Diverticulitis research (updated 8th dec 2022)

Stress -> disabled Digestion -> disabled motility-> disabled mucus production!
– Gut bacteria use adrenaline to grow more quickly

Irritable Bowel Syndrome and Diverticulitis: A Self-Help Plan by Shirlet Trickett,

Digestive Wellness: Strengthen the Immune System and Prevent Disease Through Healthy Digestion, Fifth Edition by Lipski, Elizabeth

Gut healing: phosphatydil choline, artichoke, aloe, collegen peptides, activated charcoal, resistant starches, probiotics, digestive enzymes

Low vit D + vdr SNP?
COMT / MAO SNP – moves blood away from extremities & gut for fight/flight/freeze

“Over the past decade, however, there has been an emerging proposal that perhaps the process was more inflammatory than infectious, as well as an appropriate emphasis on antibiotic restraint due to resistance issues”

” The Danish national guidelines suggested that there is no evidence for the obligate use of antibiotics in AUD, and, therefore, they should be used selectively “depending on the overall condition of the patient and the severity of the infection””

“German Society for Gastroenterology, Digestive and Metabolic disease, and the German Society for General and Visceral surgery also recommended against the use of antibiotics in AUD without any risk factors, including immunosuppression”

“They evaluated 623 patients with CT-proven left-sided AUD. Total duration of antibiotics in the treatment group was at least 7 days and antibiotics included an intravenous administration of a second- or third-generation cephalosporin and metronidazole or carbapenems or pipercillin-tazobactam. Overall rates of complication, including perforation and abscess formation, were low at 1.4%. They found no statistically significant differences between the antibiotic-treated patients (1%) and those not treated with antibiotics (1.9%). Furthermore, there were no differences in the frequency of surgery, length of hospital stay, recurrence of diverticulitis, abdominal pain, or changes in bowel habit. From these results, the authors concluded that, “antibiotic treatment of AUD does not prevent complications, accelerate recovery or prevent recurrence””

“The second RCT from the Netherlands evaluated 528 patients with CT-proven left-sided uncomplicated, acute diverticulitis, confirmed within 24 h [30]. Patients randomized to antibiotic treatments received 48 h of intravenous amoxicillin-clavulanic acid after which the route could be changed to oral for a total of 10 days of treatment. Patients were then followed up for 6 months to evaluate for complications. No differences were found between the observation and antibiotic treatment groups in terms of complicated diverticulitis, ongoing diverticulitis, recurrent diverticulitis, sigmoid resection, re-admission, adverse events, and mortality [30]. Importantly, hospital stay was actually significantly shorter in the observation group (2 days) than in the antibiotic treatment group (3 days) with a p = 0.006 [30]. The authors suggested that antibiotics could be eliminated in patients with a “first episode of uncomplicated, left-sided acute diverticulitis””

– https://www.karger.com/Article/FullText/489631


“Two RCTs (AVOD and DIABOLO) demonstrated no difference in recovery or adverse outcomes when antibiotics for acute uncomplicated diverticulitis were omitted. Both trials showed non-significantly higher rates of complicated diverticulitis and surgery in the non-antibiotic groups. This meta-analysis of individual-patient data aimed to explore adverse outcomes and identify patients at risk who may benefit from antibiotic treatment. Individual-patient data from those with uncomplicated diverticulitis from two RCTs were pooled. Risk factors for adverse outcomes and the effect of observational management were assessed using logistic regression analyses. P 

– https://www.sparrho.com/item/observational-versus-antibiotic-treatment-for-uncomplicated-diverticulitis-an-individual-patient-data-meta-analysis/264a016/

“Several papers have shown that genetic predisposition, environmental factors, and colonic dysmotility are implicated in the pathogenesis of DD. More recent studies have associated specific host immune responses, gut microbiota imbalance and therefore low-grade inflammation as contributors to symptom occurrence in DD and diverticulitis. Current and evolving evidence highlighted the role of genetic susceptibility, environment, colonic motility, visceral sensitivity, immune response, and microbiota in the pathogenesis of this disease.”

– https://www.sparrho.com/item/current-and-evolving-concepts-on-the-pathogenesis-of-diverticular-disease/22c0aea/

“Recent genome-wide association studies (GWAS) consistently identified three major genetic susceptibility factors for both conditions, but did not discriminate diverticulititis and diverticulosis in particular due the limitations of registry-based approaches. Here, we aimed to confirm the role of the identified variants for diverticulosis and diverticulitis, respectively, within a well-phenotyped cohort of patients who underwent colonoscopy. Risk variants rs4662344 in Rho GTPase-activating protein 15 (ARHGAP15), rs7609897 in collagen-like tail subunit of asymmetric acetylcholinesterase (COLQ) and rs67153654 in family with sequence similarity 155 A (FAM155A) were genotyped in 1,332 patients.”

