Forfatterarkiv: Marius

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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.

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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.

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Sulfur Amino Acids in Diet-induced Fatty Liver: A New Perspective Based on Recent Findings

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Man har sett at metionin reduserer fettlever, mens cystein øker fettlever. Nå viser ny forskning at alt dette styrt av tilgangen på svovel. Metionin gir svovel som reduserer fettlever, mens cysten tar opp svovel slik at det blir mindre svovel tilgjengelig til å redusere fettlever.

Abstract

: The relationship of sulfur amino acids to diet-induced fatty liver was established 80 years ago, with cystine promoting the condition and methionine preventing it. This relationship has renewed importance today because diet-induced fatty liver is relevant to the current epidemics of obesity, non-alcoholic fatty liver disease, metabolic syndrome, and type 2 diabetes. Two recent papers provide the first evidence linking sulfane sulfur to diet-induced fatty liver opening a new perspective on the problem. This review summarizes the early data on sulfur amino acids in fatty liver and correlates that data with current knowledge of sulfur metabolism. Evidence is reviewed showing that the lipotropic effect of methionine may be mediated by sulfane sulfur and that the hepatosteatogenic effect of cystine may be related to the removal of sulfane sulfur by cysteine catabolites. Possible preventive and therapeutic strategies are discussed.

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Heart rate variability biofeedback: how and why does it work?

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Bekrefter alle elementer jeg jobber med i Autonom pust: vagus, betennelse, m.m.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104929/

In recent years there has been substantial support for heart rate variability biofeedback (HRVB) as a treatment for a variety of disorders and for performance enhancement (Gevirtz, 2013). Since conditions as widely varied as asthma and depression seem to respond to this form of cardiorespiratory feedback training, the issue of possible mechanisms becomes more salient. The most supported possible mechanism is the strengthening of homeostasis in the baroreceptor (Vaschillo et al., 2002; Lehrer et al., 2003). Recently, the effect on the vagal afferent pathway to the frontal cortical areas has been proposed. In this article, we review these and other possible mechanisms that might explain the positive effects of HRVB.

ANTI-INFLAMMATORY EFFECTS

It is known that the vagal system interacts closely with the inflammatory system, such that increases in vagus nerve traffic (usually produced by electrical vagal stimulation) are associated with decreases in serum levels of various inflammatory cytokines (Borovikova et al., 2000; Tracey, 2002). One study did find a decrease in C-reactive proteins among hypertensive patients treated with HRV biofeedback (Nolan et al., 2012). In another study, we experimentally exposed healthy subjects to an inflammatory cytokine, lipopolysaccharide (Lehrer et al., 2010). Usually both sympathetic and parasympathetic activity is blocked by lipopolysaccharide. Although no biofeedback-induced decreases in inflammatory cytokines were found, the autonomic effects of inflammation were greatly modulated, indicating that a greater resiliency was preserved among individuals given HRV biofeedback.

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Matoverfølsomhet – et paradigmeskifte

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Artikkel skrevet i 2011 som nevner mange viktige poenger. Blandt annet at vagus svekkes ved IBS og at det gir andre plager, spesielt hudplager.

Klikk for å få tilgang til matoverfoelsomhet_aip_1_2011w_v2.pdf

Dessuten hadde mange pasienter ekstra-intesti- nale symptomer og skåret høyt på «Subjective Health Complaints» (1). Påfallende mange anga at de hadde kronisk tretthet samt leddsmerter med morgenstivhet uten påvisbar artritt. Livskvaliteten var til dels be- tydelig redusert (2).

Over 50% av pasientene tilfreds- stilte kravene til en psykiatrisk diag- nose. Men hvor mye av de psykologiske problemene kan være sekundære? Inntil for knapt 20 år siden ble også magesårsykdommen regnet som en psykosomatisk sykdom. De psykolo- giske problemene vi så hos ulcuspasi- entene var ganske like de vi nå finner hos de matoverfølsomme, og vi har enda friskt i minnet hvordan alle pro- blemene hos ulcuspasientene, in- kludert de psykologiske, «blåste bort» etter fjerning av magesårbakterien Helicobacter pylori (4).

