverse effects on the microbiome from depriving it of fermentable carbohydrates, but this can be addressed by including low-FODMAP prebiotics (such as Sunfiber and resistant starch) and by reintroducing FODMAP-containing foods as tolerated.

This article is part of the IBD Index. Last updated on April 20, 2022.

This article aims to give a high-level overview of the low-FODMAP diet, as well as practical guidance. For a deeper dive into the science, you can check out my article Is the Low-FODMAP Diet Effective for IBD?.

Table of Contents
Who came up with the low-FODMAP diet?
What is a low-FODMAP diet?
What is the theory behind the low-FODMAP diet?
Is there clinical evidence for the low-FODMAP diet in IBD?
How can I keep my microbiome healthy on a low-FODMAP diet?
Key practical tips and reminders
Resources
Review of the literature

I remember first reading about [FODMAPs] in a research paper published by Sue Shepherd and Peter Gibson in 2005. I was intrigued by the FODMAP concept because it made scientific and practical sense. I am quite proud to say that the University of Michigan was one of the first major US medical centers to adopt the low-FODMAP diet as a routine part of treating our patients with IBS. Initial discussions with our physicians and dieticians were typically met with palpable skepticism…However, as patients returned with story after story of remarkable improvement, this skepticism was quickly replaced by enthusiasm and praise. Concurrent with the gradual adoption of the low-FODMAP approach has been a dramatic shift in the behavior of our providers from viewing the low-FODMAP diet as a “rescue” strategy intended only for those that had failed all other therapies to now viewing the diet as an evidence-based, first-line treatment strategy.

William Chey, MD, from the foreword of The Complete Low-FODMAP Diet: A Revolutionary Plan for Managing IBS and Other Digestive Disorders (2011)

Who Came Up with the Low-FODMAP Diet?

The term “FODMAP” was coined in 2005 by researcher Peter Gibson in a paper titled Personal view: food for thought–western lifestyle and susceptibility to Crohn’s disease. The FODMAP hypothesis. But what started as a hypothesis regarding susceptibility to IBD quickly became an intervention almost exclusively focused on IBS, both in the research literature and mainstream information channels.

In 2011, Peter Gibson, MD and Sue Shepherd, PhD published the book The Complete Low-FODMAP Diet: A Revolutionary Plan for Managing IBS and Other Digestive Disorders. Sue Shepherd has authored a food manufacturer’s guide and two cookbooks concerning a low-FODMAP diet, and Gibson continues to publish extensively on this and other topics related to GI disorders as the Head of Luminal Gastroenterology Research at Monash University in Australia.

What is a Low-FODMAP Diet?

A low-FODMAP diet (LFD) is a diet that limits or removes foods that are high in a class of carbohydrate called “FODMAPs” (who would’ve guessed, right?). The LFD is designed in three stages: 1) a strict low-FODMAP diet for 2-6 weeks; 2) a FODMAP reintroduction phase over the course of 8-12 weeks, where one FODMAP is reintroduced at a time while tolerance is monitored; and 3) the FODMAP personalization phase, which is the long-term sustainable diet pattern based on each person’s individual tolerances. (Source)

FODMAP stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols, and they’re characterized as short-chain carbohydrates that are poorly absorbed in the small intestine and ferment rapidly in the distal small intestine and colon. These include (among others): (Source)

Fructose, the monosaccharide found mainly in fruit, honey, and anything with sugar (since fructose is half of the sucrose unit).

Lactose, the disaccharide found in dairy.

Fructans, or fructooligosaccharides (FOS); main sources are wheat and rye, with onions being another common source.

Galactooligosaccharides (GOS); most common sources are legumes, cruciferous veggies, and onions.

Polyols (aka sugar alcohols) such as sorbitol, found naturally in apples, pears, and plums. Also includes sugar alcohols used as low-calorie sweeteners, like xylitol.

What is the Theory Behind the Low-FODMAP Diet?

The basic idea is that this class of short-chain carbohydrates called FODMAPs are often poorly absorbed by humans and rapidly fermented by bacteria, leading to water being pulled into the intestine (due to osmotic effects of the unabsorbed carbohydrate molecules) and increased gas (from bacterial fermentation).

In people with sensitive GI systems, these effects can translate to symptoms like bloating, distension, abdominal pain, and diarrhea.

Is There Clinical Evidence for the Low-FODMAP Diet in IBD?

