Summary: In her 1987 book Breaking the Vicious Cycle, Elaine Gotschall proposed the hypothesis that digestive diseases – including IBD – are perpetuated by a vicious cycle of carbohydrate malabsorption, bacterial overgrowth, and intestinal injury, and can therefore be resolved by removing specific carbohydrates from the diet to break the cycle. Much of her research was quite prescient, but key claims fail to stand up to scrutiny, and the science does not support adherence to SCD principles. A modern look at Gottschall’s hypotheses reveal that modulating the intestinal bacteria through diet is indeed as important as she suspected, but that strategies other than the SCD are better able to accomplish that goal.
This article is part of the IBD Index. Last updated April 20, 2022.
This article is a deep dive into the science behind the Specific Carbohydrate Diet, and is a companion post to the high-level summary post: The Specific Carbohydrate Diet (SCD) for IBD: Everything You Need to Know.
The Specific Carbohydrate Diet as laid out in the 1987 book Breaking the Vicious Cycle (BTVC) by Elaine Gotschall is respectably science-driven. She lists dozens of references in the back of the book to support her recommendations (which is impressive considering she was conducting this research in the pre-internet era), and the book itself has been cited in the literature over 100 times. The SCD is also increasingly showing up as an intervention in clinical research, first in case studies and more recently in a large randomized controlled trial.
I said this in my main post on the SCD, but in many ways, Gottschall was truly ahead of her time with the theories she lays out in her book, although of course she leaned heavily on the work of Dr. Haas. In researching this post, I was struck by how relevant her work still is, and how many modern lines of inquiry flow naturally from her hypotheses.
That said, the big wheel of science keeps on turning, and there’s much to be critiqued in BTVC, with quite a few issues that are – in my view, at least – highly relevant to patients. When you have a dietary protocol with rules that are as specific as those of the SCD – and when the diet originator claims they must be followed with “fanatical adherence” – you gotta make sure they stand up to scrutiny, right?
So, without further ado: I’ll start by explaining the central theories and hypotheses of the SCD, so that it’s clear which claims I’ll be critiquing. Then I’ll dive into an analysis of those specific claims. Finally, I’ll take off my critiquing hat to discuss what I see as the central topics of importance relevant to the SCD in light of modern research. At the end, I’ll summarize all my main points and their practical implications (for those of you who just want the bottom line).
Table of Contents
Background: the structure and digestion of carbohydrates
Monosaccharides, disaccharides, and polysaccharides
Carbohydrate digestion
What about FODMAPs?
The central premise of the Specific Carbohydrate Diet
The “vicious cycle” problem
The “specific carbohydrate” solution
The claims
Claim 1: do people with digestive disease have an impaired ability to break down and absorb disaccharides?
Claim 2: does malabsorption of disaccharides worsen digestive disease?
Claim 3: does the SCD truly leave virtually no carbohydrates unabsorbed to be fermented by bacteria?
Claim 4: does reducing the carbohydrates available to small intestinal bacteria improve digestive disease?
Bonus claim: does carbohydrate malabsorption cause digestive disease?
SIBO, SCFA, and FODMAPs: a modern look at carbohydrate malabsorption
The bottom line
Background: The Structure and Digestion of Carbohydrates
As the name “Specific Carbohydrate Diet” implies, the key feature of the diet is – wait for it – the inclusion of only specific carbohydrates. Monosaccharides, to be precise.
Monosaccharides, Disaccharides, and Polysaccharides
The broad category of “carbohydrate” can be broken down in several ways based on their molecular structure, but the categories we care about in this case are based on their length. All carbohydrates are made up of simple sugar molecules chained together to form molecules of varying length and structure, and can be categorized as follows:
Monosaccharides are the smallest possible carbohydrate unit (mono = single, saccharide = sugar), and include glucose, fructose, and galactose.
Disaccharides consist of two monosaccharides bonded together, and include sucrose (glucose + fructose), lactose (glucose + galactose), and maltose (glucose + glucose). There are others, but those are the most common.
Polysaccharides are any carbohydrate larger than two simple sugar molecules, including all starches.