Kun sykdomspesifikk angst eller for- ventninger om plager var signifikante uavhengige prediktorer. Disse pre- diktorene forklarte dog til sammen ikke mer enn 10% av variansen i mageplagene, og alder var eneste signifikante prediktor av ekstra- intestinale plager. Det vil si at 90% av variansen i grad av somatiske plager ikke kunne forklares av psyko- logiske faktorer. Vi tror derfor nå at mange av de psykologiske problemene ved matoverfølsomhet er sekundære og at betydningen av psykologiske faktorer som årsak til matoverfølsomhet kan være betydelig overdrevet.

Vi kunne vise at et tungt fordøyelig, men fermenter- bart karbohydrat, som laktulose, ofte reproduserte pasientens plager (6). tester på klassisk IgE-sensitivisering mot spesifikke kostproteiner, deri- mot, var sjeldent positive. Det virker som om mageplagene først og fremst trigges av tungt fordøyelige karbo- hydrater og ikke spesielt av proteiner i kosten. Dessuten, at plagene kunne reproduseres av mat, viser at pasien- ten har rett – plagene kan skyldes maten! Det passer med at pasientene ikke har plager om natta, når de faster, etter tarm- skylling eller når de får tømt seg fullstendig.

Over 60% av pasientene hadde indikasjon på atopisk sykdom (Dette er hud- og slimhinnerelaterte sykdommer som allergi, tørr hud, kløe, m.m.)

Histamin øker sympatisk og redusert para- sympatisk (vagal) tonus, som også er karakteristisk for pasienter med funksjonelle mageplager (16, 17). Slik endret autonom aktivitet kan være et resultat av IgE-mediert histaminfrigjøring fra lokalt sensibili- serte mastceller (18).

Systemiske symptomer som kro- nisk tretthet og leddsmerter hos pasi- enter med IBS har tidligere ofte blitt forklart som somatisering av psykolo- giske problemer, men det finnes andre muligheter. For eksempel er det nylig rapportert at symptomer ved kronisk tretthetssyndrom kan behandles med en B-celle-antagonist (rituximab) (21). I likhet med de matoverfølsomme, har pasienter med kronisk tretthets- syndrom ofte IBS og endret mikro- flora som kan være av betydning for immunaktiveringen hos disse pasi- entene (22). Hos matoverfølsomme med IBS har vi nylig påvist økt nivå av B-celle aktiverende faktor (BAFF) i blod og tarmskyllevæske (23). BAFF er relatert til autoimmunitet og lokal immunaktivering i tarmen («lokal allergi») (24).

At karbohydrater kan reprodusere mageplagene hos pasienter med IBS og matoverfølsomhet, er verdt å merke seg, og mye tyder på at dette allerede nå bør få terapeutiske konsekvenser (27). Vi ser med andre ord for oss et paradigmeskifte når det gjelder utredning og behandling av pasienter med IBS og matoverfølsomhet.

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Central sensitisation in visceral pain disorders

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Nevner hvordan IBS skaper sentralsensitering og hyperalgesia andre steder enn bare tarmen, og bidrar til mange muskel- og ledd problemer. Nevner at dette spesielt skjer i korsryggen hvor sensoriske nerver fra tarmen treffer samme nerve i ryggmargen som de sensoriske nervene fra beina.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856337/

The concept of visceral hyperalgesia has been examined in a variety of functional gastrointestinal disorders (FGIDs), including oesophagitis, gastro‐oesophageal reflux disease, non‐ulcer dyspepsia, gastroparesis, and irritable bowel syndrome (IBS). Visceral hypersensitivity has also been demonstrated in non‐gastrointestinal disorders such as interstitial cystitis and ureteric colic.1 Although the pathophysiological mechanisms of pain and hypersensitivity in these disorders are still not well understood, exciting new developments in research have been made in the study of the brain‐gut interactions involved in the FGIDs.