As previously mentioned, the LFD is an intervention that has been studied and used clinically mostly for IBS. A review of that evidence is outside the scope of this article, but it is a fairly well-backed approach that has been shown to benefit anywhere from 50-87% of IBS sufferers compared with placebo, although it is not consistently more effective than other IBS treatments. (Source 1, 2)

Now, regarding IBD, the LFD seems to fill a very specific niche in research and clinical practice as an intervention for patients whose IBD is in remission, but who still have so-called “functional” GI symptoms (including diarrhea, bloating, etc).

In this patient population, research has absolutely shown that a LFD can be effective in reducing those functional symptoms. However, there’s little to no evidence that a LFD has an appreciable effect on the underlying inflammatory disease pathology of IBD, so while it may be extremely helpful for managing symptoms, the evidence does not support the use of this diet to get inflammation under control.

For a much more detailed look at this question, see my article Is the Low-FODMAP Diet Effective for IBD?. You can also check out the review of the literature section at the bottom of this article for an annotated bibliography of sorts, including all published research pertaining to the low-FODMAP diet and IBD specifically (as of January 2022).

How Can I Keep my Microbiome Healthy on a Low-FODMAP Diet?

One of the criticisms of the low-FODMAP diet is that it may be harmful to the intestinal microbiome long-term because it removes many of the indigestible carbohydrates that would normally feed your gut bacteria. This concern is somewhat allayed by the reintroduction of tolerated levels of FODMAP-containing foods after the initial elimination phase, but you can also include prebiotic fibers that are not FODMAPs, the primary examples being Sunfiber and resistant starch.

It’s surprisingly tricky to find reliable, clear analyses of the resistant starch content of different foods, but several foods that are commonly cited as “good” sources that would be considered low in FODMAPs include cooked and cooled rice, cooked and cooled potatoes, and unripe bananas. I imagine that any starchy food that has been cooked and then cooled will have some amount of resistant starch in it, but I could be wrong about that, and it may not be much.

Key Practical Tips and Reminders

If you have IBD and want to try a low-FODMAP diet, here are some key things to keep in mind:

  • The LFD is not intended to be a restrictive diet forever, and the creators/proponents of the diet emphasize that foods should be slowly and methodically reintroduced as tolerated to ensure long-term nutritional adequacy and microbiome health (not to mention sanity and life-enjoyment)
  • It’s possible to improve tolerance to certain foods over time. There’s evidence that certain strategies can improve lactose tolerance over time, and this is likely true of other categories of FODMAPs as well. After all, humans (and their gut bacteria) are highly adaptive creatures, and tolerance will likely improve as your health improves as well. Even if you can’t tolerate a food right now, don’t count it out forever.
  • Certain food preparation methods can reduce FODMAP content. For instance, traditional sourdough fermentation of wheat and rye bread drastically reduces the fructan content, and soaking beans overnight reduces the GOS content.
  • It’s very easy to begin to fear or demonize foods, especially if you personally experience benefits from eliminating them, so try to remember that FODMAPs are not “bad” or “unhealthy” foods. Many people eat large quantities of high-FODMAP foods with no adverse effects at all. And as far as we know, even when they produce symptoms in sensitive individuals, FODMAPs are not causing any damage to the intestine.

Resources

  • The Low-FODMAP Diet webpage from Monash University. Since Monash University has been the main hub of low-FODMAP research from the beginning, this would be my go-to source for practical advice. They have many online user-friendly resources for undertaking a LFD, as well as an app. The app purportedly has the most comprehensive FODMAP food list/database in the world.
  • The Complete Low-FODMAP Diet: A Revolutionary Plan for Managing IBS and Other Digestive Disorders by Peter Gibson, MD and Sue Shepherd, PhD (2011). The original low-FODMAP diet book. I haven’t read the whole thing, but much of it is available for free online, and (especially compared with other digestive condition “self-help” books I’ve read) does an excellent job giving background and context about various digestive disorders (with a focus on IBS), what causes them, and why the low-FODMAP diet can be helpful. It strikes a perfect balance of being layperson-friendly but still scientifically accurate. And although the book is about ten years old now, none of the science is conspicuously out of date.
  • I have not extensively vetted this source, but this appears to be a fairly simple and user-friendly chart of low-FODMAP and high-FODMAP foods. You can easily find others just by Googling.
  • The low FODMAP diet in the management of irritable bowel syndrome: an evidence-based review of FODMAP restriction, reintroduction and personalisation in clinical practice (2018). A quite thorough description of the implementation of a low-FODMAP diet in the clinical setting. Written with clinicians in mind, but could be helpful or of interest for patients as well.
  • Re-challenging FODMAPs: the low FODMAP diet phase two (2017). Also written for clinicians, but has a more specific explanation of the re-introduction phase (including a graphic and table of foods), which I found interesting and potentially helpful.

