thiamine gastroparesis

SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency?


In many of my clients, chronic upper constipation and gastroesophageal reflux disease (GERD) are misdiagnosed as bacterial overgrowth. Unfortunately, they are often non-responsive to antimicrobial treatments. Yet, sometimes the issues are fixed within a few days of vitamin B1 repletion. This has shown me that often times, the small intestinal bacterial overgrowth (SIBO) is simply a symptom of an underlying vitamin B1 or thiamine deficiency.

GI Motility and Thiamine

The gastrointestinal (GI) tract is one of the main systems affected by a deficiency of thiamine. Clinically, a severe deficiency in this nutrient can produce a condition called “Gastrointestinal Beriberi”, which in my experience is massively underdiagnosed and often mistaken for SIBO or irritable bowel syndrome with constipation (IBS-C). The symptoms may include GERD, gastroparesis, slow or paralysed GI motility, inability to digest foods, extreme abdominal pain, bloating and gas. People with this condition often experience negligible benefits from gut-focused protocols, probiotics or antimicrobial treatments. They also have a reliance on betaine HCL, digestive enzymes, and prokinetics or laxatives.

To understand how thiamine impacts gut function we have to understand the GI tract. The GI tract possesses its own individual enteric nervous system (ENS), often referred to as the second brain. Although the ENS can perform its job somewhat autonomously, inputs from both the sympathetic and parasympathetic branches of the autonomic nervous system serve to modulate gastrointestinal functions. The upper digestive organs are mainly innervated by the vagus nerve, which exerts a stimulatory effect on digestive secretions, motility, and other functions. Vagal innervation is necessary for dampening inflammatory responses in the gut and maintaining gut barrier integrity.

The lower regions of the brain responsible for coordinating the autonomic nervous system are particularly vulnerable to a deficiency of thiamine. Consequently, the metabolic derangement in these brain regions caused by deficiency produces dysfunctional autonomic outputs and misfiring, which goes on to exert detrimental effects on every bodily system – including the gastrointestinal organs.

However, the severe gut dysfunction in this context is not only caused by faulty central mechanisms in the brain, but also by tissue specific changes which occur when cells lack thiamine. The primary neurotransmitter utilized by the vagus nerve is acetylcholine. Enteric neurons also use acetylcholine to initiate peristaltic contractions necessary for proper gut motility. Thiamine is necessary for the synthesis of acetylcholine and low levels produce an acetylcholine deficit, which leads to reduced vagal tone and impaired motility in the stomach and small intestine.

In the stomach, thiamine deficiency inhibits the release of hydrochloric acid from gastric cells and leads to hypochlorydria (low stomach acid). The rate of gastric motility and emptying also grinds down to a halt, producing delayed emptying, upper GI bloating, GERD/reflux and nausea. This also reduces one’s ability to digest proteins. Due to its low pH, gastric acid is also a potent antimicrobial agent against acid-sensitive microorganisms. Hypochlorydria is considered a key risk factor for the development of bacterial overgrowth.

The pancreas is one of the richest stores of thiamine in the human body, and the metabolic derangement induced by thiamine deficiency causes a major decrease in digestive enzyme secretion. This is one of the reasons why those affected often see undigested food in stools. Another reason likely due to a lack of brush border enzymes located on the intestinal wall, which are responsible for further breaking down food pre-absorption. These enzymes include sucrase, lactase, maltase, leucine aminopeptidase and alkaline phosphatase. Thiamine deficiency was shown to reduce the activity of each of these enzymes by 42-66%.

Understand that intestinal alkaline phosphatase enzymes are responsible for cleaving phosphate from the active forms of vitamins found in foods, which is a necessary step in absorption. Without these enzymes, certain forms of vitamins including B6 (PLP), B2 (R5P), and B1 (TPP) CANNOT be absorbed and will remain in the gut. Another component of the intestinal brush border are microvilli proteins, also necessary for nutrient absorption, were reduced by 20% in the same study. Gallbladder dyskinesia, a motility disorder of the gallbladder which reduces the rate of bile flow, has also been found in thiamine deficiency.

Malnutrition Induced Malnutrition

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. In fact, this is indeed something I see frequently. And sadly, as thiamine is notoriously difficult to identify through ordinary testing methods, it is mostly missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:

  • Stomach acid secretion and gastric emptying
  • Pancreatic digestive enzyme secretion
  • Intestinal brush border enzymes
  • Intestinal contractions and motility
  • Vagal nerve function

Based on the above, is it any wonder why thiamine repletion can radically transform digestion? I have seen many cases where thiamine restores gut motility. Individuals who have been diagnosed with SIBO and/or IBS and are unable to pass a bowel movement for weeks at a time, begin having regular bowel movements and no longer require digestive aids after addressing their thiamine deficiency. In fact, the ability of thiamine to address these issues has been known for a long time in Japan.