Of note, various fibers (such as cellulose) are also considered polysaccharides, but for the purposes of the SCD, they don’t “count” as polysaccharides. As in, Gottschall does not restrict them in the diet.
Carbohydrate Digestion
Of central importance to the theory behind the SCD is the fact that all carbohydrates must be broken down into their constituent monosaccharides before they can be absorbed by the intestinal enterocytes.
Carbohydrate digestion consists of several steps, beginning with salivary amylase during chewing and continuing in the small intestine with pancreatic enzymes. But the most relevant step to the SCD is the final step, which is the breakdown of disaccharides by specific disaccharidases – sucrase, lactase, and maltase, among others. This step occurs at the microvilli of the brush border of the small intestine, as opposed to the activities of pancreatic enzymes, which occur in the intestinal lumen. Thus, this step in digestion is at risk if the structure or function of the brush border is impacted.
What about FODMAPs?
*f o r e s h a d o w i n g*
One category of carbohydrate that Gottschall does not reference in her book, but which is highly relevant to the topics to be discussed, is FODMAPs.
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. Remember this for later.
As you can gather from the acronym, the FODMAP category includes carbohydrates from all three of our SCD-relevant categories (mono, di, and polysaccharides). They 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), found mainly in wheat and onions.
Galactooligosaccharides (GOS), found mainly in 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.
The Central Premise of the Specific Carbohydrate Diet
With that background out of the way, I can now introduce the central premise of the SCD, which can be broken into two parts.
The “Vicious Cycle” Problem
The first half – the causal half – of the central premise is this: people with digestive illness have some level of injury to their small intestinal surface (the brush border), which leads to impaired digestion of disaccharides. This leads to malabsorption of disaccharides, making them available for fermentation by bacteria. This leads to bacterial overgrowth and an increase in bacterial by-products and mucus production, which perpetuates injury to the small intestinal surface.
This is the “vicious cycle” Gottschall lays out in BTVC.
The “Specific Carbohydrate” Solution
The second half of the central premise is summed up perfectly in this quote from page 19 of BTVC: “The Specific Carbohydrate Diet presents a method for breaking the cycle by maximally nourishing the individual and minimally nourishing the intestinal microbes. By this method, undesirable stresses on the intestine decrease. The diet is based on the principle that specifically selected carbohydrates, requiring minimal digestive processes, are absorbed and leave virtually none to be used for furthering microbial growth in the intestine.”
Essentially, the theory is that by only allowing monosaccharide carbohydrates in the diet, you can starve the small intestinal bacteria that are causing problems, thus allowing the intestine to heal.
The Claims
These central premises could be broken down into a variety of specific claims. For my purposes, I’ve broken down each part of the theory into two claims (given here in question format):
- Do people with digestive disease have an impaired ability to break down and absorb disaccharides? (Whether or not this is due to histological damage to the small intestine is of secondary importance.)
- Does malabsorption of disaccharides worsen digestive disease? (Whether or not this is due specifically to disaccharides feeding bacterial overgrowth in the small intestine is of secondary importance.)
- Does the SCD truly leave virtually no carbohydrates unabsorbed to be fermented by bacteria?
- Does reducing the carbohydrates available to small intestinal bacteria improve digestive disease?
Now, let’s look at each of these claims in turn.
Do people with digestive disease have an impaired ability to break down and absorb disaccharides?
The short answer to this question is “often, but not always.”
One of the frequently cited papers in BTVC describes the microscopic topography of the small intestine in children with various forms of chronic diarrhea, from celiac disease to parasitic infections to soy intolerance, and it does present good evidence for reduced disaccharidase activity in these children. (Source)
However, of note, the paper author did not find villous atrophy in all patients, or even in all patients with reduced disaccharidase activity. Further, even in patients without reduced disaccharidase activity, he still often found symptomatic carbohydrate intolerance (specifically of sucrose and lactose). Possible contributing factors cited in the paper include increased cell shedding, increased mucus production, and various metabolic actions of the intestinal microbiota.
