Denne nevner at jod mangel i befolkningen kommer mest av økt behov for jod, ikke pga mangel av jod i kosten. Et høykarbo kosthold krever mer jod enn et lavkarbokosthold. Derfor ser man jod-mangel problemer i befolkningen.
http://www.ncbi.nlm.nih.gov/pubmed/15142639
The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.
Gjennomgang av studier på PEA mot smerter som følge av nerver i klem. Ved 600mg daglig har man best og raskest effekt, men 300mg daglig gir også noe. Det tar bare lenger tid.
Fra abstract:
In total, eight clinical trials have been published in such entrapment syndromes, and 1,366 patients have been included in these trials. PEA proved to be effective and safe in nerve compression syndromes. In one pivotal, double blind, placebo controlled trial in 636 sciatic pain patients, the number needed to treat to reach 50% pain reduction compared to baseline was 1.5 after 3 weeks of treatment. Furthermore, no drug interactions or troublesome side effects have been described so far.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631430/
Veldig interessant prosjekt satt igang i WHO. Om at pasienter som kan mye om sin egen helse er viktig i helsevesenets møte med kroniske sykdommer.
http://www.who.int/management/general/decisionmaking/WhereArePatientsinDecisionMaking.pdf
Referatet fra denne konferansen har mange gullkorn:
http://www.eu-patient.eu/globalassets/campaign-patient-empowerment/pe-conference-report.pdf
“Once we stop disempowering patients, they can begin to empower themselves.”
Denne rapporten viser at når man bader med Epsom salt (Magnesium sulfat) så økes både magnesium og svovel i kroppen. Den mengden magnesium eller svovel man ikke trenger skilles bare ut med urinen.
Det blir nevnt at 2-3 ganger i uka er optimalt fordi hun når et metningspunkt om man gjør det for ofte.
I tillegg blir det nevnt at å legge epsomsalt direkte på huden (under et vanntett plaster) gir økning i både magnesium og sulfat. De forsøkspersonene som fikk dette rapporterte at deres revmatiske smerter ble borte.
«The values before the first bath were, mean 104.68 ± 20.76 ppm/ml; after the first bath the mean was 114.08 ± 25.83 ppm/ml. Continuation of bathing for 7 days in all except 2 individuals gave a rise to a mean of 140.98 ± 17.00ppm/ml.»
«Free inorganic sulfate levels in plasma rose in all subjects after bathing in Epsom salts (mean pre- bath, 3.28 nmol/mg protein ± 1.40, 2h after 1st bath, mean 5.59 nmol/mg protein ± 3.08). In some individuals, the level post-bath reached > 9 nmol/mg protein.»
«The values obtained suggest that most people would find maximal benefit by bathing 2 or 3 times/ week, using 500-600g Epsom salts each time.»
«2 volunteers wore ‘patches’ where solid MgSO4 was applied directly to the skin and sealed with a waterproof plaster. Plasma/urine analysis confirmed that both Mg and sulfate levels had increased so this is potentially a valuable way of ensuring Epsom salts dosage if bathing is not available. Interestingly, both volunteers, who were > 60 years old, commented without prompting that ‘rheumatic’ pains had disappeared.»
Klikk for å få tilgang til report_on_absorption_of_magnesium_sulfate.pdf
Dette er den desidert beste gjennomgangen av hva svovel kan bidra med i helse og medisin. Her blir de aller fleste svovel-kosttilskuddene diskutert, og MSM får en stor rolle. Den gir en komplett forståelse av alle aspekter rundt svovel og kosthold.
Den nevner hvordan tilførsel av svovel i mate kan redusere behovet for svovelholdige aminosyrer som metionin og cystein. Den nevner også hvordan svovelforbruker øker ved idrett eller sykdom, og at normal svovelinntak fra mat kanskje ikke er nok i slike tilfeller.
Den nevner at spedbarn trenger omtrent 5x mengden svovel (met og cys) pr.kg enn det voksne trenger. 2 år gamle barn trenger dobbelt så mye. Siden barn veier mye mindre enn voksne, helt ned i 30-40x mindre for spedbarn, er dosen mye mindre likevel, men det er verdt å legge merke til at barn trenger mye svovel.
Den nevner at MSM er like lite giftig som vann, altså ett av de minst giftige stoffene i naturen.
http://www.altmedrev.com/publications/7/1/22.pdf
«The biosynthesis of organic sulfur com- pounds from sulfate takes place mainly in plants and bacteria, whereas the oxidation of these com- pounds to sulfate is characteristic of animal species.»