In this issue of Gut, Sarkar and colleagues2 address the phenomenon of temporal summation of pain, termed “wind‐up”, and its relationship to central sensitisation and secondary visceral pain hyperalgesia caused by acidification of the oesophagus (see page 920). Also in this issue of Gut, Drewes and colleagues3 examine peripheral and central sensitisation using both mechanical and thermal stimuli in patients with oesophagitis compared with control subjects (see page 926). They found that in patients with oesophagitis, the interaction between central and peripheral nociceptive input may help explain patient symptoms. Understanding the implications of these two studies requires examining the concept of central sensitisation in visceral pain disorders. Both of these studies have important clinical and research ramifications for the study of FGIDs.

“Hypersensitivity in IBS patients is not just limited to the gut and more widespread alterations in central pain processing may be involved in this chronic pain disorder”

The most pronounced hyperalgesia appears to occur at the lumbosacral level at which colon and lower extremity nociceptive afferents are likely to converge onto common spinal segments, explaining why patients had higher thermal hypersensitivity in the foot than in the hand (see fig 1​1).14,15,19

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Relationship between daily physical activity level and low back pain in young, female desk-job workers.

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For mye trening og for lite trening gir ryggsmerter. Akkurat passe mye trening er best.

http://www.ncbi.nlm.nih.gov/pubmed/25261333

Abstract

OBJECTIVES:

The purpose of this study was to investigate the relationship between daily physical activity (PA) level and low back pain (LBP) in young women.

MATERIAL AND METHODS:

Two hundred forty three female, desk-job workers aged 20-40 voluntarily participated in the study. The participants were assessed by the use of Oswestry Disability Index for measuring LBP disability and by the use of the short version of the International Physical Activity Questionnaire for PA assessment. The 1-way ANOVA test was used for comparing the mean values according to the physical activity level groups. Correlations between the average LBP disability score and all the other variables were obtained using Pearson’s correlation analysis. The level of statistical significance was p < 0.05.

RESULTS:

Significant differences were found for LBP disability score between the results of 3 different PA groups (p < 0.05) (low, moderate and high PA groups). The correlation between the average LBP disability score and body weight (r = 0.187, p < 0.01), body mass index (r = 0.165, p < 0.01), vigorous MET score (r = 0.247, p < 0.01) and total PA MET score (r = 0.131, p < 0.01) were significant.

CONCLUSIONS:

The main finding of this study is that there is a U-shaped relationship between PA and LBP disability score in young women. A moderate level of daily physical activity and preventing body weight and fat gain should be recommended in young, female desk-job workers in order to prevent and manage low back pain.

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Efficacy of paced breathing for insomnia: Enhances vagal activity and improves sleep quality.

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Nevner at 0,1 Hz pust (5x minuttet) styrker vagusnerven slik at søvnen blir bedre for de som har insomnia. Her gjorde de det i 20 minutter før de la seg til å sove.

http://www.ncbi.nlm.nih.gov/pubmed/25234581

Abstract

Fourteen self-reported insomniacs (SRI) and 14 good sleepers (GS) had their cardiac neuronal activity assessed by heart rate variability (HRV) under controlled respiration at a slow frequency rate of 0.1 Hz, and a forced rate of 0.2 Hz during daytime rest. Nighttime sleep was measured by polysomnography. The SRI showed depressed high frequency power of HRV compared to the GS. An increased total power of HRV was observed among the SRI during slow, paced breathing compared with spontaneous breathing and 0.2 Hz. Sleep onset latency, number of awakenings, and awakening time during sleep were decreased and sleep efficiency was increased if SRI practiced slow, paced breathing exercises for 20 min before going to sleep. Our results indicate that there is autonomic dysfunction among insomniacs, especially in relation to vagal activity; however, this decreased vagal activity can be facilitated by practicing slow, paced breathing, thereby improving sleep quality.