Shifting focus towards IBD specifically, even a cursory PubMed search turns up plenty of evidence for both structural and functional changes to the small intestinal brush border. Damage to the small intestinal mucosa is a hallmark of Crohn’s disease, so that’s a given, but this paper reports reduced microvilli length even in small intestinal tissue that wasn’t visibly inflamed. And in this paper, researchers found reduced disaccharidase activity in both UC and CD patients, and observed that this reduced enzymatic activity was usually accompanied by abnormalities in the structure of their microvilli as well. Of note, these were also tissue samples from the seemingly-uninflamed jejunum – not the ileum or the colon, where active inflammation was present.
As a final example, this paper from 1967 (that I sadly can’t access the full text of) reports higher observed lactase deficiency in UC patients vs. controls, although the sample size was small (32 patients) and the total lactase deficiency was still quite low (46%). But the interesting bit is that they continued testing the lactase levels of these patients over time, and found that levels improved as symptoms improved, and levels declined as symptoms worsened. Nifty, right? Researchers here noticed a similar trend of lactose malabsorption waxing and waning along with disease activity, although in their larger sample of patients, they found a markedly lower total incidence of lactose intolerance (9% in UC and 6% in Crohn’s).
Of note, plenty of healthy people experience malabsorption of disaccharides with no associated clinical symptoms. For instance, many people without lactase persistence are still able to consume dairy products without ill effect. (Source)
So, the verdict? I think we can safely say that people with digestive disease often have an impaired ability to break down and absorb disaccharides, although it certainly isn’t universal. And it is often – but not always – associated with reductions in disaccharidase activity and structural changes in the microvilli.
Does malabsorption of disaccharides worsen digestive disease?
This question is surprisingly tricky to address.
There’s no doubt that malabsorption of some carbohydrates can worsen the symptoms of digestive disease. This is quite well documented; particularly in IBS, and particularly with lactose, fructose, and sorbitol malabsorption. (Source 1, 2, 3) (Gasp! Fructose? The SCD-compliant monosaccharide?? Yes. More on this later.) This also applies to “functional” symptoms in IBD patients.
Gottschall also cites evidence in her book to support this claim – largely clinical observations of children with various digestive illnesses during the early 1900s. Simply put, it was commonly observed that in children with diarrhea, removing carbohydrate from the diet would make them better, and adding it back would make them worse.
However. There are two important nuances to address here.
First: in IBD specifically, a distinction is made between worsening symptoms, and worsening the disease itself. For instance, just read the title of this paper: “Low FODMAP diet in Egyptian patients with Crohn’s disease in remission phase with functional gastrointestinal symptoms.” Yes, IBD can be in “remission” while the patient still has “functional” symptoms like diarrhea, bloating, etc. Crazy, right?
Essentially, if there is no evidence of inflammation/ulceration with colonoscopy or endoscope, and inflammatory markers are normal, then “functional” symptoms like diarrhea, constipation, and bloating are now addressed separately from the IBD. Basically, the person now has IBS. (Source)
And shockingly, it seems that the dual goals of improving functional symptoms and improving disease activity are not always aligned. For instance, check out the conclusion of this paper about introducing prebiotics in Crohn’s disease: “This strategy might be favorable for gut health in Crohn’s disease, but at the cost of inducing symptoms.” Fabulous.
To be perfectly honest, I haven’t been able to find any solid evidence of disaccharide malabsorption specifically worsening inflammation in digestive illnesses like IBD. But at a certain point, for practical purposes, I think it’s necessary to call BS on this particular distinction. For instance, look at this example:
“One patient, a farmer, had 10 to 20 watery movements a day. He applied for a disablement annuity because of extreme fatigue. Following the institution of a lactose-free diet his stools became normal within two days. In two weeks he gained 7kg in weight and insisted on his discharge because he had to go home to sow his fields.” (Source)
This patient had undergone colectomy and ileostomy, and no mention was made of a subsequent Crohn’s diagnosis or inflammation in the small intestine, so it seems likely that his watery stools would have been classified as a “functional” symptom. But I would be hard-pressed to make the semantic argument that lactose didn’t worsen “the disease itself.” (And yes, I included the quote verbatim mostly because I wanted you to know that he could go home to sow his fields.)