«Methylsulfonylmethane (MSM), an important volatile component in the sulfur cycle, is another source of sulfur found in the human diet. Sulfur is the sixth most abundant macromineral in breast milk5 (colostrum has three times more than mature milk) and the third most abundant mineral determined by percentage of total body weight in an adult.6»
Her nevnes det at svovel på huden gjør at blodkar i huden utvider seg. «Topically, sulfur can induce various histological changes, including hyperkeratosis, acanthosis, and dilation of dermal vessels.8»
«The primary sulfur-containing compounds of interest in humans are methionine, cysteine, homocysteine, cystathione, S-adenosylmethionine (SAMe), tau- rine, α-keto-γ-CH3-thiobutyrate, methanethiol, thiamin, biotin, alpha-lipoic acid (ALA), coen- zyme A, glutathione (GSH), chondroitin sulfate, glucosamine sulfate, fibrinogen, heparin, metallothionein, and inorganic sulfate.16 With the exception of the two sulfur-containing vitamins, thiamin and biotin, all of these sulfur compounds are synthesized from just one parent compound, methionine.16 In addition, sulfur is needed for a number of chemical reactions involved in the me- tabolism of drugs, steroids, and xenobiotics.»
«In animal diets deficient in cysteine, sulfate has been demonstrated to spare the physiological need for cysteine and reverse weight loss induced by cysteine-deficient diets.16 In addition cysteine, but not methionine, becomes labeled with radioactive-S when radioactive sul- fate is fed or injected into animals. Thus, sulfate can be incorporated into compounds for which cysteine is a precursor, e.g., taurine and GSH.16»
«The ex- tracellular sulfate pool in humans is among the smallest of animal species19 and is readily depleted by consumption of a low protein diet or by drugs metabolized by sulfation.19,20»
«The RDA committee recommends a com- bined SAA intake of at least 13 mg/kg per day. This is equivalent to approximately 910 mg/day for a 70 kg adult. Other authorities believe this figure to be too low and recommend an intake of 25 mg/kg/day of SAA for adults.21,22 A rule of thumb is 1 gram of protein should contain at least 17 mg of SAAs (e.g., gluten (wheat protein) or zein (corn protein)).»
«Analysis of long-term vegans living in California revealed an average protein intake of 64 g/day and an SAA intake of approximately 15 mg/kg/day or 16 mg of SAA per gram of protein.23 This level of intake would just meet the average requirement but could be marginal for adults with higher than average requirements, such as athletes or people with HIV. Although not conclusive evi- dence, this does provide evidence that vegan pa- tients should be screened for SAA deficiency.»
«Overtraining
Excessive physical stress, such as is seen in athletic overtraining, inflicts minor trauma on the athlete’s body and can deplete plasma glu- tathione levels,28,29 and increase urinary loss of sulfate.30 For the athlete in training, muscle ca- tabolism or a decrease in plasma GSH are coun- terproductive. Suboptimal intakes of sulfur amino acids during training may exert a proinflammatory influence because, at low levels of intake, cysteine is preferentially incorporated into protein rather than GSH.31 It follows that methionine and cys- teine could be used to ameliorate loss of lean tis- sue and GSH stores. Cysteine and methionine are abundant in whey protein. Methionine can be con- verted into cysteine (cysteine is the rate-limiting step in glutathione synthesis). Lipoic acid could be used to reduce oxidative stress and to preserve vitamin E and C status.»
«There is a metabolic relationship between methionine and MSM. When cows were fed D, L- methionine orally a substantial increase in urinary MSM excretion was observed.101»
«Methylsulfonylmethane is one of the least toxic substances in biology, similar in toxicity to water. The lethal dose (LD50) of DMSO for mice is over 20 g/kg body weight.106»
Denne har en solid gjennomgang av svovel som essensielt næringsstoff, og hvilke faktorer som kan bidra til at vi får for lite svovel. Den nevner også MSM som et svoveltilskudd og at det raskt blir omformet til sulfat når det kommer inn i kroppen.
De faktorer som reduserer svovel er: acetaminophen,
Den sier at GSH er en måte for kroppen å lagre svovel. Den nevner også at når man får lite SAA synker glutationsproduksjonen men over halvparten, fra 7 S i GSH pr. 10 S i protein, til ❤ S i GSH per 10 S i protein. Det viser til at kroppen prioriterer protein over GSH. Ved hard trening f.eks. vil protein prioriteres over GSH. I tillegg beskriver den hvordan økt GSH hemmer prostaglandin produksjonen og virker dermed betennelsendempende slik ibux og den type medisiner gjør.
