Hi Petite Femme
I think given you've been on antibiotics this thread will be helpful Lactobacillus rhamnosus GG and other probiotics as well as Soil Based Probiotics. The antibiotics kill off the good bacteria, and good bacteria can help reduce chrones symptoms (I'll get to that connection later) - so it's possible that antibiotics may actually make things worse.
Having some carbs to keep the critters alive is also important! Think of carbs as feeding the guys who are helping you.
Hydradenitis Suppurative is a topic I've been looking into on and off for a while, and mostly the research is very limited. Any ideas beyond surgery then are mostly hypothetical.
It does seem positively correlated to chrones and severe gut problems though, so I've been using that as a cross correlation. I've decided to take another look, and this is what I've found:
Firstly, what does the genetic side look like?
http://www.nature.com/jid/journal/v131/n7/full/jid201142a.html
Short version: the γ-secretase (gamma-secretase) enzyme is not being readily produced in those with this mutation.
A question then - is this something that will always happen in those with this mutation, or have environmental conditions caused a cascade situation?
That is, did the body need more of this because of some form of stress and Chrones/HS is the result of not being able to fulfill this demand?
http://www.nature.com/jid/journal/v133/n3/full/jid2012372a.html
Another enzyme is essential for γ-secretase production.
http://www.nature.com/nature/journal/v422/n6930/full/nature01506.html
So what can cause an increased demand for this enzyme (that would cause a failure/deficiency in those with the mutation)? Establishing cause/effect here is tricky.
http://www.ncbi.nlm.nih.gov/pubmed/17183144
One thing that causes low folate/SAMe is the MTHFR mutation - which coincidentally ties to someone else posting earlier in the thread:
And from what I posted here Hidradenitis Suppurativa
It should be noted that in cases of the MTHFR mutation, standard B12 and folate supplements will make things worse! This included eating vegetables high in folate.
Following this thread:
http://www.ncbi.nlm.nih.gov/pubmed/15259382
So an inability to handle sulphide (due to lack of SAMe) could be a causative factor in one subset of people with this condition.
http://www.biomedsearch.com/article/Inflammatory-bowel-disease-part-ulcerative/107835435.html
So in conclusion, there seems to be a potentially big connection between all of these things and the amount of methyl doners the body has or can produce.
I can't prove direct correlation and I have no idea if it will help, but the following may be worth trying:
Avoid all veg with folate in, along with standard folate/B12 supplements.
Avoid as much sulphur containing food as possible (see above).
Supplement with sub-lingual SAMe, methylfolate (go slow/low dose, it may make things worse before they get better) and sub-lingual methyl-B12 (more info here)
Also check out the suggested supplements in the article above perhaps.
I think given you've been on antibiotics this thread will be helpful Lactobacillus rhamnosus GG and other probiotics as well as Soil Based Probiotics. The antibiotics kill off the good bacteria, and good bacteria can help reduce chrones symptoms (I'll get to that connection later) - so it's possible that antibiotics may actually make things worse.
Having some carbs to keep the critters alive is also important! Think of carbs as feeding the guys who are helping you.
Hydradenitis Suppurative is a topic I've been looking into on and off for a while, and mostly the research is very limited. Any ideas beyond surgery then are mostly hypothetical.
It does seem positively correlated to chrones and severe gut problems though, so I've been using that as a cross correlation. I've decided to take another look, and this is what I've found:
Firstly, what does the genetic side look like?