The author of that same paper also notes that in a different patient who had improved dramatically on a milk-free diet, they tested adding lactose alone, and it produced the same symptoms as milk itself (severe diarrhea and cramping), proving that it was the lactose itself (and not milk protein) causing problems.
Okay, I know I said there were two important nuances to discuss. That was one. The second is this: it appears that disaccharides are not, in fact, the most relevant category of carbohydrate to consider when talking about malabsorption and digestive disease. I’ll explain further in the next section.
For now, we’ll leave it here: malabsorption of some carbohydrates (not necessarily disaccharides) can reliably worsen existing functional digestive symptoms, but it’s unclear what impact they have on underlying disease pathogenesis (eg, bacterial ecosystem, inflammation, barrier function, etc).
Does the SCD truly leave virtually no carbohydrates unabsorbed to be fermented by bacteria?
And with that less-than-satisfying assessment of the previous claim, it’s finally time to address the extensively-foreshadowed elephant in the room: FODMAPs.
Here’s the thing: Gottschall got a lot right, or almost right. But, in my humble opinion, she got the actual selection of her “specific carbohydrates” wrong. I propose that, if the goal is indeed to limit the availability of unabsorbed carbohydrates that are easily fermented by bacteria in the small intestine, the eliminated class of carbohydrates should be FODMAPs.
Recall now the brief definition of FODMAPs I gave you earlier in this article that I told you to remember. FODMAPs are defined by 1) their tendency to be poorly absorbed, and 2) their tendency to be rapidly fermented by bacteria.
Of note, starch is not a FODMAP. I’m not going to make the argument here that starch is never a problem and is wrongly maligned by the SCD, because I don’t know that that’s true, and a sincere treatment of that topic would require its own article.
So, I will focus on the question asked by our third claim: does the SCD actually do what it says? Are the “specifically selected carbohydrates, requiring minimal digestive processes,” (ie, monosaccharides) “absorbed and leave virtually none to be used for furthering microbial growth”?
To this I say: no way.
First of all, setting FODMAPs aside for a moment: the SCD does not only contain monosaccharides.
For one thing, most fruits contain sucrose, a disaccharide (see chart below). Some contain quite a lot of it. This is a well-known fact, and – to my knowledge – has been well known for some time, yet Gottschall doesn’t mention or account for this anywhere in BTVC.
Further, the “allowed” legumes contain starch, a polysaccharide, a fact that Gottschall simply steps over by saying these starches “have been shown to be tolerated” (BTVC, p. 27). Judging things by whether they’re tolerated or not is all well and good, if that’s the consistent framework you’re applying. But you can’t selectively (and seemingly arbitrarily) invoke “tolerance” when the rest of the diet is built on specific rules that call for “fanatical adherence” regardless of tolerance. I digress.
Now back to FODMAPs. Even if the SCD did only include monosaccharides, it would still not be successful in eliminating the class of carbohydrates most likely to be malabsorbed and fermented by bacteria. Because that class of carbohydrates is FODMAPs (again, by definition). And fructose, which is one of the very few carbohydrates allowed on the SCD, is a FODMAP.
Now, granted, a large proportion of the “fructose malabsorption” literature is misleading, because they administer isolated fructose in amounts that far exceed what you could get from, say, fruit. And isolated fructose is very poorly absorbed, but is absorbed much better in combination with glucose. (Source) And wouldn’t you know it – fructose is never found in nature without glucose.
That said, there are several natural foods that contain more fructose than glucose, and the excess fructose in those foods is liable to be poorly absorbed (and therefore available for bacteria to ferment). (Source) And one of the prime offenders – apple juice – is a key component of the SCD intro diet!
Sorbitol is also a FODMAP, and is found naturally in many fruits, including apples. I even came across several studies showing diarrhea caused by malabsorption of carbohydrates from apple juice specifically. (Source 1, 2, 3) Again, apple juice is one of the very few foods allowed in the early stages of the SCD.