Denne studien har det viktigste bildet over mulige svovelunderskudd ved forskjellige diett typer. Her blir det vist at vegetarianere, veganere, eldre, slankedietter og det de kaller «health conscious diet» får direkte svovelmangel om de tar paracet som trekker enda mer svovel ut av kroppen. Eller om de har andre tilstander som trekker svovel ut av kroppen, som f.eks. betennelser.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2198910/
Cartilage, less essential for survival, may not fare well under conditions of sulfur deprivation, explaining why dietary supplements containing sulfur (chondroitin sulfate, glucosamine sulfate, MSM (Methylsulfonylmethane), etc.) may be of benefit in the treatment of joint diseases [20].
Since all the dietary supplements investigated containing sulfate, including MSM [27] are readily metabolized prior or shortly after absorption to sulfate or small molecular weight intermediates, they should be able to spare losses of GSH associated with dietary deficiencies, increased utilization due to disease or altered immune function.
In an isotopic study in rats, when diets with various SAA contents were fed at adequate levels, 7 molecules of S were incorporated into GSH for every 10 incorporated into protein [34]. At inadequate levels of intake the ratio fell to <3:10. This response to a low intake of SAA is causes antioxidant defenses to become compromised.
GroupSAA (g/day) IHigh-protein6.8 IIHigh-protein low-calorie5.0 IIIOriental-American4.8 IVAverage balanced4.3 VFast-food4.1VIDieter3.5 VIILacto-ovo-vegetarian3.0 VIII»health conscious diet2.6 IXVegan2.3 Xelderly people (75 yr old)1.8
Denne nevner at svovel har 2 typer «body pools» i kroppen: en med rask gjennomstrømning (10 dagers halveringstid) og en med sakte gjennomstrømning (175 dagers halveringstid). Den raske består hovedsaklig av GSH (glutation), og den sakte består av muskelvev med Taurin som svovelkilde. Og den nevner at GSH har 2 typer «pools», en med 4 timers halveringstid i leveren, og med 4 dagers halveringstid i blodet.
Den nevner også at svovel i urin synker med 87% etter 10 dager med svovelfattig diett (vegetar).
Den konkluderer med at SAA-fattig kost gir lite svovel i «total body pool», og homocystein økes som en konsekvens. Situasjonen blir bare forverret om man har en betennelsestilstand i tillegg.
http://jn.nutrition.org/content/136/6/1641S.long
Our view is that hyperhomocysteinemia principally results from a state of chronic N and Met deprivation undermining the TBN reserves of exposed populations and whose magnitude is best appraised by the inverse correlation linking declining TTR values to rising Hcy concentrations (61,129; Fig. 3). This harmful situation may become even worse with the occurrence of any inflammatory burden further deteriorating the negative N balance (142) or by its coexistence with a cobalamin –deficiency as frequently encountered in low-income countries (156).
Ny gjennomgang av hva PEA kan gjøre for nervebetennelser. Nevner bl.a. at «microniced» PEA er bedre enn vanlig, men dette er nok bare en del av en markedsføringsgimmik. Nevner også at det er bedre å blande med luteolin.
http://www.ncbi.nlm.nih.gov/pubmed/26055231
Inflammation is fundamentally a protective cellular response aimed at removing injurious stimuli and initiating the healing process. However, when prolonged, it can override the bounds of physiological control and becomes destructive. Inflammation is a key element in the pathobiology of chronic pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders. Glia, key players in such nervous system disorders, are not only capable of expressing a pro-inflammatory phenotype but respond also to inflammatory signals released from cells of immune origin such as mast cells. Chronic inflammatory processes may be counteracted by a program of resolution that includes the production of lipid mediators endowed with the capacity to switch off inflammation. These naturally occurring lipid signaling molecules include the N-acylethanolamines, N-arachidonoylethanolamine (an endocannabinoid), and its congener N-palmitoylethanolamine (palmitoylethanolamide or PEA). PEA may play a role in maintaining cellular homeostasis when faced with external stressors provoking, for example, inflammation. PEA is efficacious in mast cell-mediated models of neurogenic inflammation and neuropathic pain and is neuroprotective in models of stroke, spinal cord injury, traumatic brain injury, and Parkinson disease. PEA in micronized/ultramicronized form shows superior oral efficacy in inflammatory pain models when compared to naïve PEA. Intriguingly, while PEA has no antioxidant effects per se, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treat neuroinflammation. This review is intended to discuss the role of mast cells and glia in neuroinflammation and strategies to modulate their activation based on leveraging natural mechanisms with the capacity for self-defense against inflammation.