– https://www.sparrho.com/item/common-variation-in-fam155a-is-associated-with-diverticulitis-but-not-diverticulosis/2611108/

“total of 50,019 participants were included. Over 24years of follow-up, there were 4343 incident cases of acute diverticulitis. The highest quintile of fiber intake in the study population (mean, 28.5 g/d) was associated with a lower risk of diverticulitis compared to the lowest quintile (12.5 g/d). Compared with the lowest quintile of total fiber intake, hazard ratios for the second, third, fourth, and fifth quintiles were 0.96, 0.95, 0.91, and 0.86, respectively, representing amodest reduction in risk. Inclusion of red meat consumption in the models did not alter the hazard ratios or P value. Intake of total fiber, cereal fiber, and fruit fiber were each associated with a statistically significant decrease in incident diverticulitis when the trend across the quintiles was evaluated with multivariable models. Analysis of specific foods revealed reduced risk of diverticulitis with increasing consumption of whole fruits, apples, pears, and prunes, but notfruit juice. Neither vegetable fiber nor total vegetable intake were associated with diverticulitis. Interestingly, insoluble – but not soluble – fiber intake was associated with a decreased risk of diverticulitis (highest quintile compared with lowest quintile: hazard ratio, 0.86; 95% confidence interval, 0.78–0.95;Ptrend¼.004). The authors conclude that insoluble fiber may be protective against diverticulitis, and that consumption of specific foods, including whole fruits, may also reduce the risk for diverticulitis.”

– [https://www.gastrojournal.org/article/S0016-5085(20)30108-6/pdf](https://www.gastrojournal.org/article/S0016-5085%2820%2930108-6/pdf)

“Symptomatic Uncomplicated Diverticular Disease (SUDD) is the most common clinical form of Diverticular Disease (DD). The therapy should be aimed at reducing both the intensity and frequency of symptoms as well as preventing complications. The pharmacological treatments include fibers, not absorbable antibiotics (for example rifaximin), anti-inflammatory drugs (for example 5-amino-salycilic acid) and probiotics, alone or in combination with other drugs. Although some of these treatments seem to be effective in treating SUDD, but their efficacy in preventing complications of the disease is still uncertain. It has been hypothesized that microbial imbalance associated with bacterial overgrowth of the colon, may be the key to the development of diverticular disease (DD). Therefore, drugs that can manipulate gut microbiota such as probiotics or rifaximine are considered as a potential key therapy. Rifaximine is able to modulate the intestinal ecosystem, restoring eubiosis. …. In SUDD probiotics have been proven as an effective therapy in reducing abdominal symptoms, but unfortunately there has been limited number of relevant studies regarding efficacy of this therapy.”

– https://www.sparrho.com/item/hot-topics-in-medical-treatment-of-diverticular-disease-evidence-pro-and-cons/25c9121/