TTFD and Gut Motility

While there are many formulations of thiamine for supplementation, the form of thiamine shown to be superior in several studies is called thiamine tetrahydrofurfuryl disulfide or TTFD for short. One study investigated the effect of TTFD on the jejunal loop of non-anesthetized and anesthetized dogs. They showed that intravenous administration induced a slight increase in tone and a “remarkable increase” in the amplitude of rhythmic contractions for twenty minutes. Furthermore, TTFD applied topically inside lumen of the intestine also elicited excitation.

Another study performed on isolated guinea pig intestines provided similar results, where the authors concluded that the action of TTFD was specifically through acting on the enteric neurons rather than smooth muscle cells. Along with TTFD, other derivatives have also been shown to influence gut motility. One study in rats showed an increase in intestinal contractions for all forms of thiamine including thiamine hydrochloride (thiamine HCL), S-Benzoyl thiamine disulphide (BTDS -a formulation that is  somewhat similar to benfotiamine), TTFD, and thiamine diphosphate (TPD). A separate study in white rats also found most thiamine derivatives to be effective within minutes.

Most interestingly, in another study, this time using mice, the effects of thiamine derivatives on artificially induced constipation by atropine and papaverine was analyzed. The researchers tested whether several thiamine derivatives could counteract the constipation including thiamine pyrophosphate (TPP), in addition to the HCL, TTFD and BTDS forms. Of all the forms of thiamine tested, TTFD was the ONLY one which could increase gut motility. Furthermore, they ALSO showed that TTFD did not increase motility in the non-treatment group (non-poisoned with atropine). This indicated that TTFD did not increase motility indiscriminately, but only when motility was dysfunctional. Finally, severe constipation and gastroparesis identified in patients with post-gastrectomy thiamine deficiency, was alleviated within a few weeks after a treatment that included three days of IV TTFD at 100mg followed by a daily dose of 75mg oral TTFD. Other symptoms also improved, including lower limb polyneuropathy.

To learn more about how thiamine affects gut health:

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This article was first published on HM on June 1, 2020. 


More about Eosinophilic Esophagitis


Seeing some of the comments following the appearance of my post Eosinophilic Esophagitis May Be a Sugar Sensitive Disease, it seemed that it was necessary to provide a little more explanation for how the conclusions were reached. Hopefully this may produce less misunderstanding.

Compartmentalized Medicine

The present model for disease is being rapidly outdated, so let me first of all review how a diagnosis is made in modern medicine. When a patient pays a visit to a physician, a medical history is recorded. The history begins by the patient describing symptoms, the sensory afflictions experienced since the loss of health began. This is followed by a physical examination when the physician is looking for evidence of malfunction. For example, this may include finding enlargement of a given organ, point tenderness when pain is elicited or a neurological deficit. Family history and the history of previous illnesses are both taken into account. The physician may or may not have a working idea of the nature of the disease process at this stage and a series of laboratory tests are requested. All of this is put together and the physician then has to consider what is generally referred to as a differential diagnosis. Which part of the physical examination, combined with the tests, all point conclusively to a diagnostic category?

This method of making a diagnosis was derived from the Flexner report initiated by Rockefeller in 1910. It was adopted from the German method in which laboratory confirmation was emphasized. This gave rise to the methodology that we now call “scientific medicine”. The symptoms, signs and laboratory reports are then put together and a given disease is named as the most likely fit.

So let us examine for a moment how this confuses us. All sensations are perceived in the brain and symptoms are merely a method by which the brain/body provides a warning that something is wrong. The “wrongness” has to be interpreted. In the present model, each constellation of symptoms, signs and laboratory reports are then given a name. For example, because somebody by the name of Parkinson was the first to describe a given constellation, it is called Parkinson’s disease, even though the underlying cause is completely unknown. Research has been aimed at finding a cure for that disease without giving full recognition to the fact that the constellation of findings overlaps with the constellations exhibited in other brain diseases, each being named separately. Furthermore, if the constellation points to an organ as the seat of a given problem (such as the intestine), the patient is referred to a specialist (a gastroenterologist) whose practice is confined to diseases of that organ (organic disease). An attempt to improve the symptoms by prescribing drugs is the chosen method, without considering the complex connection of the sick organ with the brain. An “anti-inflammatory” drug is prescribed, without asking why or what caused the organ to become sick.

In the case that I wrote about previously, the disease process called eosinophilic esophagitis or EoE, results from ingesting food. The presently accepted cause is “food allergy”.