Review of the Literature

Note: the vast majority of literature you’ll find regarding FODMAPs is related to IBS, not IBD. Here, I’ve included all IBD-specific papers I could find.

*COMING SOON* Ford, Alexander C. MODULATE: a study to evaluate the effectiveness of either amitriptyline, ondansetron, loperamide, or dietary intervention (the low FODMAP diet) against standard dietary advice for the treatment of diarrhoea in patients with stable ulcerative colitis.

*COMING SOON* Milajerdi et al. A randomized controlled trial investigating the effect of a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols on the intestinal microbiome and inflammation in patients with ulcerative colitis: study protocol for a randomized controlled trial. 2020. Trials.

  • This is a proposed protocol for a study that hasn’t happened yet, but if it does, 30 patients with mild to moderate UC will be randomly assigned to a LFD or to continue their usual diet for 4 weeks. Primary outcomes will be fecal calprotectin and lactoferrin, as well as gut microbial composition measured via stool sample.

Simões et al. FODMAPs, inflammatory bowel disease and gut microbiota: updated overview on the current evidence. 2022. Eur J Nutr.

  • Reviews the differential effects of individual FODMAPs on gut bacteria
  • Concludes that a LFD may effectively improve clinical outcomes, but may adversely impact gut microbiota and suggests individualizing the diet to achieve the least possible dietary restriction

Grammatikopoulou et al. Low FODMAP Diet for Functional Gastrointestinal Symptoms in Quiescent Inflammatory Bowel Disease: A Systematic Review of Randomized Controlled Trials. 2020. Nutrients.

  • An updated review of the evidence for the efficacy of a low-FODMAP diet in IBD patients in remission with functional digestive symptoms
  • (Side note: they shared an image of their PubMed search strategy in here including all the search terms, Boolean operators, etc, which I found interesting.)
  • Four RCTs included in the analysis (marked below with an asterisk: Cox, Bodini, Pedersen, and Halmos)
  • “Careful inspection revealed that the RCTs were highly heterogeneous in terms of design, participants, and outcomes. Accordingly, any attempt to recommend adherence to the LFD for relief from FGS in patients with IBD will be based on inadequate evidence. The four retrieved RCTs yielded inconsistent findings concerning all outcome domains, including disease severity, QoL, FGS relief, gut microbiota, nutrient intake, immunity and inflammation markers, stool characteristics, and fecal composition.”
  • Markers of inflammation (such as CRP) and immune response were unchanged, indicating that improvement in symptoms is separate from improvement in disease activity
  • Most RCTs failed to include objective outcomes like immune activation markers, changes in the gut microbiota or in the gut lumen, and when objective outcomes (such as CRP, fCAL, or T-cell phenotype) were assessed, the lack of significant differences post-LFD adherence was apparent.
  • Makes the point that IBS trials comparing the LFD to conventional IBS medical nutrition therapy (MNT) did not show that LFD was superior, so the comparison diet in IBD trials should be some other IBD-specific dietary intervention, rather than no diet change.

*Cox et al. Effects of Low FODMAP Diet on Symptoms, Fecal Microbiome, and Markers of Inflammation in Patients With Quiescent Inflammatory Bowel Disease in a Randomized Trial. 2020. Gastroenterology.

  • Fifty-two patients with IBD in remission but persistent gut symptoms were randomized to a 4-week LFD or control diet.
  • 52% of those on the LFD reported adequate relief of gut symptoms, compared to 16% of the control group. The LFD group also had a non-statistically-significant greater reduction in IBS severity scores, and slightly higher quality of life scores.
  • Stool samples from the LFD revealed lower levels of a couple Bifidobacteria species and Faecalibacterium prausnitzii, but microbiome diversity and markers of inflammation did not differ significantly between groups.
  • Conclusions: In a trial of the low FODMAP diet vs a control diet in patients with quiescent IBD, we found no significant difference after 4 weeks in change in irritable bowel syndrome severity scores, but significant improvements in specific symptom scores and numbers reporting adequate symptom relief. The low FODMAP diet reduced fecal abundance of microbes believed to regulate the immune response, compared with the control diet, but had no significant effect on markers of inflammation. We conclude that a 4-week diet low in FODMAPs is safe and effective for managing persistent gut symptoms in patients with quiescent IBD. 