“The aim was to evaluate the efficacy and safety of DIVER-100® in patients with SUDD. We conducted a prospective observational study to evaluate the efficacy of DIVER-100® in consecutive patients with SUDD, confirmed by radiology or endoscopy. All patients were treated with DIVER-100® 2 capsules/day 10 days per month, for 3 months. The primary endpoint was the clinical remission rate, defined as the reduction of abdominal pain and bloating, improvement of bowel habits and prevention of acute diverticulitis (AD). The secondary endpoint was the rate of adverse events. One hundred and one patients were consecutively enrolled at the Internal Medicine and Gastroenterology Unit, Sant’Orsola Hospital, Bologna, Italy. DIVER-100® was effective in inducing remission of symptoms in 12 patients (11.9%) at 3 months and in 10 patients (9.9%) at 6 months. DIVER-100® significantly reduced abdominal pain and bloating in 45.5% and 57.4% of patients respectively (p <0.001)  ![11-03-20_103856-DIVER 100® compresse - shop-farmacia.it - Waterfox Classic.jpg](file:///home/gaz/.config/joplin-desktop/resources/bf8c386d1f434adca9eeaea8586be8a7.jpg) https://www.shop-farmacia.it/benessere/IT924997428/diver-100-compresse.htm - [https://www.sparrho.com/item/efficacy-of-a-new-nutraceutical-formulation-in-patients-with-symptomatic-uncomplicated-diverticular-disease-sudd-a-prospective--observational-study/25c92a9/](https://www.sparrho.com/item/efficacy-of-a-new-nutraceutical-formulation-in-patients-with-symptomatic-uncomplicated-diverticular-disease-sudd-a-prospective-observational-study/25c92a9/) "Acute Uncomplicated Diverticulitis (AUD) is defined as the inflammation of a colon diverticulum, often involving colic wall and pericolic fat. Conventional treatment of AUD includes antibiotics, usually ciprofloxacin and metronidazole, fasting, and fluid therapy. The aim of this study was to test the efficacy of a mix of three probiotic strains (Bifidobacterium lactis LA 304, Lactobacillus salivarius LA 302, Lactobacillus acidophilus LA 201; Lactibiane Iki®, Biocure [PiLeJe Groupe], Italy/PiLeJe Laboratoire, France) in association with conventional antibiotics in treating AUD compared to conventional antibiotics used alone. We enrolled 84 (25M/59F mean age 61.5 ± 11.5 years) consecutive patients who came to the Emergency Department of the Fondazione Policlinico Universitario A. Gemelli - IRCCS, Rome, Italy, with a diagnosis of AUD confirmed by CT scan. After routine blood test and dosage of C-reactive protein (C-RP), patients were randomly divided into two groups: Probiotic group (42 patients, 10M/32F mean age 32.23 ± 10.3 years) was treated with ciprofloxacin 400 mg twice a day and metronidazole 500 mg three times a day for one week and simultaneously supplemented with the probiotic mix, 1 sachet twice a day for 10 days. Control group (42 patients, 15M/27F mean age 59.01 ± 11.3 years) received the same antibiotic treatment without the probiotic mix. All patients filled a daily Visual Analog Scale (VAS) for assessment of abdominal pain, with a range value from 0 (asymptomatic) to 10, and CRP value was determined on admission and at discharge. As regards abdominal pain, on Day 3, Group A showed a significant decrease of 4.06 points (51.4%) in VAS score compared to a decrease of 2.79 points (34.9%) in Group B. On Day 5 the decrease was of 6.3 points (80%) in Group A and of 4.85 points (61%) in Group B. VAS score was reduced by 7.59 points (96%) in Group A and 6.1 points (76%) in Group B on Day 7 +, and by 7.8 points (99%) in Group A and 7.2 points (90%) in Group B on Day 10. About inflammation, Group A showed a decrease in C-RP value of 64%, compared to a decrease of only 35% in Group B. We also observed that the duration of hospitalization was significantly shorter for patients in Group A: 89 h (3.7 days) in Group A vs. 101 h (4.2 days) in Group B (p=0.03). Our results indicated showed that the supplement with the probiotic mix of Bifidobacterium lactis LA 304, Lactobacillus salivarius LA 302, and Lactobacillus acidophilus LA 201 in combination with the standard antibiotic therapy for AUD reduced abdominal pain and inflammation significantly more than antibiotic treatment used alone. These findings could be due to the anti-inflammatory activity of the probiotic mix. Larger studies are needed to validate its use in the clinical practice." - https://www.sparrho.com/item/the-efficacy-of-a-mix-of-three-probiotic-strains-in-reducing-abdominal-pain-and-inflammatory-biomarkers-in-acute-uncomplicated-diverticulitis/24c09cc/ "Different structural and functional alterations have been described in the colon wall with