So, I think the answer to this claim is clear: the SCD does not actually limit carbohydrates to those that are easily digested and absorbed. In other words: it does not do what it says it does.
Does reducing the carbohydrates available to small intestinal bacteria improve digestive disease?
And with that, we come to our final claim, and find that it has lost its relevance to the discussion at hand. Because while the question of “starving” bacteria in the small intestine is highly relevant and deserves to be addressed, it should be assessed in light of a diet that actually does leave very little carbohydrate available to small intestinal bacteria, such as a low-FODMAP, ketogenic, or carnivore diet.
Bonus Claim: Does Carbohydrate Malabsorption Cause Digestive Disease?
But you signed up for four claims, and four claims you shall get!
This claim is not central to the SCD, which is concerned with resolving digestive disease once it’s present. However, Gottschall nevertheless appears to claim, at various points, that carbohydrate malabsorption can also cause digestive disease in the first place (or at least be a significant contributor).
See for yourself:
“The presence of undigested and unabsorbed carbohydrates within the small intestine can encourage microbes from the colon to take up residence in the small intestine and to continue to multiply. This, in turn, may lead to the formation of products, in addition to gas, which injure the small intestine.” (BTVC p. 18)
“Is the fermentation of undigested, unabsorbed starch by intestinal bacteria in the human colon causing an acidic environment which could cause harmless bacteria to change to harmful forms?” (BTVC p. 19)
“While the underlying causes of the various intestinal disorders cannot be stated with certainty, faulty digestion and malabsorption of dietary carbohydrates may be, in large part, responsible for these disorders.” (BTVC p. 21)
If there’s one fallacy you’ll find everywhere in the world of health science, it’s conflating causes and solutions. But just because an intervention has therapeutic value for an illness does not mean that the absence of that intervention caused the problem in the first place.
Regarding whether carbohydrate malabsorption causes digestive disease, it does appear that there’s a debate to be had here. In fact, the debate is being had in the literature as we speak. But the central theme is this: not all carbohydrate malabsorption is created equal.
Gottschall, of course, already knew this – at least to some extent. She glossed completely over the fiber question, and even allowed for the consumption of starches from certain ‘approved’ legumes, as discussed above.
Dr. Peter R Gibson is one researcher who would probably agree with Gottschall that carbohydrate malabsorption is a significant contributing factor underlying the development of various digestive diseases, but his focus is (unsurprisingly) on FODMAPs. (Source) The mechanism he posits is almost exactly the mechanism Gottschall posited back in 1987: that the fermentation of FODMAPs in the distal small intestine could lead to bacterial overgrowth, which leads to increased intestinal permeability and potentially diseases like IBS, Crohn’s, or celiac disease.
However, like Gottschall, his reasoning is largely mechanistic/theoretical, and is based mostly on animal research and correlational epidemiology data. He first put forth his hypothesis in 2005 (Source), and although he’s still beating the low-FODMAP drum to this day, a review paper published in 2020 contributed no further evidence aside from some more animal studies with extremely dubious relevance to humans. (Source)
And I hate to say it, but he also misrepresented the results of one study in humans, claiming that the addition of dietary fructans resulted in an increase in fecal calprotectin (thus implicating dietary FODMAPs in intestinal inflammation). What the study actually measured was fecal calprotectin at the very beginning of the study, and at the very end, so the rise could just as easily have been caused by the low-FODMAP diet, or any of the FODMAP challenges (including fructans), or all of those factors together. (Source)
All that said, the position he’s advocating is not all that radical. The broad category of “FODMAPs” is interesting because while it includes many foods we’d consider healthful, like beans, crucifers, onions, garlic, and fruits, the standard American diet is also high in FODMAPs due to its copious quantities of HFCS, dairy products, and wheat, plus rising amounts of sugar alcohols and other food additives that fall into the FODMAP category (such as inulin, which is increasingly added to processed foods for its purported prebiotic benefits).
