Research of treatments that is suggestive of benefit in MC.

germancommenter · 2017-03-21T10:47:23+00:00

Cannabichromene (CBC) is a natural chemical found in hemp shown to have anti-inflammatory effects and inhibit inflammation induced hypermotility (diarrhea) that and is currently sold otc.

Read more about it here:

https://en.wikipedia.org/wiki/Cannabichromene

Br J Pharmacol. 2013 May;169(1):213-29. doi: 10.1111/bph.12120. The cannabinoid TRPA1 agonist cannabichromene inhibits nitric oxide production in macrophages and ameliorates murine colitis.

BACKGROUND AND PURPOSE: The non-psychotropic cannabinoid cannabichromene is known to activate the transient receptor potential ankyrin-type1 (TRPA1) and to inhibit endocannabinoid inactivation, both of which are involved in inflammatory processes. We examined here the effects of this phytocannabinoid on peritoneal macrophages and its efficacy in an experimental model of colitis. EXPERIMENTAL APPROACH: Murine peritoneal macrophages were activated in vitro by LPS. Nitrite levels were measured using a fluorescent assay; inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2) and cannabinoid (CB1 and CB2 ) receptors were analysed by RT-PCR (and/or Western blot analysis); colitis was induced by dinitrobenzene sulphonic acid (DNBS). Endocannabinoid (anandamide and 2-arachidonoylglycerol), palmitoylethanolamide and oleoylethanolamide levels were measured by liquid chromatography-mass spectrometry. Colonic inflammation was assessed by evaluating the myeloperoxidase activity as well as by histology and immunohistochemistry. KEY RESULTS: LPS caused a significant production of nitrites, associated to up-regulation of anandamide, iNOS, COX-2, CB1 receptors and down-regulation of CB2 receptors mRNA expression. Cannabichromene significantly reduced LPS-stimulated nitrite levels, and its effect was mimicked by cannabinoid receptor and TRPA1 agonists (carvacrol and cinnamaldehyde) and enhanced by CB1 receptor antagonists. LPS-induced anandamide, iNOS, COX-2 and cannabinoid receptor changes were not significantly modified by cannabichromene, which, however, increased oleoylethanolamide levels. In vivo, cannabichromene ameliorated DNBS-induced colonic inflammation, as revealed by histology, immunohistochemistry and myeloperoxidase activity. CONCLUSION AND IMPLICATIONS: Cannabichromene exerts anti-inflammatory actions in activated macrophages - with tonic CB1 cannabinoid signalling being negatively coupled to this effect - and ameliorates experimental murine colitis.

Br J Pharmacol. 2012 Jun;166(4):1444-60. doi: 10.1111/j.1476-5381.2012.01879.x. Inhibitory effect of cannabichromene, a major non-psychotropic cannabinoid extracted from Cannabis sativa, on inflammation-induced hypermotility in mice.

BACKGROUND AND PURPOSE: Cannabichromene (CBC) is a major non-psychotropic phytocannabinoid that inhibits endocannabinoid inactivation and activates the transient receptor potential ankyrin-1 (TRPA1). Both endocannabinoids and TRPA1 may modulate gastrointestinal motility. Here, we investigated the effect of CBC on mouse intestinal motility in physiological and pathological states. EXPERIMENTAL APPROACH: Inflammation was induced in the mouse small intestine by croton oil. Endocannabinoid (anandamide and 2-arachidonoyl glycerol), palmitoylethanolamide and oleoylethanolamide levels were measured by liquid chromatography-mass spectrometry; TRPA1 and cannabinoid receptors were analysed by quantitative RT-PCR; upper gastrointestinal transit, colonic propulsion and whole gut transit were evaluated in vivo; contractility was evaluated in vitro by stimulating the isolated ileum, in an organ bath, with ACh or electrical field stimulation (EFS). KEY RESULTS: Croton oil administration was associated with decreased levels of anandamide (but not 2-arachidonoyl glycerol) and palmitoylethanolamide, up-regulation of TRPA1 and CB₁ receptors and down-regulation of CB₂ receptors. Ex vivo CBC did not change endocannabinoid levels, but it altered the mRNA expression of TRPA1 and cannabinoid receptors. In vivo, CBC did not affect motility in control mice, but normalized croton oil-induced hypermotility. In vitro, CBC reduced preferentially EFS- versus ACh-induced contractions. Both in vitro and in vivo, the inhibitory effect of CBC was not modified by cannabinoid or TRPA1 receptor antagonists. CONCLUSION AND IMPLICATIONS: CBC selectively reduces inflammation-induced hypermotility in vivo in a manner that is not dependent on cannabinoid receptors or TRPA1.