*Bodini et al. A randomized, 6-wk trial of a low FODMAP diet in patients with inflammatory bowel disease. 2019. Nutrition.

  • Fifty-five patients with IBD in remission or with mild disease activity were randomized to a 6-wk LFD or standard diet (SD).
  • Disease activity (measured by the Harvey-Bradshaw index and partial Mayo score) and fecal calprotectin decreased and disease-specific quality of life increased in the LFD group, with no changes in any of those measures in the control group.
  • Conclusions: A short-term, LFD is safe for patients with IBD, and is associated with an amelioration of fecal inflammatory markers and quality of life even in patients with mainly quiescent disease.
  • Note: basically no placebo response in the control group

Gibson, Peter R. Use of the low-FODMAP diet in inflammatory bowel disease. 2017. J Gastroenterol Hepatol.

  • Review article covering the existing FODMAP/IBD research from four angles: whether IBD patients consume significantly more or fewer FODMAPs compared to the healthy population (not really); whether IBD patients are more likely to have lactose/fructose malabsorption (yes); whether reducing FODMAPs improves IBD symptoms (yes); and whether the prebiotic effect of FODMAPs can be helpful to IBD patients (maybe).
  • Also does quite a good job summarizing the relevant risks/considerations pertaining to IBD patients, particularly the effect of FODMAPs on inflammation and the microbiota.
  • Conclusions: Evidence from unblinded and observational studies regarding the efficacy of reducing FODMAP intake for IBS-like symptoms in patients with quiescent IBD is compelling despite the lack of high-quality evidence. However, the risks associated with such dietary change have to be seriously considered in this patient group. Dietitian-led implementation of the diet is strongly recommended.

*Pedersen et al. Low-FODMAP diet reduces irritable bowel symptoms in patients with inflammatory bowel disease. 2017. World J Gastroenterol.

  • Eighty-nine patients with IBD in remission or with mild-to-moderate disease and coexisting IBS-like symptoms were randomized to a 6-week LFD or a normal diet.
  • 81% of the LFD group had at least a 50-point reduction in IBS symptom severity, compared to 46% of the normal diet group. The LFD also had significantly lower IBS symptom severity overall and experienced a greater increase in quality of life compared with the normal diet group.
  • Conclusions: In a prospective study, a low-FODMAP diet reduced IBS-like symptoms and increased quality of life in patients with IBD in remission.
  • Note: large placebo response in control group for all endpoints.

Pedersen et al. Sa1245 Gut Microbiota in IBD Patients With IBS Before and After 6 Weeks of Low FODMAP Diet. 2014. (Note: this poster abstract was based on an interim analysis of the above Pedersen study, published in its final version in 2017)

  • Fifty IBD patients with IBS-like symptoms were randomized to a 6-week LFD or a normal diet.
  • At baseline, most (70%) had dysbiosis, 20% had normal biosis, and 10% were inconclusive. These proportions did not change significantly over the course of the 6-week study, although 10% had missing follow-up data, so that could’ve affected the significance of the results.

Cox et al. Fermentable Carbohydrates [FODMAPs] Exacerbate Functional Gastrointestinal Symptoms in Patients With Inflammatory Bowel Disease: A Randomised, Double-blind, Placebo-controlled, Cross-over, Re-challenge Trial. 2017. J Crohns Colitis.