http://www.nature.com/jid/journal/v131/n7/full/jid201142a.html
Our results provide further evidence that mutations resulting in haploinsufficiency of the γ-secretase genes, NCSTN and PSENEN, are involved in the pathogenesis of some familial cases of HS. To our knowledge, these findings have not previously been reported in Caucasian individuals. These results indicate the involvement of γ-secretase in the development of HS, which is further supported by the development of cysts in γ-secretase-deficient mice (Pan et al., 2004). γ-Secretase is involved in the cleavage of a wide array of transmembrane proteins; however, it is noteworthy that the hair follicle and sebaceous glands of mice deficient in γ-secretase are phenotypically identical to those of mice deficient in Notch 1 and 2 (Pan et al., 2004), potentially indicating the involvement of the Notch cell signalling pathway in HS. The binding of ligands to the extracellular domain of Notch receptors induces γ-secretase-driven cleavage of the intracellular domain which, in the nucleus, affects gene expression (Oswald et al., 2001). Our investigations highlight the γ-secretase–Notch pathway as a potential therapeutic target in HS. However, it is notable that screening of NCSTN, PSEN1, and PSENEN did not reveal mutations in five of the seven pedigrees. These HS pedigrees may therefore represent HS alleles comprising non-coding or undetected coding variants, represent phenocopies of HS, or be explained by further locus heterogeneity in HS. Further loci may include genes encoding other proteins involved in the γ-secretase–Notch pathway. Investigations of additional familial and sporadic cases are required to establish the contributions of γ-secretase alleles in HS and identify further genes underlying this debilitating disease. The pathophysiological mechanisms underlying HS may also provide insight into the basis of more common conditions such as acne vulgaris.
Short version: the γ-secretase (gamma-secretase) enzyme is not being readily produced in those with this mutation.
A question then - is this something that will always happen in those with this mutation, or have environmental conditions caused a cascade situation?
That is, did the body need more of this because of some form of stress and Chrones/HS is the result of not being able to fulfill this demand?
http://www.nature.com/jid/journal/v133/n3/full/jid2012372a.html
There are both human and animal data to functionally support a role for γ-secretase in the skin. A number of individuals involved in the recent trial of the γ-secretase inhibitor Semagacestat for Alzheimer’s disease reported cutaneous side effects including nonspecific skin rashes, hair color changes, and an increased risk of skin cancer (Kelleher and Shen, 2010; Panza et al., 2010). It is unclear whether the skin changes resembled HS; however, the alterations in hair color would be consistent with a biological role for γ-secretase in the hair follicle.
A greater body of work has focused on the function of γ-secretase in the skin of mice where disrupture (PSEN1−/PSEN2−, PSEN1−, and NCT+/−) results in follicular keratinization, follicular atrophy, the formation of epidermal cysts, absent sebaceous glands, and epidermal hyperplasia, all histological features of HS in humans (Xia et al., 2001; Pan et al., 2004; Li et al., 2007). These cutaneous manifestations initially appeared around the nose and mouth, inguinal and perineal areas, and around the sebaceous glands of the eyelids and ears (the post-auricular area, inguinal, and perineal areas are commonly affected in HS). Some nodules on the PSEN1− and NCSTN+/− mice became dysplastic and developed into SCC, which may correlate with the rare development of SCC in HS-affected skin in humans. γ-Secretase would therefore seem to act as a tumor suppressor in the skin, a function potentially mediated by its effects on Notch signaling (known to be a tumor suppressor) and EGFR (γ-secretase inhibition results in an upregulation of EGFR, known to be upregulated in over 90% of head and neck SCCs; Li et al., 2007).
Mice treated with a γ-secretase enzyme inhibitor (LY-411,575), which leaves the γ-secretase complex intact and at normal levels, develop lesions similar to NCT+/− mice (Li et al., 2007). This therefore suggests that it is the reduced enzyme activity in the genetically γ-secretase-deficient mice rather than the effect of any individual components of the complex that underlies the skin changes observed. The fact that mutations have been reported in three of the four subunits of γ-secretase in familial cases of HS suggests that this is likely to be the case in humans.
Another enzyme is essential for γ-secretase production.
http://www.nature.com/nature/journal/v422/n6930/full/nature01506.html
Presenilin {PSEN - see study above} is essential for γ-secretase activity, a proteolytic activity involved in intramembrane cleavage of Notch and β-amyloid precursor protein (βAPP)1, 2.