Understanding Disease Differently: A Connected System

Let me provide an example to illustrate the change in perspective that occurs if the whole person is considered. On one of these posts a mother reported that her daughter had eosinophilic esophagitis, “associated with idiopathic gastroparesis” (partial or complete paralysis of the intestine). The word idiopathic stands for the simple sentence “the cause is unknown”. Evidently, no attempt had been made to connect the two conditions together. Is it likely that two unusual conditions will exist at the same time in one individual? By recognizing that the brain is always involved with body disease and brain disease is always involved with the body, it is possible to provide a solution for a connection between eosinophilic esophagitis and gastroparesis. It depends completely on an understanding of the profound genius of the brain/body interconnection.

The post that led to all of these comments asks the question, is this disease caused by the ingestion of sugar? We know that ingestion of sugar can easily induce thiamine deficiency because we have the ancient model of beriberi where white rice (without its surrounding cusp) ingestion, consumed as a staple, was found to be the cause. (Rice grain is starch and is broken down in the body to glucose. The cusp around the grain contains the vitamins. When the cusp of the rice is removed, as it is in white rice, the vitamins are removed leaving only the starch, which is converted to glucose.)

Digestion: Where Mechanical Meets Chemical

The vagus nerve is the 10th cranial nerve. Its action, initiated in the lower part of the brain, is to send outgoing messages to the spleen, an important organ that is used for controlling inflammation. The vagus nerve uses a neurotransmitter called acetylcholine and it also deploys messages to the esophagus and the entire intestinal tract. The wave pattern in the respective parts of the intestine that is induced by this nerve is called peristalsis. It pushes the contents along while the complex process of digestion occurs. Without going into details, the synthesis of acetylcholine depends on vitamin B complex, dominated by thiamine. Without thiamine, there is less acetylcholine and without this vital neurotransmitter, the control of inflammation and peristalsis in the esophagus, the intestinal tract, or both, are all compromised.

Eosinophilic Esophagitis and Food Allergy

In EoE, food sensitivity, occurring for whatever reason and known as food allergy, is causing inflammation that might occur in either the esophagus or any other part of the intestinal tract. When it occurs in the intestine it is called eosinophilic enteritis. Although the mechanism is the same, the locality differs but the esophagus is more commonly the affected part. The inflammatory response gets out of control because the vagus nerve, lacking acetylcholine to transmit the necessary information, is failing to suppress esophageal inflammation by sending a proper message to the spleen. The association of eosinophilic penetration into the intestinal tissue is part of the inflammation and it is interesting that a similar event has been associated with asthma in bronchial tubes. Asthma was a recurrent problem in the history of my patient.

Like the famous poem:

“for the want of a nail a shoe was lost; for the want of a shoe a horse was lost; for the want of a horse a battle was lost; for the want of a battle a kingdom was lost”.

To paraphrase this in biochemical terms “for the want of thiamine (vitamin B1), action of the citric acid cycle (engine of the cell) was lost; for the want of the citric acid cycle, acetylcholine (neurotransmitter) was lost; for the want of acetylcholine, suppression of inflammation was lost; for the want of acetylcholine, normal peristalsis (wavelike action) in the esophagus and intestinal tract was lost.

The loss of the peristaltic wave in the intestine was given the name “idiopathic gastroparesis”, a clear indication by the diagnostician that “its cause is unknown”. Like the blind men and the elephant the present medical model looks at a segment of the problem and fails to see the big picture. The trouble with this failure to understand the full nature of the problem is because we have divided brain disease from body disease. If it is suspected that the brain is the cause of the problem and all laboratory studies are negative, it is assumed that the symptoms are psychosomatic in nature and have been “imagined by the patient”. When the patient is told that it is “psychological”, it naturally induces anger.

My patient’s symptoms, recurring through infancy to the age of 8 years, were thought to be psychosomatic until endoscopy revealed the esophagitis. The “psychosomatic symptoms” were resulting from thiamine deficiency affecting the brain. His dramatic growth spurt during treatment strongly suggested that the autonomic (automatic) nervous system was at the seat of the complex problem. That conclusion can be supported by the medical literature concerning a well known genetically determined disease called Familial Dysautonomia, a disease whose clinical course results in growth failure. In the case of my patient, the dysautonomia was reversible and the result of thiamine deficiency, hence the growth spurt.

Nobody is looking for evidence of a vitamin deficiency because it has been assumed that that kind of disease is of only historical interest. This idea is so impregnated in the modern medical psyche that we can actually miss such a diagnosis when it is staring us in the face! That was the case here and may be the case in many other instances of eosinophilic esophagitis or enteritis.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.