  • Thirty-two patients with quiescent IBD but ongoing functional symptoms who had already experienced “adequate relief” of their symptoms on a low-FODMAP diet were allocated to a series of 3-day fermentable carbohydrate challenges in random order (fructans, galacto-oligosaccharides [GOS], sorbitol, and glucose placebo), each separated by a washout period.
  • Note: the dose of fructans was twice as high as the dose of GOS or sorbitol to reflect that the standard UK diet contains fructans in greater quantities than the other two FODMAPs
  • Significantly fewer participants reported adequate relief of gastrointestinal symptoms on the final day of the fructan challenge compared with placebo (glucose). There was also a greater incidence of moderate or severe abdominal pain, bloating, and flatulence during the fructan challenge compared with placebo (glucose) and greater severity of abdominal pain, bloating, flatulence, and faecal urgency on the final day of the fructan challenge compared with placebo [glucose]. These statistically significant findings for fructans compared with placebo were not observed during the GOS and sorbitol challenges.
  • Note: most, but not all (89.7%), patients continued to experience “adequate relief” after the glucose (placebo) challenge, which means that three participants either had a negative reaction to glucose or had a “nocebo” response to the glucose.
  • The CD patients, but not the UC patients, experienced a small but statistically significant increase in fecal calprotectin between the beginning and end of the trial, indicating that the increased functional gut symptoms experienced with the FODMAP challenges might have affected disease activity as well.
  • Conclusions: At the relatively high doses used, fructans, but not GOS or sorbitol, exacerbated FGS in quiescent IBD. (This prompted the authors to speculate whether the low-FODMAP diet as currently instated is unnecessarily restrictive.)

Zhan et al. Is a low FODMAP diet beneficial for patients with inflammatory bowel disease? A meta-analysis and systematic review. 2017. Clin Nutr.

  • Can’t access full text
  • Results: Two RCTs and four before-after studies with a total of 319 patients (96% in remission) were identified. Except for the constipation response, there was a significant improvement in other symptoms, including diarrhea response, satisfaction with gut symptoms, abdominal bloating and pain, fatigue, and nausea.
  • Conclusions: “The present meta-analysis offers proof to support that a low FODMAP diet is beneficial for reducing gastrointestinal symptoms in patients with quiescent IBD.”

*Halmos et al. Consistent Prebiotic Effect on Gut Microbiota With Altered FODMAP Intake in Patients with Crohn’s Disease: A Randomised, Controlled Cross-Over Trial of Well-Defined Diets. 2016. Clin Transl Gastroenterol.

  • This appears to be by far the most methodologically sound and thorough RCT we have in IBD thus far.
  • Eight patients completed the study, and were randomized to consume either a LFD or a high-FODMAP “typical Australian” diet for 21 days, then all patients underwent a 21-day washout period of their usual diet, then they followed 21 days of the interventional diet that they hadn’t gotten in the first round (ie, a crossover design).
  • Not only were all meals and snacks provided, they ALSO controlled for total fiber content by adding psyllium husk and resistant starch to the LFD.
  • Analyses were based on data collected from 5-day fecal samples from each of the three segments of the study (so they had information from 15 days of poop per person)
  • Compared with symptoms while consuming the participants’ habitual diet, the low FODMAP diet did not alter the severity of symptoms, but, the typical Australian diet increased overall gastrointestinal symptoms (the “typical Australian diet” was higher in FODMAPs than the participants’ habitual diet, which the study authors noted as an interesting observation in itself; perhaps the Crohn’s patients naturally restricted FODMAP intake in their habitual diets from experience, without knowing what “FODMAPs” were)
  • There were no differences in bacterial abundance, fecal pH, or total or specific fecal SCFA on the habitual diet compared with the provided diets. The habitual diet and LFD both had a reduced absolute and relative abundance of the butyrate-producing C. cluster XIVa and the mucus-associated A. muciniphila compared with the typical Australian diet.
  • The subjects were relatively asymptomatic on their habitual diet and remained so on the low FODMAP diet, but gastrointestinal symptoms significantly increased with the higher FODMAP intake on the typical Australian diet without changing disease activity. 
  • “The patterns of change in the measured bacteria were almost identical to those observed in the IBS/healthy cohort who underwent the same interventions and had identical methodological dissection of the fecal microbiota. It is reassuring that the same dietary manipulations of FODMAPs produce consistent effects irrespective of the underlying disease state.”
  • “The lower relative abundance of A. muciniphila on the low FODMAP diet was also accompanied by a higher relative abundance of R. torques as previously observed by Png et al. R. torques is commonly seen in higher abundance in patients with IBD, suggests that a reduced FODMAP intake may encourage an environment that is unfavorable to health.”
  • “These data suggest that if, patients with Crohn’s disease had a FODMAP intake similar to that of the designed typical Australian diet, their microbiome would approach a putatively better structure.”
  • Conclusions: In clinically quiescent Crohn’s disease, altering dietary FODMAP intake is associated with marked changes in fecal microbiota, most consistent with a prebiotic effect of increasing FODMAPs as shown in an irritable bowel/healthy cohort. This strategy might be favorable for gut health in Crohn’s disease, but at the cost of inducing symptoms.