So what can cause an increased demand for this enzyme (that would cause a failure/deficiency in those with the mutation)? Establishing cause/effect here is tricky.
http://www.ncbi.nlm.nih.gov/pubmed/17183144
Herein, we demonstrate that dietary deficiency in folate and vitamin E increased PS-1 expression in juvenile and adult normal C57B1/6J and ApoE-/- mice and in aged normal mice.[..]
Prior studies demonstrate that impaired DNA methylation resulting from a deficiency in S-adenosylmethionine (SAM, which is rapidly depleted following folate deprivation) leads to PS-1 overexpression, and that direct supplementation with SAM attenuates PS-1 overexpression.
One thing that causes low folate/SAMe is the MTHFR mutation - which coincidentally ties to someone else posting earlier in the thread:
cdwrites4 said:You don't need more iron, you need B vitamins: B12, B6, B3, Folate
I also have MTHMR gene mutation c677T, homozygous. I've apparently been deficient in Bs all my life because of the mutation. So, since about January, I've been injecting methylcobalamin (B12) once per week. I also take all the B vitamins in a active form and try to eat some green leafy veggies every day. I think I'm slowly feeling better from all this. On my blood test, my B 12 shows up as super high out of range.
And from what I posted here Hidradenitis Suppurativa
CASE REPORTS:
The first case had pouchitis complicated by perianal abscesses and a recto-vaginal fistula. The second case had biopsy proven hidradenitis suppurativa affecting the perianal, inguinal and pubic skin. High dose vitamin B₁₂ appeared to be the major factor in preventing the recurrence of suppuration in both patients. Neither patient had vitamin B₁₂ deficiency. Open label experience: high dose vitamin B₁₂ treatment of a further 10 consecutive IBD patients with dermatoses was thought to provide benefit to six of them, but did not appear useful in four patients with perianal Crohn's disease with fistulae as the only manifestation of cutaneous disease.
CONCLUSIONS:
There appears to be a subset of IBD patients with perianal and more distant inflammatory dermatoses, who benefit from high dose vitamin B₁₂ treatment. Clinical trials in IBD patients with biopsy-characterised suppurative dermatoses will be required in order to properly define the role of this safe and economical therapy.
It should be noted that in cases of the MTHFR mutation, standard B12 and folate supplements will make things worse! This included eating vegetables high in folate.
Following this thread:
http://www.ncbi.nlm.nih.gov/pubmed/15259382
Low S-adenosylmethionine concentrations found in patients with severe inflammatory bowel disease.
S-adenosylmethionine is a methyl donor in many cellular reactions including detoxification of constantly produced hydrogen sulphide in the colon. A reduced capacity to detoxify hydrogen sulphide may be implicated in the pathogenesis of inflammatory bowel disease. S-adenosylmethionine could be low if this assumption is correct. We compared S-adenosylmethionine concentrations in whole blood in patients with severe and moderate inflammatory bowel disease with healthy reference persons.
METHODS:
S-adenosylmethionine concentrations in whole blood were measured using high-pressure liquid chromatography. Patients with Crohn's disease (n=21), ulcerative colitis (n=7) and healthy age-matched reference persons (or controls) (n=17) were studied.
RESULTS:
S-adenosylmethionine concentrations were significantly decreased in patients with severe inflammatory bowel disease (mean 1.10 mg/l) as compared to patients with moderate Crohn's disease and ulcerative colitis (mean 1.83 mg/l) and reference persons (mean 1.84 mg/l). Statistically significant inverse correlations were found between S-adenosylmethionine concentration and activity index (p<0.01 and R2=0.86) as well as Crohn's disease activity index (p<0.01 and R2=0.50) scores.
CONCLUSIONS:
Low concentrations of S-adenosylmethionine were found in patients with severe inflammatory bowel disease. Future studies will show whether S-adenosylmethionine is a marker for disease activity and a possible tool for investigation of sulphur toxicity as a causative mechanism in inflammatory bowel disease.