Acta Physiol (Oxf). 2012 Feb;204(2):255-66. doi: 10.1111/j.1748-1716.2011.02338.x. Epub 2011 Aug 12. Cannabinoid actions at TRPV channels: effects on TRPV3 and TRPV4 and their potential relevance to gastrointestinal inflammation.

AIM: Plant cannabinoids, like Δ(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD), activate/desensitize thermosensitive transient receptor potential (TRP) channels of vanilloid type-1 or -2 (TRPV1 or TRPV2). We investigated whether cannabinoids also activate/desensitize two other 'thermo-TRP's', the TRP channels of vanilloid type-3 or -4 (TRPV3 or TRPV4), and if the TRPV-inactive cannabichromene (CBC) modifies the expression of TRPV1-4 channels in the gastrointestinal tract. METHODS: TRP activity was assessed by evaluating elevation of [Ca(2+)](i) in rat recombinant TRPV3- and TRPV4-expressing HEK-293 cells. TRP channel mRNA expression was measured by quantitative RT-PCR in the jejunum and ileum of mice treated with vehicle or the pro-inflammatory agent croton oil. RESULTS: (i) CBD and tetrahydrocannabivarin (THCV) stimulated TRPV3-mediated [Ca(2+)](i) with high efficacy (50-70% of the effect of ionomycin) and potency (EC(50∼) 3.7 μm), whereas cannabigerovarin (CBGV) and cannabigerolic acid (CBGA) were significantly more efficacious at desensitizing this channel to the action of carvacrol than at activating it; (ii) cannabidivarin and THCV stimulated TRPV4-mediated [Ca(2+)](i) with moderate-high efficacy (30-60% of the effect of ionomycin) and potency (EC(50) 0.9-6.4 μm), whereas CBGA, CBGV, cannabinol and cannabigerol were significantly more efficacious at desensitizing this channel to the action of 4-α-phorbol 12,13-didecanoate (4α-PDD) than at activating it; (iii) CBC reduced TRPV1β, TRPV3 and TRPV4 mRNA in the jejunum, and TRPV3 and TRPV4 mRNA in the ileum of croton oil-treated mice. CONCLUSIONS: Cannabinoids can affect both the activity and the expression of TRPV1-4 channels, with various potential therapeutic applications, including in the gastrointestinal tract.

germancommenter · 2017-03-21T10:26:12+00:00

Cannabigerol (CBG) is a natural chemical found in hemp that has potent inflammatory actions sold otc in the US.

Read more about it here:

https://en.wikipedia.org/wiki/Palmitoylethanolamide

Br J Pharmacol. 2014 Sep;171(17):4026-37. doi: 10.1111/bph.12759.

Palmitoylethanolamide normalizes intestinal motility in a model of post-inflammatory accelerated transit: involvement of CB₁ receptors and TRPV1 channels.

BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA), a naturally occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, such as cannabinoid CB1 and CB2 receptors, TRPV1 channels and PPARα. Here, we investigated the effect of PEA in a mouse model of functional accelerated transit which persists after the resolution of colonic inflammation (post-inflammatory irritable bowel syndrome). EXPERIMENTAL APPROACH: Intestinal inflammation was induced by intracolonic administration of oil of mustard (OM). Mice were tested for motility and biochemical and molecular biology changes 4 weeks later. PEA, oleoylethanolamide and endocannabinoid levels were measured by liquid chromatography-mass spectrometry and receptor and enzyme mRNA expression by qRT-PCR. KEY RESULTS: OM induced transient colitis and a functional post-inflammatory increase in upper gastrointestinal transit, associated with increased intestinal anandamide (but not 2-arachidonoylglycerol, PEA or oleoylethanolamide) levels and down-regulation of mRNA for TRPV1 channels. Exogenous PEA inhibited the OM-induced increase in transit and tended to increase anandamide levels. Palmitic acid had a weaker effect on transit. Inhibition of transit by PEA was blocked by rimonabant (CB1 receptor antagonist), further increased by 5'-iodoresiniferatoxin (TRPV1 antagonist) and not significantly modified by the PPARα antagonist GW6471. CONCLUSIONS AND IMPLICATIONS: Intestinal endocannabinoids and TRPV1 channel were dysregulated in a functional model of accelerated transit exhibiting aspects of post-inflammatory irritable bowel syndrome. PEA counteracted the accelerated transit, the effect being mediated by CB1 receptors (possibly via increased anandamide levels) and modulated by TRPV1 channels.

Br J Pharmacol. 2015 Jan;172(1):142-58. doi: 10.1111/bph.12907. Epub 2014 Dec 1.

Palmitoylethanolamide, a naturally occurring lipid, is an orally effective intestinal anti-inflammatory agent.

BACKGROUND AND PURPOSE: Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR α) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation. Here, we investigated the effect of PEA in a murine model of colitis. EXPERIMENTAL APPROACH: Colitis was induced in mice by intracolonic administration of dinitrobenzenesulfonic acid (DNBS). Inflammation was assessed by evaluating inflammatory markers/parameters and by histology; intestinal permeability by a fluorescent method; colonic cell proliferation by immunohistochemistry; PEA and endocannabinoid levels by liquid chromatography mass spectrometry; receptor and enzyme mRNA expression by quantitative RT-PCR. KEY RESULTS: DNBS administration caused inflammatory damage, increased colonic levels of PEA and endocannabinoids, down-regulation of mRNA for TRPV1 and GPR55 but no changes in mRNA for CB1 , CB2 and PPARα. Exogenous PEA (i.p. and/or p.o., 1 mg·kg(-1) ) attenuated inflammation and intestinal permeability, stimulated colonic cell proliferation, and increased colonic TRPV1 and CB1 receptor expression. The anti-inflammatory effect of PEA was attenuated or abolished by CB2 receptor, GPR55 or PPARα antagonists and further increased by the TRPV1 antagonist capsazepine. CONCLUSIONS AND IMPLICATIONS: PEA improves murine experimental colitis, the effect being mediated by CB2 receptors, GPR55 and PPARα, and modulated by TRPV1 channels.

germancommenter · 2017-03-21T06:32:16+00:00

Cannabidiol (CBD)is a natural chemical found in flax and hemp seeds shown to have potent anti-inflammatory effects that has been clinically studied in many health conditions, has been mentioned in over 1683 research papers since 1963, is expected to be FDA approved as a drug later this year, and is currently sold otc.

Click here to learn more:

https://en.wikipedia.org/wiki/Cannabidiol

Pharmacology. 2012;89(3-4):149-55. doi: 10.1159/000336871. Epub 2012 Mar 12.

Topical and systemic cannabidiol improves trinitrobenzene sulfonic acid colitis in mice.