diverticula, involving all the parietal layers, from mucosa to muscular tunica. The potential role of minimal inflammatory infiltrate in DD mucosa was firstly proposed in 2008 [20]. An increased number of lymphocytes, but not neutrophils [20,21], has been reported in some studies, creating the so-called “subclinical inflammation” [22]. In one study, the mean content of lymphocytes (10 colonic fields with high power field) was 4.1 in controls, 5.9 in asymptomatic DD and 7.3 in symptomatic DD patients [20]. Using a semi-quantitative grading from 0 (normal) to 4 (diffuse presence of lymphocytes), the median grade was 1 in DD and 0.5 in controls [23]. Although statistically significant, the difference among groups in these studies does not seem so impressive. Moreover, the content of different inflammatory cytokines and molecules involved in mucosal repair (tumor necrosis factor [TNF]-α, syndecan, basic fibroblast growth factor, etc.) has been reported to be increased in DD compared to controls [21]. However, other studies failed to confirm these findings. Using flow cytometric evaluation, lymphocyte percentage and composition (CD4+, CD8+/CD103+, CD25+, and CD62L+) in the sigmoid mucosa did not differ between DD and controls [24]. Moreover, a fine study with biopsies specifically taken around the diverticular, failed to find a difference in interleukin [IL]2, IL4, IL5, IL8, IL10, IL12p70, IL13, interferon-γ, TNF-α, transforming growth factor-β, and caspase-9 content between DD and matched controls [25]. Likewise, a recent study found a similar content of lymphocytes, mast cells, IL10, and TNF-α in the colonic mucosa of DD and controls, and a reduced expression of IL6 was even detected in DD [26]. Finally, a recent case-control study involving 254 subjects found no association between DD and either histological or serological (C-reactive protein [CRP]) inflammatory markers, or between these markers and diarrhea or abdominal pain [27]. Consequently, the proposed role of minimal inflammation of the colonic mucosa in generating abdominal symptoms in DD patients remains to be proven [22,26]. For instance, the density of overall immune cells in colon mucosa decreased (30.66±1.07 vs.25.25±0.96; P=0.008) in patients with irritable bowel syndrome (IBS) following mesalazine therapy, but abdominal pain and bloating did not significantly improve [28].Alterations in both the amount and the composition of collagen in the extracellular matrix of colon wall with diverticula have been documented, paralleling the DD stage [29]. Indeed, the content of type I (mature) collagen progressively decreases, whilst type III (immature) accumulates, as does the cross-linking among fibers [29]. This shifting was linked to a perturbation of metalloproteinase (MMP-1 and MMP-2) function due to increased production of their inhibitors. More specifically, an 18- and 3-fold increase of MMP-1 and MMP-2 inhibitors, respectively, has been found in DD, so that the normal collagen synthesis is not balanced by an appropriate demolition [29]. Notably, similar alterations have been demonstrated in both Crohn’s disease and collagenous colitis [30]. Besides collagen, other alterations in the matrix microenvironment have been found in the colon wall with diverticula. Intriguingly, angiogenic factors (vascular endothelial growth factor, endothelial and smooth muscle derived-neuropilin, MMP-13), cell proliferation regulators (p53, p27, c-erb-2, cyclin D1), and cyclooxygenase-2 were found to be equally expressed in colon with either DD or CRC [31].Altered colonic pressure profiles were commonly thought to play a role in the etiology and pathophysiology of DD [32]. However, a review showed that there was only a limited volume of literature investigating pressure in patients with diverticulosis [33]. Indeed, pooled data from the existing studies showed no difference in intrasigmoid pressure or the duration of activity when patients with diverticulosis/DD were compared with controls, suggesting that there is only weak evidence to support the role of characteristic patterns of pressure activity in this condition [33]. Nevertheless, more recent findings demonstrated alterations in the enteric neural function. An experimental study found cholinergic denervation hypersensitivity in DD patients compared with controls, due to a lower choline acetyltransferase activity, upregulation of M3 receptors, and increased sensitivity to exogenous acetylcholine [34]. A disturbed glial cell line-derived neurotrophic factor responsiveness was proposed as a contributory factor to the development of these alterations [35]. In addition, the presence