Stikkordarkiv: metylsulfonylmetan

Metabolic Fingerprint of Dimethyl Sulfone (DMSO2) in Microbial-Mammalian Co-metabolism.

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Nevner mye om hvordan MSM produseres naturlig i kroppen av bakterier som omformer metionin. Spesielt dette avsnittet om hvordan Chrons og IBS har mangel på svovel i tarmen fordi de ikke greier å omforme metionin.

http://www.ncbi.nlm.nih.gov/pubmed/25245235

There is evidence that supports the existence of an altered co- metabolic pathway of methionine in inflammatory bowel disease (IBD) patients. For example, the fecal metagenome of ileal Crohn’s disease (CD) patients exhibits a significant increase in genes related to cysteine and methionine metabolism compared with that in healthy subjects.39 Additionally, fecal sulfur-containing compounds (such as MT, DMS, methyl propyl sulfide, and methyl-2-propenyl disulfide) are significantly lower in CD patients compared with that in healthy subjects, whereas H2S production is higher.40,41 Interestingly, Dawiskiba et al. reported that serum DMSO2 is significantly lower in IBD patients (24 UC and 19 CD patients) compared with that in healthy controls.42 It is therefore possible that these intestinal diseases are associated with both a disruption of microbial methionine degradation as well as the host detoxification pathways (discussed in Section 4.2) that reshape the sulfur-compound distribution in the host metabolic profile.

Nutritional essentiality of sulfur in health and disease.

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Denne beskriver det aller meste om svovel og hvorfor det er et viktig næringsstoff å fokusere på. Den nevner bl.a. at svovel tilskudd, f.eks. MSM, går inn i TBS (total body sulfur pool) som en svovelkilde for glutation. Sammen med metionin og cystein fra maten.

Den nevner også hvordan stress og betennelser skaper en større «turnover» av proteiner, som ofte ikke samsvarer med inntaket av proteiner. Man blir da kronisk på underskudd av svovel og proteiner. Dette forklarer hvorfor proteintilskudd er viktig ved betennelsestilstander og stress tilstander som f.eks. kronisk smerte.

Svovel og Nitrogen har et forhold på 1:14 og er tett sammenkoblet. Når nitrogen forsvinner forsvinner også svovel. Muligens kan man måle svoveltilgjengeligheten i kroppen ved å måle nitrogen med urinstix.

http://www.ncbi.nlm.nih.gov/pubmed/23815141

Hele artikkelen er i min dropbox.

HYPERHOMOCYSTEINEMIA AS A RESPONSE TO STRESS

N and S maintain tightly correlated ratios in tissues of both healthy subjects8 and diseased patients.167 Acute stressful conditions of any cause unleash a shower of many cytokines that fulfill a myriad of autocrine, para- crine, and endocrine functions.168 As a consequence, enhanced tissue proteolysis throughout the body ensues, allowing the redirection of AA residues toward the pref- erential overproduction of acute-phase reactants and repair proteins by the liver and at the site of injury.169 The rate of protein degradation usually exceeds that of protein undergoing neosynthesis,170,171 leading to a negative N balance with subsequent depletion of TBN reserves. The increased urinary excretion of N catabolites (mainly urea, but also creatinine, NH4+, 3-CH3-histidine, and other minor compounds) demonstrates that both metabolic and structural tissues participate in the adap- tive responses to injury in proportion to the magnitude of initial impact.31,170,171 In very aggressive conditions (burns) affecting adult men, urinary output of N may be as high as 250 g of N per week, which corresponds to a loss of 6–7 kg of LBM31 or 12–14% of metabolically active tissues.30 Major stressful disorders are associated with massive urinary excretion of S,167,172 which depletes endogenous pools of TBS. In stressors of medium severity (bone fracture), S spillover has been estimated to be 17 g of S per week, or more than 10% of TBS body stores. Interestingly enough, measurement of S and N urinary losses yields values very close to the 1:14 ratio that char- acterizes mammalian tissues,8,167 indicating that TBN and TBS pools exhibit concomitant degradation patterns throughout the course of injury.