So an inability to handle sulphide (due to lack of SAMe) could be a causative factor in one subset of people with this condition.
http://www.biomedsearch.com/article/Inflammatory-bowel-disease-part-ulcerative/107835435.html
The Sulfur-Butyric Acid Connection
Butyric acid, a four-carbon short chain fatty acid, and several other SCFAs, including propionic and acetic acids, are produced in a healthy colon by fermentation of fiber and other carbohydrates. Butyric acid provides the primary fuel for colonocytes. Proper ion transfer, mucus synthesis, phase II detoxification, and lipid synthesis for cell membrane integrity in the colonocytes depend on butyrate oxidation. (47) Impaired metabolism of SCFAs has been implicated as a factor in UC.
Hond et al compared butyrate metabolism in healthy controls with that of 25 hospitalized patients with severe ulcerative colitis and 11 UC patients in remission. They measured butyrate metabolism after rectal instillation of [sup.14]C-labeled butyrate by measuring [sup.14]C[O.sup.2] in the breath. Patients with active UC had significantly lower butyrate oxidation than patients in remission (who had normal butyrate oxidation) or controls. Three patients with inactive disease had decreased butyrate oxidation and interestingly, all three relapsed within a few weeks. (48) Perhaps decreased oxidation of SCFAs is a good predictor of possible relapse and occurs before other signs of inflammation. Because normal oxidation was observed in patients in remission, faulty SCFA oxidation is likely to be a result rather than a primary cause of ulcerative colitis. {One wonders if the same process of oxidation of the fatty acid is occurring inside the body, perhaps due to leaky guts? I remember finding a possible correlation between oxidation of fatty acid and HS somewhere earlier in the thread}
Other researchers compared the rate of butyrate, glucose, and glutamine oxidation to carbon dioxide in colonoscopy biopsy specimens from 15 patients with quiescent or mild colitis to specimens from 28 controls with normal colonic mucosa. Butyrate, but not glucose or glutamine, oxidation was significantly impaired in the UC patients compared to controls, even though the disease was mild. (49)
High concentrations of sulfate-reducing bacteria with concomitant elevation of hydrogen sulfide have been noted in patients with UC. Hydrogen sulfide can potentially damage the gut mucosa by inhibiting butyrate oxidation in the mitochondria, essentially starving the cotonocyte (Figure 3). In experiments on human colonocytes isolated from colectomy patients, hydrogen sulfide and other sulfur compounds inhibited butyrate oxidation by 75 percent in the distal colon and 43 percent in the ascending colon. The authors of the study conclude that the "metabolic effects of sodium hydrogen sulfide on butyrate oxidation along the length of the colon closely mirror metabolic abnormalities observed in active ulcerative colitis." (50)
[FIGURE 3 OMITTED]
Animal studies on rabbits and guinea pigs have demonstrated that feeding sulfated polysaccharides (such as carrageenan), but not unsulfated polysaccharides, can induce lesions similar to ulcerative colitis. (51)
Researchers note higher counts of sulfur-reducing bacteria in the feces of patients with active UC than in patients in remission. (52) A commonly used drug for treatment of ulcerative colitis, 5-aminosalicylic acid (5-ASA; mesalamine) has been shown to lower sulfide concentrations in feces. (53) {The bacteria could be helping the body handle the sulphur it can't - without them damage occurs in greater amounts. But only if the person doesn't have or can't produce adequate methyl donors.}
Methylation is believed to be an important route for sulfide detoxification in the colonocyte. {Right back to methyl donors/folate deficiency and/or MTHFR mutations} (54) A study was conducted to determine if methyl donors could reverse the damaging effect of sulfides on colonocytes. Isolated colonocytes from rat and human specimens were tested by measuring the oxidation of butyrate in the presence of hydrogen sulfide, followed by introduction of methyl donors to the suspension. Sulfide toxicity was reversible most potently by S-adenosylmethionine 1,4 butane disulfonate (stable form of SAMe), followed by DL-methionine-S-methyl-sulfonium and L-methionine. Methyl donors may have therapeutic value in UC. (55)