In any case, it will be tough to separate the effects of the FODMAPs in the Western diet from all the other harmful effects. And judging by the progression of research between 2005 and 2020, I don’t imagine we’ll get convincing evidence anytime soon that FODMAPs (by virtue of being malabsorbed carbohydrates) cause digestive disease. And if/when we do, I wouldn’t be surprised if the conclusion is that “bad” FODMAPs cause problems, but “good” FODMAPs don’t. (Who wants to tell the Blue Zones that their high consumption of FODMAPs in the form of beans is going to give them digestive diseases?)
And what’s more – we also have lots of evidence indicating that carbohydrate malabsorption (FODMAP and otherwise) not only doesn’t cause digestive disease, but may actually protect against it.
Exhibit A: Primary adult lactose intolerance protects against development of inflammatory bowel disease. Now, this is simply observational research, a negative correlation between lactose malabsorption and IBD. But if lactose malabsorption caused (or contributed to) the pathology of IBD, this would be a highly unexpected correlation to find.
Exhibit B: Physiological small bowel malabsorption of carbohydrates protects against large bowel diseases in Africans. This paper discusses the potential role of lactose, fructose, and starch malabsorption in South African blacks in their markedly reduced rates of diseases such as IBD and diverticulitis, compared with South African whites. Researchers found that a test meal of maize was completely absorbed by whites, but incompletely absorbed by blacks, and hypothesized that this tendency to incompletely absorb carbohydrate in blacks was protective due to increased production of SCFA in the colon. And indeed, they found significantly higher levels of SCFA in South African blacks compared with whites, despite similarly low intakes of dietary fiber in the two groups.
Exhibit C: Does super efficient starch absorption promote diverticular disease? This fascinating little study found that patients with symptomatic diverticular disease absorb starch better than controls, and consequently, less starch reaches their colon. They conclude: “our findings confirm that unabsorbed starch is an important source of carbohydrate reaching the colon…In populations having a comparatively low intake of fibre, super efficient starch absorption, by reducing the provision of carbohydrate to the colon, may be an important determinant of a person’s susceptibility to diverticular disease.”
Plenty more where that came from, but you get the idea.
I think it’s clear that, while there is some preliminary evidence indicating that malabsorption of certain types of carbohydrate may cause problems, malabsorption of carbohydrate in general absolutely does not cause digestive disease, and may in fact protect against it.
SIBO, SCFA, and FODMAPs: A Modern Look at Carbohydrate Malabsorption
Now let’s talk about this field from the perspective of our best modern understanding, rather than from the perspective of critiquing an old hypothesis.
We’ve already touched on how Gottschall’s early research feeds into modern research on FODMAPs. But astute readers may also have picked up on the fact that Gottschall was arguably somewhat of a pioneer in the burgeoning field of small intestinal bacterial overgrowth (SIBO) research.
From pages 11-13 of BTVC: “The stomach and most of the small intestine do not normally harbor more than a sparse population of microbial flora…However, bacterial overgrowth in the stomach and small intestine can and does occur for various reasons among which are: 1) interference with the high acidity of the stomach through the continual use of antacids; 2) A decrease in the acidity of the stomach such as occurs in the aging process; 3) Malnutrition or a diet of poor quality, and the resulting weakening of the body’s immune system; 4) Antibiotic therapy which can cause a wide range of microbial changes. Once the normal equilibrium of the colon is disturbed for any reason, its microbes can migrate into the small intestine and stomach hampering digestion, competing for nutrients, and overloading the intestinal tract with their waste products.”
Now, bearing in mind that a search of PubMed titles for “small intestinal bacterial overgrowth” or “SIBO” turns up 1 paper published in each of 1984 and 1986, then near-exponential growth up to 56 papers published in 2020, I for one am impressed with Gottschall’s very prescient take on small intestinal bacteria as a key factor in the etiology of digestive diseases. Because although our understanding is rapidly evolving (for instance, recent research indicates that the issue is more likely to be dysbiosis than “overgrowth” per se), there’s no doubt that bacteria in the small intestine is hugely relevant to digestive health.