Influence of breathing frequency on the pattern of respiratory sinus arrhythmia and blood pressure: old questions revisited (2010) – describes how the breathing frequency controls HRV, or RSA (Respiratory Sinusoid Arythmia) as it is called in this article. It mentiones that 6 bpm (breath per minute), or 0.1Hz, gives a 1,8 times higher HRV than 12 bpm. And it confirms that it is the Vagus nerve that controls HRV since betablockers (reducing blood pressure) does not affect HRV. http://ajpheart.physiology.org/content/298/5/H1588
Cardiovascular and Respiratory Effect of Yogic Slow Breathing in the Yoga Beginner: What Is the Best Approach? (2013) – describes how 5-6 bpm gives the best activation of the Vagus nerve, and that its better to use the same length on both in- and outbreath. http://www.hindawi.com/journals/ecam/2013/743504/
Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure (2002) – mentiones that 6 bpm gives the best response on the HRV and Vagus nerve, in addition to a significant lowering of the blood pressure. This study showed results after only 4 minutes of the breathing exercise. http://circ.ahajournals.org/content/105/2/143.full
Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension (2005) – mentiones how 6 bpm increases HRV and the vagus nerves effect on the heart, and that it is the best way to breathe to lower bloodpressure. http://hyper.ahajournals.org/content/46/4/714.full
Heartbeat Synchronizes With Respiratory Rhythm Only Under Specific Circumstances (2004) – shows that HRV is highest at 5-6 bpm. http://journal.publications.chestnet.org/article.aspx?articleid=1082860
Autonomic system modification in zen practitioners (2013) – says a lot about how breathing frequency affects HRV and other factors. And especially interesting is how it changes the normal breathing in the long run. They confirm that 6 bpm gives the highest HRV. http://www.ncbi.nlm.nih.gov/pubmed/24469560
Breathing at a rate of 5.5 breaths per minute with equal inhalation-to-exhalation ratio increases heart rate variability. (2014) – this one mentions that 5.5bpm gives the best HRV and that inbreath and outbeath should be the same length to get the best results. http://www.ncbi.nlm.nih.gov/pubmed/24380741
Modulatory effects of respiration (2001) – shows that HRV is highest at 5-6 bpm and that is sinks when the breathing frequency gets higher or lower. http://www.sciencedirect.com/science/article/pii/S1566070201002673
Matter Over Mind: A Randomised-Controlled Trial of Single-Session Biofeedback Training on Performance Anxiety and Heart Rate Variability in Musicians (2012) – shows that you get the same results if you breath 6bpm or use biofeedback. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3464298
Heart Rate Variability Biofeedback Increases Baroreflex Gain and Peak Expiratory Flow (2003) – mentions that the HRV training with breathing exercises have long term effects on heart diseases and thet it involves neurplasticity. Confirms that 6bpm increases the vagal tone. Thay also show that you get reultst with only the breathing exercise, but that the vagus nerve responds better with biofeedback. http://www.ncbi.nlm.nih.gov/pubmed/14508023
Nevner at mettet fett har fått feil rykte. Det er oksidering av flerumettet fett og sukker som skaper alle livsstilssykdommer som mettetfett feilaktig har blitt koblet til.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650498/
Saturated fats are benign with regard to inflammatory effects, as are the MUFAs. The meager effect that saturated fats have on serum cholesterol levels when modest but adequate amounts of polyunsaturated oils are included in the diet, and the lack of any clear evidence that saturated fats are promoting any of the conditions that can be attributed to PUFA makes one wonder how saturated fats got such a bad reputation in the health literature. The influence of dietary fats on serum cholesterol has been overstated, and a physiological mechanism for saturated fats causing heart disease is still missing.
Various aldehydes produced in the oxidation of PUFAs, as well as sugars, are known to initiate or augment several diseases, such as cancer, inflammation, asthma, type 2 diabetes, atherosclerosis, and endothelial dysfunction. Saturated fats per se may not be responsible for many of the adverse health effects with which they have been associated; instead, oxidation of PUFAs in those foods may be the cause of any associations that have been found. Consequently, the dietary recommendations to restrict saturated fats in the diet should be revised to reflect differences in handling before consumption, e.g., dairy fats are generally not heated to high temperatures. It is time to reevaluate the dietary recommendations that focus on lowering serum cholesterol and to use a more holistic approach to dietary policy.
Verkstedet Bodywork & Breathing System 