Interestingly, hyperhomocysteinemia, a condition of inadequate methylation, has been found to occur more commonly in patients with IBD (17 of 64; 26.5%) than controls (4 of 121; 3.3%). (56) Other researchers confirm homocysteine levels tend to be higher in IBD (8.7 mmol/L) than in healthy controls (6.6 [micro]mol/L). (57) While hyperhomocysteinemia may likely be, at least in part, a result of folate or vitamin B12 deficiency associated with the disease process or medications used, it may also be a contributing factor to the pathogenesis of UC. {i.e. a viscous cycle. It should be noted that methyl donors and B12 get depleted from severe long term stress, such as having one of these diseases. Thus the longer the disease and stress lasts, the less capacity the body has to protect from the disease flaring up!}
At least two in vitro studies have attempted to determine whether activity of certain enzymes involving sulfur metabolism are up- or down-regulated in UC. One found thiolmethyltransferase (TMT) activity did not seem to be associated with sulfide-induced colonocyte toxicity). (54) A second in vitro study found TMT activity was significantly higher in UC. The authors speculate TMT might be up-regulated in UC in an attempt to detoxify excess hydrogen sulfide. (58)
Potential sulfate toxicity may have implications for diet as both an etiological and therapeutic factor. The Western diet, which by one analysis contains an average of 16.6 mmol sulfate/day compared to the rural African diet that contains an average of 2.7 mmol sulfate/day, (51) has been implicated as one of the risk factors in ulcerative colitis. Sulfur may be acquired in the diet by consumption of food preservatives and additives such as sulfites, sulfur dioxide, and carrageenan, and foods high in sulfur amino acids (eggs, whole milk, cheese, meat, cruciferous vegetables, onions, and garlic). The effects of low-sulfur diets on UC are discussed in the dietary treatment section.
Similar to sulfides, nitrogen derivatives may inhibit butyrate metabolism. An in vitro study found nitric oxide interfered with fatty acid metabolism in colonocytes. However, co-administration of peroxide and sulfide was necessary to cause injury to the colonocyte. (59)
[..]
Less Conventional Treatments for Ulcerative Colitis Connection between Smoking, Nicotine, and UC
Epidemiological data have found smoking may confer some level of protection from UC. Thirty newly diagnosed UC patients were matched for age, sex, and marital and economic status with healthy controls. Patients with UC were three times less likely to smoke but seven times more likely to have quit smoking an average of 27 months prior to diagnosis. (73)
Because of the possible link between smoking and protection from UC, a number of studies have been conducted using transdermal nicotine patches or nicotine gum for the treatment of ulcerative colitis. A small, double-blind, crossover trial examined seven UC patients individually (single-patient trial) for eight weeks. Therapy was alternated every two weeks between nicotine gum (20 rag/day) and placebo gum. Evaluation was on the basis of self-reported symptoms and proctoscopic exam. Three of seven patients, all former smokers, demonstrated significant enough improvement to warrant incorporating nicotine gum into their treatment regimens. (74)
The effectiveness of transdermal patches has been examined in several double-blind trials. Seventy-two patients with active UC were randomized to receive either daily 15-25 mg transdermal nicotine patches or placebo patches for six weeks. All patients remained on previous medications--mesalamine in all patients and low-dose glucocorticoids in 12 patients. Seventeen of 35 patients in the nicotine group experienced complete remission, compared to nine of 37 in the placebo group. The nicotine group also had greater improvement in clinical signs, symptoms, and histological findings, and decreased stool frequency, abdominal pain, and urgency. Twenty-three patients in the nicotine group experience side effects (mainly lightheadedness, nausea, headache, and sleep disturbances), compared to only 11 in the placebo group. (75)
A study published the following year, involving some of these same researchers, did not find significant positive effects from the use of transdermal nicotine. Eighty UC patients in remission were assigned in double-blind fashion to either transdermal nicotine (15 mg patch for 16 hours daily) or placebo patch for six months. As soon as a maintenance dose of nicotine was reached, mesalamine was discontinued in all patients. No significant differences in number of relapses were noted between groups. The researchers observed serum nicotine levels were lower than expected in the active treatment group, which may reflect poor compliance. (76)
