thiamine SIBO

SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency?

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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. 

The Thiamine Connection: From POTS to Wernicke’s and Everything in Between

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Cushing’s Syndrome With a Pituitary Tumor

As a pharmacist, I always believed I had a good handle on most health conditions and the proper steps for diagnosis. It wasn’t until my daughter became very ill in 2014 that I would learn that not all conditions are so simple. After many months of dealing with her mystery illness and through much study, I came upon Cushing’s Disease, which is a condition of excess cortisol production. All of her symptoms seemed to coincide with this disease. She had insomnia, central weight gain, substantial stretch marks, a buffalo hump, flushing, anxiety, difficulty concentrating, muscle weakness, constipation and diarrhea, extreme fatigue and several others. However, her labs were not so clear cut. After two months of rigorous testing and a confirmation of a pituitary tumor on an MRI, she had a diagnosis and a surgery date.

At first, her surgery seemed to be very successful. Her anxiety, flushing, and fatigue went away. Stretch marks stopped appearing and the old ones began to heal. She showed improvement for awhile, and then her health began to decline again. Some of the old symptoms were returning. Then, she developed new symptoms similar to what are seen in the condition referred to as POTS, or postural orthostatic tachycardia syndrome. She had low blood pressure, orthostatic hypotension, temperature dysregulation, and many others. Her pathology report had always troubled me since her surgery and I wondered if the excess cortisol production was actually due to an underlying stress not yet identified.

As I began my journey into functional medicine, I became more aware of the microbiome and what a vital role it can play in our health. I studied small intestinal bacterial overgrowth (SIBO), small intestinal fungal overgrowth (SIFO), and dietary induced vitamin and mineral deficiencies. Each of these areas were clues that I needed in order to put together all the pieces of this incredibly intricate puzzle.

Maybe It Was Thiamine Deficiency

It was not until I came upon a book entitled “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition” that all the pieces really started to fall into place. Could a thiamine deficiency be the underlying cause for all of this? I began to wonder if it was not just the surgery that improved her health, but also the IV of vital nutrients that maybe her poor body was unable to absorb. Magnesium is always given prior to brain surgery which activates thiamine into its active form. And, I’m sure her IV nutrition would have contained vitamins such as thiamine. This would have explained some of the improvements we saw that seemed to have no explanation.

We started a regimen of high dose thiamine along with a stronger gut healing protocol for SIBO and SIFO. I wanted to make sure we alleviated any issues that could cause malabsorption of thiamine. Within 3 months on thiamine, my daughter’s lab work improved dramatically. For the first time, she had normal levels of platelets and serum calcium. Also, her cholesterol dropped 35 points and was finally within normal range. Many other markers of concern also showed great improvement. She also had no more symptoms of POTS. Finally, I had found my answer.

I became obsessed on obtaining as much information I could about this deficiency. I researched the mild to severe symptoms and how this nutrient deficiency was prevalent in so many disease states. At this point, I had no idea that this information, which was helping my daughter, would prove to be life-saving knowledge for my grandmother.

Acute Onset Wernicke’s Syndrome In a Hospitalized Elderly Woman

I faced my worst nightmare recently, watching my 90 year old grandmother undergo a descent into severe thiamine deficiency. She has been in the hospital for a bad fall that fractured several ribs and gave her a lung puncture. In addition to the infection from the lung puncture, she had a UTI and then developed pneumonia. All of these factors increased her risk of thiamine deficiency due to the infection, which is clearly stated as a source of thiamine deficiency in the literature.

When I finally made it to the hospital, I could see that she had progressed to Wernicke’s encephalopathy. This was absolutely horrifying. She had severe eye paralysis and it was as if she was looking straight through me. She could not focus her pupils on my face at all. She was able to focus only for one split second and then a tear rolled down her cheek. I literally thought I was going to pass out. I had been studying all the symptoms to look out for in severe thiamine deficiency and now it was staring me in the face. I knew without a shadow of a doubt this was what was wrong, but I wondered “will the doctors listen to me?”

I had asked them several days prior to give her IV thiamine and I was under the impression that they were administering it, but they were only giving her an oral dose of 100 mg daily per the recommendations of one of the physicians. She went into respiratory distress in front of me and I had to agree to let them put her on a ventilator. They wanted to check a thiamine level before giving, and I said that was not always accurate according to studies. I had to beg the nurse practitioner that night to give her something and she agreed to a 100mg injection. I finally saw the doctor the next morning and she agreed to one of the accepted regimens for Wernicke’s Encephalopathy which is 200mg IV three times daily. She agreed that there was no real risk to giving it to her and I was grateful that she trusted my recommendation. I went home and waited for a miracle.

Thankfully, the next day she woke up from this coma-like state. Two days later she was off the ventilator and able to speak with me showing incredible improvement. She has been confused on and off since this incident, but according to studies, this may last for weeks or possibly months. She is 90, so I know this has been very hard on her frail body and her recovery will probably take much longer than a younger person.

Both Chronic and Acute Thiamine Deficiency Go Unnoticed

I hope this was a real wake up call to the staff at the hospital where she is staying. How many other people are suffering from this condition and it goes unnoticed? How many people are dying that could be saved? This is not a rare condition and is certainly not limited to alcoholism. My grandma has not had alcohol in years. She had low thiamine levels going into the hospital, and the infection just pushed her over the edge.

I had prayed for years to determine what could be causing my daughter’s health issues and I believe there was divine intervention that finally led me to thiamine deficiency. To be given this knowledge which is helping to heal my daughter and soon afterward be able to utilize it to save my grandmother’s life is absolutely incredible.

My daughter was suffering from a long term, chronic, mild to moderate thiamine deficiency and my grandmother was experiencing a severe acute deficiency. Both of these can be difficult to diagnose due to the perception that this is a rare condition and typically only affects alcoholics. We need awareness and I am committed to sharing this information with anyone who will listen.

The Progression to Wernicke’s Encephalopathy and Respiratory Distress

We Need Your Help

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. 

This article was published originally on April 30, 2020.