of interstitial cells of Cajal, gut pacemaker cells and glial cells was found to be decreased in colonic DD [36]. [(<<< Vitamin-A connection???)] All these neural abnormalities, overall configuring an “enteric neuropathy”, lead to disturbed motility and visceral hypersensitivity in the sigmoid tract, which, in turn, may be responsible, at least in part, for some abdominal symptoms in DD patients [37]. Therefore, DD might be considered as a “transumural” rather than a “mucosal” disease.Recent data suggest a certain genetic predisposition towards developing diverticulosis and diverticulitis [38,39]." - http://www.annalsgastro.gr/files/journals/1/earlyview/2019/ev-08-2019-03-AG4668-0410.pdf https://chronoceuticals.com/discovered-gut-bacteria-use-vitamin-a-to-regulate-the-immune-system/ https://hackyourgut.com/2016/11/14/nutrients-essential-to-hacking-your-gut-number-1/ https://www.ncbi.nlm.nih.gov/pubmed/30081517 The role of probiotics as modulators of immune system and chronic inflammation has been investigated. At the moment, probiotics are considered as a third choice for the treatment of SUDD and no evidences exist in the treatment and prevention of acute diverticulitis. Some studies, summarized by Elisei and Tursi in a systematic review, seem to demonstrate a role in reduction of SUDD recurrence. - [https://www.dovepress.com/inflammation-management-in-acute-diverticulitis-current-perspectives-peer-reviewed-fulltext-article-JIR#](https://www.dovepress.com/inflammation-management-in-acute-diverticulitis-current-perspectives-peer-reviewed-fulltext-article-JIR) check for SIBO & Disbiosis!! no NSAIDs - damage the gut reduce stress (cortisol reduces stomach acid - and therefore the availability of nutrients - eventually effecting serotonin levels negatively -> chew food thoroughly!)
begin with low fibre, slowly increase to moderate-high fibre diet (cooked food is best for a weakened gut)
remove inflammatory foods – dairy/gluten/grains
l-glutamate 5g twice daily with meal
SBOs – shaijit
Deglycrrhizinated Licorice Extract
curcumin for inflammation (with black pepper)
omega 3s
probiotics (ferments)
flaxseed oil?
bone broth (made from grass-fed and finished animals including bone, fat, and meat close to the bone.)
coconut oil?
unsulphered blackstrap molasses? (processed without sulphur dioxide – bleaching agent!) (if no active SULT? SNP – sulphur processing issues. )
relax vagus nerve (gargle and gag)
reduce caffeine (dehydrates colon, and speeds food transit – lowering nutrient absorption)
use squatty-potty to reduce pressure on colon
MSM (sulphur – if no SULT? SNP active.)
chamomile oil (German chamomile reduces inflammation and calms digestion in the gut and urinary system especially)
frankincense oil (for inflammation)
lavender oil (diffuse for relaxation – lowers stress, enables parasympathetic nervous system, leading to healing)
selenium? (relieves oxidative stress)
oregano oil (antibiotic – can help heal the gut. can be taken to help fight off infection during a flare.)
peppermint oil tea (stomach pain and disorders/gallbladder pain & disease/indigestion/halitosis (bad breath)/gas pain and bloating/diarrhea/ulcers/IBS and SIBO. alleviates digestive upset like bloating and gas. Aids indigestion.)
iron? (study found that iron supplementation increased an anti-inflammatory bacterial metabolite and enhanced the number of gut bacteria.)
hibiscus tea (calms gut)
inulin to feed microbiome
castor oil hot compress (for pain)
Colloidal silver – extremely helpful during a flare-up and can help fight off infection (nano-silver only??)
DGL Licorice – 300mg per day twenty minutes before meals to help lubricate and calm the digestive tract and reduce inflammation in the colon.
Digestive enzymes – take 1-2 capsules of digestive enzymes before every meal to help your body digest foods more completely.
Ginger tea – reduces inflammation, gas, bloating, and stomach upset.
High-quality aloe vera juice – soothes and heals the intestinal lining (with ‘Aloin’ (sp?) removed)
Probiotics – take 20-50 billion active strains daily to help fight infection and prevent inflammation, constipation, bloating, and gas. those with diverticulosis can take 5 billion per day to maintain healthy gut flora.
Psyllium fiber – a form of insoluble fiber that helps bulk up stools and prevent flare-ups.
Slippery elm – soothes and protects the mucous membranes of the colon and reduces inflammation
calendula extract / tea – (calendula extract reduced inflammation in rats with induced edemas. Researchers noted that this response might result from calendula’s ability to inhibit certain pro-inflammatory biomarkers.)