Several small Italian studies yielded some positive findings. In seven of 10 patients with relapsing UC on mesalamine who did not tolerate steroids well, 15 mg transdermal nicotine daily for four weeks resulted in clinical remission that persisted for as long as three months after nicotine withdrawal. (77)
Another small study compared the effects of transdermal nicotine with those of prednisone in patients on mesalamine maintenance therapy. Patients in clinical relapse were randomly assigned to add either prednisone or transdermal nicotine to mesalamine for five weeks. The first 15 in each group with clinical and endoscopic signs of remission were followed for six months. The relapse rate was 20 percent in the nicotine group and 60 percent in the prednisone group. (78) In a further evaluation, follow-up continued for 12 months with patients in remission due to either nicotine or prednisone. If patients relapsed, they were crossed over to the other treatment regimen. After 12 months, relapse occurred in 14 of 15 patients originally on prednisone and seven of 15 Oil nicotine. (79)
Transdermal nicotine has been compared to oral mesalamine in the treatment of distal colitis. Thirty patients who failed to respond to mesalamine enemas (4 g at bedtime) were randomly assigned to 15 mg transdermal nicotine daily or 800 mg mesalamine three times daily for four weeks. Clinical and sigmoidoscopic remission was observed in 12 of 15 patients on nicotine, but only five of 15 on oral mesalamine. (80)
Transdermal nicotine appears to offer effective co-treatment for UC, both for patients during relapse and for maintaining remission. In the negative study, patients were asked to discontinue mesalamine, unlike other studies where patients remained on their maintenance treatment. Although nicotine's mechanism of action is unknown, it may exert its effects through inflammatory mediators, (81) changes in mucus production, (82) or alterations in blood flow. (83)
Heparin: An Unexpected Find
Patients with UC have a greater risk of developing coagulation problems such as deep vein thrombosis (DVT). {This is also a really common problem for those with the MTHFR mutation. Heparin also seems to help with some MTHFR problems such as miscarriage} In treating patients for DVT with heparin, an unexpected improvement in UC was noted, Heparin consists of a group of GAGs that have anticoagulant as well as potential anti-inflammatory effects.
[..]
Folic Acid
Folic acid status in ulcerative colitis patients may be influenced by a number of factors, including reduced dietary intake, red cell hemolysis secondary to chronic drug therapy, (104) chronic diarrhea, (105) and sulfasalazine therapy that interferes with absorption of folate. (106) Impaired intestinal transport and absorption results in structural alteration of intestinal mucosal cells, thus promoting further malabsorption and cell transformation. (105,107)
As mentioned, folate deficiency may be associated with high homocysteine levels often seen in UC patients. A Greek study examined serum folate and homocysteine levels in 108 IBD patients, 53 of whom had UC. It was determined that UC patients had significantly higher homocysteine levels, while folate levels were lower when compared to control subjects. (108) {Classic symptons of one of the MTHFR mutations, but could also be caused by just having a B12/folate deficiency for some other reason such as chronic stress}
[..]
Elimination of Sulfur-containing Amino Acids
Based on the known contribution of sulfides to the pathogenesis of UC, a pilot study was conducted on eight patients taking sulfasalazine for maintenance and prednisolone for acute attacks (four who had suffered a first acute attack and four with chronic UC). The patients were asked to eliminate dietary sources of sulfur-containing amino acids, including eggs, cheese, whole milk, ice cream, mayonnaise, soy milk, mineral water, sulfited drinks such as wine and cordials, nuts, and cruciferous vegetables. They were also asked to decrease intake of red meat, substituting chicken, fish, and skim milk as protein sources. During the 12-month follow-up, the patients experienced no relapses or attacks (expected relapse rate on sulfasalazine was 22.6 percent). In addition, all showed marked histological improvement. The number of bowel movements daily in the four chronic UC patients decreased from an average of 6/day to 1.5/day. Two patients stopped the diet, but resumed it when they noticed adverse effects. (126) A larger controlled trial is warranted.