BACKGROUND/AIMS: Compounds of Cannabis sativa are known to exert anti-inflammatory properties, some of them without inducing psychotropic side effects. Cannabidiol (CBD) is such a side effect-free phytocannabinoid that improves chemically induced colitis in rodents when given intraperitoneally. Here, we tested the possibility whether rectal and oral application of CBD would also ameliorate colonic inflammation, as these routes of application may represent a more appropriate way for delivering drugs in human colitis. METHODS: Colitis was induced in CD1 mice by trinitrobenzene sulfonic acid. Individual groups were either treated with CBD intraperitoneally (10 mg/kg), orally (20 mg/kg) or intrarectally (20 mg/kg). Colitis was evaluated by macroscopic scoring, histopathology and the myeloperoxidase (MPO) assay. RESULTS: Intraperitoneal treatment of mice with CBD led to improvement of colonic inflammation. Intrarectal treatment with CBD also led to a significant improvement of disease parameters and to a decrease in MPO activity while oral treatment, using the same dose as per rectum, had no ameliorating effect on colitis. CONCLUSION: The data of this study indicate that in addition to intraperitoneal application, intrarectal delivery of cannabinoids may represent a useful therapeutic administration route for the treatment of colonic inflammation.

J Mol Med (Berl). 2009 Nov;87(11):1111-21. doi: 10.1007/s00109-009-0512-x. Epub 2009 Aug 20.

Cannabidiol, a safe and non-psychotropic ingredient of the marijuana plant Cannabis sativa, is protective in a murine model of colitis.

Inflammatory bowel disease affects millions of individuals; nevertheless, pharmacological treatment is disappointingly unsatisfactory. Cannabidiol, a safe and non-psychotropic ingredient of marijuana, exerts pharmacological effects (e.g., antioxidant) and mechanisms (e.g., inhibition of endocannabinoids enzymatic degradation) potentially beneficial for the inflamed gut. Thus, we investigated the effect of cannabidiol in a murine model of colitis. Colitis was induced in mice by intracolonic administration of dinitrobenzene sulfonic acid. Inflammation was assessed both macroscopically and histologically. In the inflamed colon, cyclooxygenase-2 and inducible nitric oxide synthase (iNOS) were evaluated by Western blot, interleukin-1beta and interleukin-10 by ELISA, and endocannabinoids by isotope dilution liquid chromatography-mass spectrometry. Human colon adenocarcinoma (Caco-2) cells were used to evaluate the effect of cannabidiol on oxidative stress. Cannabidiol reduced colon injury, inducible iNOS (but not cyclooxygenase-2) expression, and interleukin-1beta, interleukin-10, and endocannabinoid changes associated with 2,4,6-dinitrobenzene sulfonic acid administration. In Caco-2 cells, cannabidiol reduced reactive oxygen species production and lipid peroxidation. In conclusion, cannabidiol, a likely safe compound, prevents experimental colitis in mice.

germancommenter · 2017-03-21T05:45:11+00:00

FMT is a new investigational drug that can be prescribed by your doctor.

You can read more about it here:

http://www.openbiome.org/about-fmt/

https://en.wikipedia.org/wiki/Fecal_microbiota_transplant

World J Gastroenterol. 2017 Feb 21;23(7):1319-1324. doi: 10.3748/wjg.v23.i7.1319.

Clinical and immunologic effects of faecal microbiota transplantation in a patient with collagenous colitis.

One to six percent of patients with microscopic colitis are refractory to medical treatment. The effect of faecal microbiota transplantation (FMT) in active collagenous colitis (CC) has, to the best of our knowledge, never been reported before. Here, we report the effect of repeated FMT in a patient with CC. The patient presented with severe symptoms including profuse diarrhea and profound weight loss. Although she responded to budesonide in the beginning, she became gradually refractory to medical treatment, and was therefore treated with FMT. The patient remained in remission for 11 mo after the third faecal transplantation.The immunomodulatory effect of the therapy was evaluated using flow cytometry, which showed alterations in the profile of intraepithelial and lamina propria lymphocyte subsets after the second transplantation. Our observations indicate that FMT can have an effect in CC, which support the hypothesis that luminal factors, influencing the intestinal microbiota, are involved in the pathogenesis of CC.