As for FODMAP research, one randomized clinical trial published in 2017 pretty well confirmed that – at least for functional digestive illness – a low-FODMAP diet is superior to the SCD. Seventy-three patients with IBS were divided into two groups: one low-FODMAP, and one SCD. After three months, patients on the low-FODMAP diet had experienced significant improvement in symptoms, while patients on the SCD showed a small improvement that was not statistically significant.
One area of modern research in this field that is conspicuously absent from BTVC is the importance of short-chain fatty acids (SCFAs) to intestinal health. In fact, the only mention from Gottschall is in a negative light: “The production of large amounts of short-chain organic acids by bacterial fermentation in the intestine may ultimately prove to be an important clue in discovering the cause of some forms of inflammatory bowel disease.” (BTVC p.19) Certainly she never mentions the importance of providing adequate substrate to large intestinal bacteria so they can produce butyrate; the focus is exclusively on starving bacteria.
But interestingly, what may at first appear to be an oversight or a misunderstanding turns out to have some merit. Because although modern research has almost unilaterally emphasized the importance of adequate SCFA to intestinal health, a little digging reveals that (like anything else) this is not a simple case of “more is always better.”
I’m not one to reinvent the wheel, so I’d like to direct you to Dr. Lucy Mailing’s thorough and brilliant (as always) article series on SCFAs for further analysis of this topic – particularly part 2 on the benefits of butyrate and part 3 on the “butyrate paradox.” But the upshot is that while it appears unlikely at this point that excess SCFAs are a significant causal factor in digestive disease (as Gottschall suggests), it certainly looks like excess SCFAs may cause problems in the context of active disease, especially when epithelial ulceration is present (as in IBD).
The Bottom Line
We’ve covered a lot of ground in this article, so briefly, here are the high points:
- The SCD is based on the theory that digestive disease is caused/perpetuated by the harmful activities of bacteria in the small intestine, which is promoted by the consumption of carbohydrates that are not absorbed and instead feed these bacteria.
- The goal of the SCD is to reduce or eliminate the fermentation of carbohydrates in the small intestine by limiting dietary carbohydrates to monosaccharides.
- However, some of the carbohydrates allowed on the SCD are notoriously malabsorbed and available for bacterial fermentation, so the diet does not do what it purports to do.
- Because a low-FODMAP diet specifically excludes carbohydrates that are poorly absorbed and readily fermented by bacteria, it could be argued that the SCD is obsolete and should be replaced by a low-FODMAP diet in cases where the goal is to reduce bacterial fermentation in the small intestine; this suggestion is supported by one clinical trial in IBS where a low-FODMAP diet significantly improved symptoms, while the SCD did not.
Ultimately, the role of carbohydrate malabsorption and bacterial fermentation in digestive diseases is highly nuanced and far from being fully understood. Bacterial fermentation of carbohydrate can be desirable and beneficial, undesirable and deleterious, or anywhere in between, depending on the substrate, the location in the gut, the health of the intestinal epithelium, and any number of other factors.
In a practical sense, much of it boils down to the question of whether to “starve the bad” or “feed the good,” and I don’t expect we’ll have clear answers anytime soon.
As for the Specific Carbohydrate Diet – Gottschall has a remarkable story, and has done a remarkable amount of good for a great many people, and much of the science in BTVC is still highly relevant today. And even where the somewhat basic and flawed mechanistic science behind the book fails, there’s no doubt the SCD works well for many people on a practical level.
That said, the science overwhelmingly fails to support the rules of the diet as written. And while I do believe Gottschall approached the design and implementation of the SCD from a largely practical standpoint (growing out of the hands-on clinical work of Dr. Haas and her own experiences with her daughter), those practical underpinnings are at risk of being drowned out by the rigid presentation of the diet’s extremely specific rules and over-emphasis on seemingly arbitrary factors that simply do not stand up to scientific scrutiny.
If the diet, as written, in all of its specific carbohydrate glory, works for you or anyone else – that’s excellent! But where the diet works, it’s unlikely that the mechanisms at play are exactly as described in the book, despite Gottschall’s confidence in her presentation of the disease mechanisms. In reality, things are quite a bit more complicated. And where the diet doesn’t work, patients would be well served to leave the SCD behind and experiment with other approaches.
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