[..]
Short Chain Fatty Acids
Because of the vital role they play in the maintenance of colonic integrity and energy metabolism, SCFA supplementation using butyrate enemas has been the focus of several studies in UC patients. Enema administration is thought to enhance and prolong the contact of butyrate with the colonic cells when compared to other routes of administration. The use of butyrate enemas in UC patients has produced varied results, making conclusions regarding their effectiveness difficult. Harig et al administered enemas containing sodium salts of butyrate, propionatc, and acetate to patients with diversion colitis (microscopically indistinguishable from UC) twice daily over a six-week period and demonstrated an improvement in inflammation and a significant reduction in symptoms. (164)
In a multicenter trial, 51 patients with chronically active mild-to-moderate distal UC received enemas of either butyrate plus 5-ASA or saline plus 5 ASA twice daily. After eight weeks endoscopic and histological parameters, laboratory data, stool frequency and consistency, and other UC symptoms were assessed. The administration of 5-ASA plus butyrate was significantly more effective than 5-ASA plus saline in achieving disease improvement or remission. (165)
Two six-week studies reported either statistically insignificant (166) or no improvement (167) in UC disease activity or remission status in patients supplemented with butyrate enemas, when compared to a saline enema placebo.
Glutamine
In addition to being the main fuel source for the mucosal cells in the ileum, (168) glutamine is also utilized by colonocytes as a respiratory fuel source. (169) A rat study investigated the effect of various agents (prednisolone, 5-ASA, L-glutamine, or SCFAs) applied by enema twice daily for seven days alter induction of colitis with trinitrobenzene sulfonic acid in ethanol. L-glutamine enemas provided the most benefit when compared to the other agents, resulting in a decrease in severity of colitis and lipid peroxidation, without altering mucosal absorption capacity. None of the other three agents yielded such comprehensive benefit. (170)
Research using other animal models of UC has shown glutamine addition to elemental diets decreases endotoxin levels (171) and promotes more rapid healing of colonic lesions. (172)
Phosphatidyicholine/Phosphatidylinositol
Research using a rat model of induced colitis indicates oral supplementation with phosphatidylcholine (PC) prevents collagen deposition and subsequent stricture formation in inflamed colonic tissue. Two of 15 rats fed 100 mg PC daily developed strictures, compared to 12 of 16 colitic rats not receiving PC. Non-colitic control rats had no stricture development, in addition, collagenase activity in colonic tissue was significantly higher in colitic rats given PC than in non-colitic rats and colitic rats receiving no PC. The authors conclude the reduced rate of stricture formation in the treated rats was due to PC enhancement of collagen breakdown. (173)
A study of rats with acetic-acid induced colitis investigated the therapeutic benefits of colonically administered PC and phosphatidylinositol (PI). Both phospholipids were found to have therapeutic benefit when given in a dose-dependent and time-dependent manner over a three-day period. Beneficial effect (prevention of colitis induction and reduction of mucosal permeability) was most pronounced when either PC or PI was given to rats immediately after colitis induction (acetic acid administration). Both phospholipids resulted in significant mucosal recovery and decreased permeability. (174)
So in conclusion, there seems to be a potentially big connection between all of these things and the amount of methyl doners the body has or can produce.
I can't prove direct correlation and I have no idea if it will help, but the following may be worth trying:
Avoid all veg with folate in, along with standard folate/B12 supplements.
Avoid as much sulphur containing food as possible (see above).
Supplement with sub-lingual SAMe, methylfolate (go slow/low dose, it may make things worse before they get better) and sub-lingual methyl-B12 (more info here)
Also check out the suggested supplements in the article above perhaps.