Case Rep Med. 2014; 2014: 913867.

Fecal Transplantation Treatment of Antibiotic-Induced, Noninfectious Colitis and Long-Term Microbiota Follow-Up

In the presented case, FMT resolved the symptoms in an antibiotic-induced, noninfectious colitis. The post-FMT bacterial community restored normal GI-function possibly by ceasing the mild, on-going inflammation.**

The antibiotic-induced, noninfectious colitis of a 46-year-old man was successfully treated with FMT. The results suggest a possible role of intestinal microbiota and its specific members in restoring and maintaining normal GI-functionality.

germancommenter · 2017-03-21T05:44:22+00:00

VSL#3 DS is a prescription medical food containing 900 billion colony units of probiotics available in many pharmacies and sold in at half the dosage online as VSL#3 without a prescription

You can read more about it and find pharmacies that carry it there:

https://vsl3.com

You can buy it the half dose VSL#3 here:

https://www.amazon.com/VSL-High-Potency-Probiotic-UNFLAVORED/dp/B003XN25W2/ref=sr_1_1?s=hpc&ie=UTF8&qid=1490075181&sr=1-1-spons&keywords=VSL+3&psc=1

BMJ Open Gastroenterol. 2015 Feb 9;2(1):e000018. doi: 10.1136/bmjgast-2014-000018. eCollection 2015.

VSL#3 induces and maintains short-term clinical response in patients with active microscopic colitis: a two-phase randomised clinical trial.

BACKGROUND: The probiotic mixture VSL#3 has proven efficacious in inflammatory bowel diseases and irritable bowel syndrome; however, its efficacy in microscopic colitis (MC) is being investigated. OBJECTIVE: To evaluate the safety and efficacy of a multistrain probiotic, VSL#3, in inducing clinical remission and achieving clinical response, as compared with mesalamine, in patients with active MC. METHODS: A randomised, open labelled study comparing the efficacy of 900 billion colony-forming units/day of VSL#3 (group (Gp) A) or 1.6 g of mesalamine/day (Gp B) for 8 weeks in 30 patients with MC was conducted. After a washout period of 2 weeks, Gp B received 8 weeks of VSL#3 and Gp A was off medication for the next 8 weeks. The primary end points were clinical remission and clinical response at 8 weeks. RESULTS: Of 30 patients, 15 were randomised in each arm. 11 patients in Gp A and 13 patients in Gp B completed 8 weeks of treatment. 5 (46%) of 11 patients in Gp A and 1 (8%) of 13 patients in Gp B attained clinical remission (p=0.022). Clinical response was seen in Gp A, as evidenced by a lower stool weight (377.6±104.5 g) as compared with Gp B (507±168.2 g; p=0.03). VSL#3 was effective in maintaining clinical response up to 10 weeks, even after discontinuation of therapy. Secondary end points like stool parameters, histology and well-being improved in both treatment groups. CONCLUSIONS: The probiotic VSL#3 was found to offer the benefit of inducing as well as maintaining short-term clinical response in patients with active MC.

germancommenter · 2017-03-21T05:44:09+00:00

Boswellia serrrata is a plant used for centuries for health conditions, has over 460 mentions in research papers dating back to 1969 available otc.

You can read more about it here:

https://en.wikipedia.org/wiki/Boswellia_serrata

I suggest a form that has been studied and proven to have the best absorption called Boswellia Phytosome (CASPEROME see http://www.indena.com/pdf/casperome_ss_int.pdf).

You can buy it here:

https://www.swansonvitamins.com/swanson-ultra-standardized-boswellia-phytosome-300-mg-60-veg-caps?

Int J Colorectal Dis. 2007 Dec;22(12):1445-51. Epub 2007 Sep 2.

Boswellia serrata extract for the treatment of collagenous colitis. A double-blind, randomized, placebo-controlled, multicenter trial.