Prince et al. Fermentable Carbohydrate Restriction (Low FODMAP Diet) in Clinical Practice Improves Functional Gastrointestinal Symptoms in Patients with Inflammatory Bowel Disease. 2016. Inflamm Bowel Dis.

  • This was a retrospective case-note review of 88 patients with IBD whose inflammation was well-controlled and who had received dietary counseling in the low-FODMAP diet to manage ongoing functional gut symptoms.
  • There was a large and significant increase in the percentage of patients reporting satisfactory symptom relief between baseline (16%) and follow-up (78%) after following a LFD for an average of ~2-3 months, as well as decreases in symptom severity score and improvements in stool consistency.
  • Note that adherence to the diet was not assessed, so these numbers could include patients who improved while not maintaining a LFD, patients who did not improve because they didn’t follow the diet, as well as a placebo response in general.

Gearry et al. Reduction of dietary poorly absorbed short-chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease-a pilot study. 2009. J Crohns Colitis.

  • This was a retrospective telephone questionnaire of 52 patients with IBD whose inflammation was well-controlled and who had previously received dietary counseling in the low-FODMAP diet to manage ongoing functional gut symptoms.
  • About half of the patients were considered “responders” to a low-FODMAP diet, with improvements in diarrhea, bloating, gas, and abdominal pain most common. Constipation tended to not improve or even slightly worsen.
  • Of note, it doesn’t appear that they analyzed patients who were adherent to the diet separately from patients who were not adherent; if that’s the case, the true response rate is likely higher than 50%.

Related

Therapeutic Diets for IBD carbohydrates, Crohn's disease, fiber, fodmap, gut bacteria, IBD, low-FODMAP, microbiome, prebiotics, ulcerative colitis

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Hi! I’m Alyssa. I like thunderstorms and cats, hate wearing shoes, and enjoy devising extensive research projects for myself in my free time. This is me in Bali with a monkey on my shoulder. And this is my blog, where I muse about health-related topics and document my relentless self-guinea pigging. If you want to know more about me, click here!

alyssa.luck

alyssa.luck
If you've seen "vagus nerve exercises" that have y If you've seen "vagus nerve exercises" that have you moving your eyes or tilting your head, you've probably encountered the work of Stanley Rosenberg. The exercises he created and introduced in his 2017 book now appear in instructional videos all over the internet. 
 
The book itself has much to recommend it: it's accessible, it's practical, it's inspiring. But it has one major flaw: the solid practical and informational content regarding the cranial nerves is framed in terms of the scientifically dubious polyvagal theory. 
 
I particularly enjoyed the book as an introduction to the therapeutic arena of bodywork, of which Rosenberg is a skilled practitioner. His book is full of case reports that demonstrate how immensely powerful extremely subtle movements and physical manipulations can be. These do need to be kept in perspective: it's a small sample size of the most remarkable cases, and the results were achieved within the supportive clinical environment of a skilled practitioner. You can tell from his descriptions how refined his technique is. But nevertheless, it was a paradigm-shifting read for me, and the exercises give you something concrete to play around with. 
 
The book also brought the cranial nerves and the concept of “social engagement” to the fore as arbiters of health. Rosenberg has a solid background in cranial nerve anatomy and shares many interesting tidbits and considerations that you don’t typically hear; for instance, the potential impact of dental and orthodontic work on cranial nerve function.
 
So, is it worth reading? If any of the above piques your interest, go for it! Just read my post on polyvagal theory first – you can use the book to practice separating the wheat (solid informational content) from the chaff (pseudoscientific framing). If nothing else, the book is a nice reminder that genuine healers who get lasting results for their patients do exist.

But if you just want to try the exercises, you can easily find them all on YouTube. 

“You learn techniques to understand principles. When you understand the principles, you will create your own techniques.” -Stanley Rosenberg
I first stumbled upon polyvagal theory during the I first stumbled upon polyvagal theory during the course of my heart rate variability research. I was surprised to encounter it again "in the wild" shortly after, in the book "Accessing the Healing Power of the Vagus Nerve." Before long, I saw it popping up everywhere, (Baader-Meinhof, anyone?) 
 
