Diverticulitis research

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

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

“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 < 0·025 was considered statistically significant owing to multiple testing adjustment. In total, 545 patients in the observational group and 564 in the antibiotics group were included. No statistical differences were found in 1-year follow-up rates of ongoing diverticulitis (7·2 versus 5·0 per cent in observation versus antibiotics groups respectively; P = 0·062), recurrent diverticulitis (8·6 versus 9·6 per cent; P = 0·610), complicated diverticulitis (4·0 versus 2·1 per cent; P = 0·079) and sigmoid resection (5·0 versus 2·5 per cent; P = 0·214). An initial pain score greater than 7, white blood cell count exceeding 13·5 × 10 /l and previous diverticulitis at presentation were risk factors for adverse outcomes. Antibiotic treatment did not prevent adverse outcomes in patients at high risk of adverse events. Observational management of acute uncomplicated diverticulitis is safe. Some statistical uncertainty remains, depending on the thresholds of clinical relevance, owing to small differences, but no subgroup that would benefit from antibiotic treatment was apparent. © 2020 The Authors. BJS published by John Wiley & Sons Ltd on behalf of BJS Society Ltd-" - 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 not fruit 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 "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) after 3 months. No episodes of AD and no adverse events related to DIVER--100® were recorded at month 6 in the study population. DIVER-100® is a safe and effective nutraceutical compound in obtaining remission and symptom relief in SUDD patients. Further randomized, placebo-controlled clinical trials are needed to confirm these preliminary data." 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/ "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# pathogenesis: * check for SIBO & Disbiosis!! * obesity? * lack of exercise? * low fibre 'SAD' diet? * microbiota imbalance? remove: * inflammatory foods - dairy? gluten? * no NSAIDs - damage the gut * reduce stress (cortisol reduces stomach acid - and therefore the availability of nutrients - eventually effecting serotonin levels negatively) * reduce caffeine (dehydrates colon, and speeds food transit - lowering nutrient absorption) actions/additions: * immediately start with LOW FIBRE, slowly increase to moderate-high fibre diet * DIGESTIVE ENZYMES with meals -betaine/HCL/enzymes etc (take 1-2 capsules of digestive enzymes before every meal to help your body digest foods more completely.) * L-GLUTAMATE (5g twice daily with meal) * L-GLUTAMINE * ZINC carnosine? - (heals gut lining) * CURCUMIN for inflammation (with black pepper) * OMEGA3S & ESSENTIAL FATTY ACIDS * FERMENTED FOODS - (probiotics - kefir(with goat milk), sauerkraut, kimchi)) * FLAXSEED OIL? * BONE BROTH (chicken?) * COCONUT OIL? * UNSULPHERED BLACKSTRAP MOLASSES? (processed without sulfur dioxide - bleaching agent!) * RELAX VAGUS NERVE (gargle and gag) * EXERCISE * use SQUATTY POTTY to reduce pressure on colon * MSM (sulfur) * CHAMOMILE OIL (German chamomile reduces inflammation in the gut and urinary system especially. diffuse/topical?) * FRANKINCENSE OIL (for inflammation. diffuse/topical?) * LAVENDER OIL (diffuse for relaxation - lowers stress, enables parasympathetic nervous system, leading to healing. diffuse/topical?) * SELENIUM? (relieves oxidative stress) * GINGER OIL - (heals gut. diffuse/topical?) * OREGANO OIL - (antibiotic. diffuse/topical?k * PEPPERMINT OIL - (aids stomach pain and disorders/gallbladder pain & disease/indigestion/halitosis (bad breath)/gas pain and bloating/diarrhea/ulcers/IBS and SIBO. diffuse/topical?) * IRON? (study found that iron supplementation increased an anti-inflammatory bacterial metabolite and enhanced the number of gut bacteria.) * B-COMPLEX * HIBISCUS TEA (calms gut) * INULIN? (to feed microbiome - AFTER flare-up subsides, since it's fibre) * CRANBERRY? * CASTOR OIL warm compress (for pain) * CHAMOMILE TEA – (reduces intestinal inflammation and calms digestion.) * COLLOIDAL SILVER – (extremely helpful during a flare-up and can help fight off infection) * DGL LICORICE – (300mg per day twenty minutes before meals to help lubricate and calm the digestive tract and reduce inflammation in the colon.) * GINGER TEA – (reduces inflammation, gas, bloating, and stomach upset.) * PATCHOULI OIL - (soothes