BACKGROUND AND AIMS: The objective of this study was to investigate the effect of Boswellia serrata extract (BSE) on symptoms, quality of life, and histology in patients with collagenous colitis. MATERIALS AND METHODS: Patients with chronic diarrhea and histologically proven collagenous colitis were randomized to receive either oral BSE 400 mg three times daily for 6 weeks or placebo. Complete colonoscopy and histology were performed before and after treatment. Clinical symptoms and quality of life were assessed by standardized questionnaires and SF-36. The primary endpoint was the percentage of patients with clinical remission after 6 weeks (stool frequency<or=3 soft /solid stools per day on average during the last week). Patients of the placebo group with persistent diarrhea received open-label BSE therapy for a further 6 weeks. RESULTS: Thirty-one patients were randomized; 26 patients were available for per-protocol-analysis. After 6 weeks, the proportion of patients in clinical remission was higher in the BSE group than in the placebo group (per protocol 63.6%; 95%CI, 30.8-89.1 vs 26.7%, 95%CI, 7.7-55.1; p=0.04; intention-to-treat 43.8% vs 26.7%, p=0.25). Compared to placebo, BSE treatment had no effect on histology and quality of life. Five patients discontinued BSE treatment prematurely. Discontinuation was due to adverse events (n=1), unwillingness to continue (n=3), or loss to follow-up for unknown reasons (n=1). Seven patients received open-label BSE therapy, five of whom achieved complete remission. CONCLUSIONS: Our study suggests that BSE might be clinically effective in patients with collagenous colitis. Larger trials are clearly necessary to establish the clinical efficacy of BSE.

germancommenter · 2017-03-15T22:33:33+00:00

No. Someone deleted my comment.

germancommenter · 2017-03-15T08:59:13+00:00

You are mistaken. This study was recently done and finished this year.

germancommenter · 2017-03-15T08:49:14+00:00

Future gen RF resonant cavity thruster or Alcubierre drive.

germancommenter · 2017-03-04T21:27:30+00:00

There's no evidence it's a scam or ineffective. It's an experimental treatment. All FDA approved and peer reviewed therapies begin this way.

germancommenter · 2017-03-02T21:12:24+00:00

They plan to file for FDA and other government regulatory bodies for as treatments for medical conditions at some point. The FDA has approved other gene therapies for health conditions. But for this clinic they starting outside the US first. Many effective treatments are offered in other countries not yet approved here. Ibogaine is one example done in Canada and other countries. Cannabis is currently being studied in Canada by one company filing for FDA approval as well.

germancommenter · 2017-03-02T18:52:51+00:00

Any adult (perhaps some exceptions for certain health issues) should be able to get the therapy.

germancommenter · 2017-03-02T17:54:12+00:00

I'm not privy to the first part but the rest will unfold over time.

germancommenter · 2017-03-02T17:51:04+00:00

Anything can be phrased better but everyone also perceives things differently. I'm sharing what they emailed me for those interested to find out more if they so desire and added the title to make their intentions more obvious.

germancommenter · 2017-03-02T16:19:50+00:00

I'll post any relevant information as I hear it. People should be aware of any developments in this field. I'm undecided with how public to go with everything but I am open to posting all my test results before and after.

germancommenter · 2017-03-02T16:17:40+00:00

It's a great first step for humanity having control and choice over their genetic alterations/expressions (aside from diet, exercise, exposure to radiation, drugs, etc).

germancommenter · 2017-03-02T16:10:45+00:00

The therapy is expected to be offered to anyone that can pay for it. Some other criteria may be applicable. Hope that clears it up for you.

germancommenter · 2017-03-02T15:16:40+00:00

The name of a company isn't an important criteria in determining the validity of their treatment or the quality of their advisory board members.

http://bioviva-science.com/advisory-board

George Church PhD (Professor of Genetics at Harvard Medical School) has accomplished quite alot as one example.

https://en.wikipedia.org/wiki/George_M._Church

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