Homeopathy for Diverticulitis:

Homeopathic remedies can be taken at a 30C potency to help alleviate symptoms of diverticulitis.

Take the remedy that fits your symptoms 4x daily for 2-3 days to see if there is any improvement. If there is an improvement, you can stop taking the homeopathic remedy unless symptoms return.

Arsenicum Album is for burning pain in the abdomen that is relieved by heat. This may be accompanied by feelings of anxiety and restlessness.

Bryonia Alba is for sharp pains in the left side of the abdomen that becomes worse with movement.

Belladonna is for abdominal throbbing or burning pain that is sudden accompanied by a fever. The pain is worse with movement.

Colocynthis is for sharp, gassy, colicky pain in the abdomen that is relieved by pressure.

Ignatia Amara is for spasms in the colon that occur after emotional stress.

Magnesia Phosphorica is for abdominal cramping that is relieved by heat but worse with pressure.

Nux Vomica is for cramping pain in the digestive tract accompanied by irritability and chill extremities.

Sulphur is for those who are awakened by diarrhea that is urgent.

essential oils:

Try a dilution of 2 drops in 1tsp of carrier oil and apply it over the abdomen.

Anise – use before or after meals to aid digestion

Fennel – great for use before and after meals to prevent or treat gas and bloating

German chamomile – Great for reducing pain and inflammation

Ginger – warming and soothing for cramps

Nutmeg – warming and soothing. Good for aiding digestion (dilute very well, 1 drop per 1tsp)

Patchouli – great to use on the abdomen to prevent nausea and vomiting

Peppermint – cooling and soothing for cramps

serotonin is an important player in gut motility. Serotonin concentrations in those with colonic diverticulosis are significantly lower than normal controls and contribute to the type of bowel habit following a test meal. (29) Serotonin transporter (SERT) transcript levels are also lower in those with a history of diverticulitis compared to controls and those with asymptomatic diverticulosis. (30) Inflammation is also known to decrease SERT expression and function (31, 32), so following the recommendations to lower intestinal inflammation is of course the first step to improving gut motility. In addition, it is also likely that supplementation with 5-HTP (a precursor to serotonin) may alleviate constipation and increase motility since it will increase serotonin levels. Note: do not take 5-HTP without talking to your doctor first if you are on an SSRI medication.


This inability to store glycogen is one factor which helps to explain the strong tendency towards hypoglycemia seen in many people with a thiamine deficiency.

In short, the bioenergetic state of the cell governs its ability to retain potassium ions and structure water into a gel-like phase. A cell with plentiful ATP can maintain this ability, independent of the “sodium potassium pump”. On the other hand, cells lacking energy lose their capacity to retain potassium, intracellular water becomes “unstructured” and intracellular concentration of sodium ions increases and the electronic state of the cell is changed. This causes water to “leak” out of the cells into the extracellular space to produce a localised edema of sorts. Thiamine, playing a central role in energy metabolism, is partially responsible for maintaining healthy redox balance and a continuous supply of ATP. Hence, it is no wonder why a deficiency of this essential nutrient produces such drastic changes in the cellular electrolyte balance.

In thiamine deficiency, an underlying intracellular potassium deficiency may be going unnoticed due to unremarkable blood levels. In cases where potassium deficiency is suggested, thiamine deficiency may be indicated, and TTFD might used to more safely correct the electrolyte balance.

see: Thiamine Deficiency and Associated Clinical Disorder – David W. McCandless

see: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition – Derrick Lonsdale & Chandler Marrs


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.

Helpful digestive treatment:

2 parts: dioscorea villosa = wild yam 1 part: valeriana officinalis = valerian 1 part: viburnum opulus = cramp bark 1 part: mentha piperita = peppermint 5ml 3x daily an infusion of matricaria(German chamomile) or mentha piperita speed slowly throughout the day will help Bentonite clay In an animal study observing rats with skin wounds, researchers observed that calendula extract reduces inflammation during the healing process. The anti-inflammatory activity was attributed to the presence of triterpenes, especially taraxasterol and faradiol esters. Another animal study found that calendula extract reduced inflammation in rats with induced edemas. Researchers noted that this response might result from calendula’s ability to inhibit certain pro-inflammatory biomarkers. A recent animal trial observing ulcerative colitis (UC) in rats discovered that two different forms of calendula extract have significantly high treatment rates. Both extract forms eradicated the inflammation and atrophy caused by UC. In a lab-based study, calendula extract exerted anti-inflammatory effects on stomach lining cells. These results occurred due to the inhibition of pro-inflammatory biomarkers. The government organization German Commission E recommends calendula for throat and mouth inflammation. Respected herbalists Thomas Easley and Steven Horne mention in their herbal text, The Modern Herbal Dispensatory (2014), that “[c]alendula is a wonderful remedy for gastrointestinal inflammation” and may be used specifically for “[c]rohn’s disease, colitis, and gastritis.” David Hoffmann, registered herbalist of the American Herbalist Guild, writes in his text, Medical Herbalism (2003), that calendula has “anti-inflammatory actions in the digestive system” and could be helpful in ailments like “gastric and duodenal ulcers.” Famed herbalist, Rosemary Gladstar, writes that calendula is noted for its anti-inflammatory properties and can be applied topically or internally. She also states that calendula is a “wonderful herb for babies” as it gently soothes inflammatory skin conditions like cradle cap and diaper rash