Digging deeper, I discovered scientific controversy bubbling just beneath the smooth surface of polyvagal theory's popular presentation. Three months later, I posted a 13k word analysis of the topic. 
 
The technical details are far below the level of practicality for the average person, but the way polyvagal theory has propagated outside of academia has some important ramifications for clinical and scientific progress. 
 
In the wake of a wave of health complaints that our current medical model is poorly equipped to treat, it's clearer than ever that a new paradigm is needed. The grassroots push to emphasize diet and lifestyle factors has been a huge step in the right direction, but it's becoming more and more common to see people who have done everything "right" and are still struggling with persistent health complaints that could range anywhere from mildly annoying to debilitating. 
 
What we need is a genuine integration of mind and body in medicine – not the weak lip service that our current paradigm pays to "stress reduction," like the vague suggestion to relax more and maybe try meditation. And if we're going to develop a sophisticated mind-body medicine, we need a sophisticated mind-body science. And if we want a sophisticated mind-body science, we must subject such topics to the same standards of inquiry as we expect from molecular biomedicine. And that means rejecting pseudoscience like polyvagal theory. 
 
Full analysis and references at alyssaluck.com/polyvagal-theory-a-critical-appraisal
To continue my recounting of the health things I'm To continue my recounting of the health things I'm experimenting with, let me tell you about DNRS: the slightly cheesy, arguably outdated “brain rewiring” program that has changed my life. 

I found it because I was looking for ways to “retrain” my nervous system. I watched some success stories. None of the “target” health conditions matched mine, but I went for it anyway. Probably the best decision I’ve ever made for my health. 

The core of DNRS is built on the principles of neuroplasticity. They call it "brain rewiring" because you intentionally take triggers that would normally stimulate a negative response in your body or mind, and associate them repeatedly with neural signals of safety. If that sounds pseudosciencey, I hear ya – one of my goals with future posts is to bring some concreteness and specificity to the topic. I imagine there are lots of people who could benefit from this type of thing who are turned off by the overly abstract or touchy-feely language. 

There are tons of "brain rewiring" programs like DNRS, but they're all built on similar ideas. Most bring in elements of other popular approaches, ranging from the scientifically validated (cognitive behavioral therapy, mindfulness, acceptance and commitment therapy) to the type of new-agey stuff I always scoffed at (shadow work, inner child work, parts work). 

For me, DNRS has provided the perfect framework to finally achieve what meditation experts and therapists and mystics alike are always advocating – the ability to step into the role of “curious observer.” It's given me everything therapy and meditation promised but could never deliver, helping me recognize my own patterns of thought and behavior and consciously redirect unhelpful ones. If this sounds vague, that's because there isn't a single area of my life that hasn't been improved by using this framework. 

I spend far more time in states of joy and peace and gratitude, and less time in states of anxiety or depression or frenzy. Many chronic worries that used to occupy my mind or keep me up at night – whether related to health, relationships, or my future – have disappeared, and the others are on their way out. (Cont. in comments)
Isn’t it crazy how something can be so easy and Isn’t it crazy how something can be so easy and natural for one person, but so hard for another? 

Me doing food: I can totally cook everything I eat from scratch, no prob

Me doing mental health: just doing my hour of daily mindful cognitive gratitudinal journalization

Me doing physical therapy: I can’t do it I don’t have that muscle

I’ve done many hard things in the name of health, but I think they’ve all been the types of hard things that come naturally to me. And frankly, that hasn’t gotten me where I want to be. 

So I’ve decided to finally tackle something that feels very unnatural: developing a real relationship with my muscles and bones, and learning - through experience, not from a book - how they coordinate with each other and how to use them. 

I never really considered my musculoskeletal system a key player in autoimmune or digestive woes, but now I realize it’s naïve to think dysfunction in one part of the body doesn’t affect another. And since this is so obviously my weakest link, it’s high time to make it a priority!

Even though I’ve done strength training in the past, I never dedicated the time and focus to figure out what my body actually needed to function better, and workouts often felt awkward or led to injury. 

I’ve always dreaded PT-type exercises because they felt simultaneously like “not enough” and also SO HARD, especially when there’s no way to confirm whether I’m doing them “right” (my nightmare). 

But I’m pretty sure the fact that targeted “mind-muscle” work is so hard for me means it’s what I need the most. (That’s how that works, right?)