MSM sitt forhold til homocystein

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Homocystein er sett på som utgangspunktet for mange livsstilssykdommer. Homocystein økes av det moderne kostholdet med mye kjøtt spesielt.

Denn studien nevner at MSM reduserer homocystein-økning etter trening. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507661/

Aside from measures of antioxidant status (TEAC and glutathione), we included the measure of homocysteine in the current design. Homocysteine is a non-protein amino acid, with elevated levels in circulation thought to be associated with an increased risk of cardiovascular disease; although recent evidence questions this association [22]. A study by Kim et al. reported a statistically significant lowering of homocysteine (8.0 to 7.2 μmol·L-1) in a sample of knee osteoarthritis patients following intake of MSM at a dosage of 6 grams per day for 12 weeks [4]. Data from the present investigation somewhat corroborate the work of Kim and colleagues, as we noted a lowering of homocysteine during the post-exercise period after subjects were supplemented with MSM for four weeks (Figure ​(Figure3).3). The mechanism of action of this effect may be linked to methyl group donation by MSM, in much the same way as done by B-vitamins [23].

Og denne nevner at homocystein har en direkte giftig effekt på sirkulasjonssystemet og nervesystemt og er assosiert med mange nevrologiske sykdommer. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198708/

Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12. Physiologic Hcy levels are determined primarily by dietary intake and vitamin status. Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof. Certain genetic factors also cause eHcy, such as C667T substitution of the gene encoding methylenetetrahydrofolate reductase. eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, minimal cognitive impairment, dementia, Parkinson’s disease, multiple sclerosis, epilepsy, and eclampsia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders.

Studien nevner at homocystin transformeres tilbake til methionin ved hjelp av B12, med hjelp av folat og B6 (svovel-holdig b-vitamin). Som den første studien viser vil også MSM virke direkte reduserende på homocystein og dermed kan vi forklare den smerte- og symptomreduserende effekten MSM har på nevrologiske problemer.

Nuclear Magnetic Resonance–Based Metabolomics Enable Detection of the Effects of a Whole Grain Rye and Rye Bran Diet on the Metabolic Profile of Plasma in Prostate Cancer Patients1,2

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Denne nevner at MSM (dimetyl sulfone) økes når vi spiser helkorn.

 

Effect of RP on the metabolism of homocysteine and dimethyl sulfone.

WG and bran fractions are rich sources of betaine (36), which may explain the increased betaine level observed after RP in our study. An increase in betaine was previously reported in postprandial plasma collected from pigs fed a WG rye diet (37), but our study shows that it is measurable even in overnight fasting plasma. Betaine acts as a methyl donor in the betaine-homocysteine methyl transferase reaction, which converts homocysteine and betaine to methionine and N,N-dimethylglycine (38). We also observed a reduction in homocysteine and an increase in plasma N,N-dimethylglycine after RP, which indicates a favorable shift in homocysteine metabolism. Elevated circulating homocysteine levels are an independent risk factor for cardiovascular diseases (39–41). Insulin suppresses the expression of betaine homocysteine methyl transferase and consequently reduces the rate of the betaine-homocysteine methyl transferase reaction (42). Therefore, the favorable shift in homocysteine metabolism in our study could be explained by reduced insulin secretion (5) as well as higher bioavailability of betaine as reaction precursor after RP treatment.

We also observed an increase in the organic sulfur compound dimethyl sulfone after RP treatment. Dimethyl sulfone is a metabolite occurring in the plasma and cerebrospinal fluid of normal humans (43). It derives from dietary sources, from intestinal bacterial metabolism and human endogenous methanethiol metabolism (43). It is plausible that higher dimethyl sulfone is associated with a higher rate of intestinal fermentation after RP intake (16). SCFA are also the products of intestinal fermentation (44), but they were not detected in our NMR analysis, possibly because of their limit of detection in plasma.