inflammation) * High-quality ALOE VERA JUICE – (soothes and heals the intestinal lining) * OIL OF OREGANO – (can be taken to help fight off infection during a flare.) * PEPPERMINT TEA –(alleviates digestive upset like bloating and gas. Aids indigestion.) * 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. (SBOs - shaijit)) * PSYLLIUM FIBER – (a form of insoluble fiber that helps bulk up stools and prevent flare-ups. - AFTER flare-up subsides) * SLIPPERY ELM – (soothes and protects the mucous membranes of the colon and reduces inflammation. - AFTER flare-up subsides) * GRAPEFRUIT OIL - (100% pure. particularly effective in treating infections of the colon, stomach, intestines, urinary system, excretory system, and kidneys) * VITAMIN-D (essential for lowering inflammation, along with zinc and selenium. "VDR [vitamin d receptor] plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium. Therefore, vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD…D3 markedly enhanced tight junctions formed by Caco-2 monolayers by increasing junction protein expression and TER and preserved the structural integrity of tight junctions” — PubMed #17962355. * * “The anti-inflammation and anti-infection functions for Vitamin D are newly identified and highly significant activities. Vitamin D/VDR have multiple critical functions in regulating the response to intestinal homeostasis, tight junctions, pathogen invasion, commensal bacterial colonization, antimicrobe peptide secretion, and mucosal defense. Interestingly, microorganisms modulate the VDR (Vitamin D Receptor) signaling pathway.” — PubMed #PMC2955835. * * “Many studies have implicated Vitamin D and VDR in inflammatory bowel disease (IBD). Low Vitamin D levels have been reported in patients with IBD. The VDR protein is significantly lower in IBD and colitis-associated colon cancer patients… It has also been shown that VDR stabilizes cell tight junction structures in the intestinal epithelial cells; hence, proper functioning of VDR is needed to control intestinal homeostasis…Consistent with its anti-inflammatory role, 1,25(OH)2D3 downregulates the expression of many proinflammatory cytokines…. Cells of the gastrointestinal tract, including epithelial cells and lamina propria macrophages, are constantly exposed to lumenal bacteria, which play key roles in normal intestinal development and innate immunity. The intestinal Paneth cells are known to secrete antimicrobial peptides, which are regulated by VDR signaling.” — PubMed #PMC2955835. * * “The involvement of Vitamin D/VDR in anti-inflammation and anti-infection represents a newly identified and highly significant activity for VDR. Studies have indicated that the dysregulation of VDR may lead to exaggerated inflammatory responses, raising the possibility that defects in Vitamin D and VDR signaling transduction may be linked to bacterial infection and chronic inflammation.” — PubMed #20639756. note: Glycine (available in bone broth), and Vitamin-D are very protective of UV radiation damage and inflammation. * CLARY SAGE - (has been used to boost the secretion of gastric juices and bile, which speeds up and eases the digestive process - massage into abdomen) * YARROW - (Animal studies have uncovered evidence that it can reduce smooth muscle spasms that contribute to GI complaints and even inflammatory bowel diseases.) * abdomen oil rub - (2 drops peppermint, 1 drop chamomile, 3 drops rosemary, 1 drop clove, diluted in 1tsp coconut or almond oil, applied twice daily) * ROSEMARY - (fantastic liver cleanser and booster. choleretic(increases bile), hepatoprotective, lowers cortisol) 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 OIL(antidepressant, antiphlogistic, antiseptic, aphrodisiac, astringent, cicatrizant, cytophylactic, deodorant, diuretic, febrifuge, fungicide, insecticide, sedative, tonic(tones organs and systems). soothes inflammation (including internal), particularly if the inflammation or irritation is a result of fever. Great to use on the abdomen to prevent nausea and vomiting. speeds the healing process of cuts and wounds, hastens the fading of scars, boils, acne, pox, and measles) Peppermint – cooling and soothing for cramps calprotectin (found in the gut, and stool) when there's inflammation. binds zinc and protein. so when levels are high, deficiency can occur. 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. Mercury (vaccines, filings, contact lens fluid, etc) makes changes to the gut, allowing pathogenic bacteria, fungi, yeast, parasites to take hold.