Anyway, I’m happy to report that I’m finally through both the initial phase of being a giant baby because I have to do something I’m bad at, AND the second phase of neurotically worrying about doing it “wrong.” And hopefully I’m on my way to better posture, improved breathing, and greater strength! 

Super thankful to have people in my life who remind me to have fun and stay curious, when my natural disposition is to write a 27-step plan to “fixing” everything “wrong” with me. And to remind me that it is, in fact, a JOY to be a novice at something (as @_john_the_savage_ would say).
"If your nervous system is balanced, your heart is "If your nervous system is balanced, your heart is constantly being told to beat slower by your parasympathetic system, and beat faster by your sympathetic system. This causes a fluctuation in your heart rate: HRV." (whoop.com) 
 
This statement is a formidable example of one of the biggest misconceptions about heart rate variability (HRV). 
 
HRV is highest during rest or sleep, when sympathetic input is lowest. If HRV was the result of an autonomic “tug-of-war,” why would it be greatest when one of the contenders has entirely dropped the rope? 
 
Part of the misunderstanding may stem from failure to recognize that the heart has an intrinsic rate, well above the resting heart rate maintained by the vagus nerve. Varying vagal impulses create HRV without any sympathetic input at all. 
 
There are many other common misconceptions, such as the notion that HRV metrics measure autonomic tone, or that HRV itself is a metric with one interpretation. 
 
Such misconceptions aren’t only found in layscience – they also pervade academic and clinical literature. For instance, you’ll see LF used as a measurement of “sympathetic tone” and LF/HF as a measurement of “sympathovagal balance,” even though it’s been clear for decades that those interpretations are not physiologically accurate.
 
This post (and the associated article at alyssaluck.com/hrv101) can be thought of as “foundations for understanding HRV research.” And it provides a good example not only of the insufficiency of “sound-byte” science, but also of real science in action. 
 
The unfortunate reality is that we can’t always take researchers’ conclusions at face value. Few have the time to adequately assess a field before adopting one of their metrics, and once a misinterpretation has taken root it can easily become an accepted fact that propagates through repetition, becoming more entrenched with each published paper.
 
Thankfully the ramifications in this case are not very serious - misdirection of experimental design and analysis, and many false statements, but no dire consequences. Nevertheless, it’s a good reminder that science is a human institution, and it never hurts to question oft-repeated “facts.”
My latest diet experiment: the bean protocol! This My latest diet experiment: the bean protocol! This was one of the changes I made immediately prior to my drastic increase in HRV. 

Brief background: the bean protocol entails eating lots of soluble fiber (particularly beans) as a way to support detox. It rests on the assumption that most chronic health issues are the result of fat-soluble environmental toxins, excess hormones, and other fat-soluble things being recirculated in the body rather than eliminated. 

There is some scientific merit to this: the liver does eliminate many toxins and other compounds through the bile, these things can be subject to reabsorption via enterohepatic recirculation, and certain types of fibers do interrupt this process by binding bile, preventing reabsorption and allowing excretion in the feces.

That said, there are many unanswered questions that would need to be answered for me to be on board with that as the sole or even primary explanation for the anecdotal success of those on the protocol. I think there are almost certainly other mechanisms at play, and I doubt things work exactly as proponents of the protocol describe. 

But at the end of the day, what matters is not mechanisms, but practical outcome. And whatever the reason, it works for many! It seems especially popular and effective for hormonal issues and acne, but the preeminent bean spokesperson @uniquehammond cured her severe Crohn’s with it. 

For me, I experienced better digestion and clearer skin, among other benefits (like not having to wear deodorant). On the less-good side, I lost weight I didn't need to lose, had cold hands and feet, and developed some dry patches on my skin. 

(The dry patches [and perhaps weight loss] were probably because I kept fat too low – mostly because their favored fat source, nuts, is a no-go for me.)

I'm continuing to experiment, hoping to find a balance that lets me reclaim the benefits (which I lost after returning to my normal eating pattern) while avoiding the pitfalls. I’ll share any exciting developments, and will eventually dig into the science behind it too. 

For info about what the protocol entails, you can visit alyssaluck.com/the-bean-protocol-for-ibd!
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Recent Posts

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  • Heart Rate Variability 101: What It Is, How It’s Measured, and Controversies in the Literature
  • Autonomic Nervous System 101: Anatomy and Physiology
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