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Rheumatoid Arthritis Is A Metabolic Disease; Vitamin K And Niacinamide May Treat It

Discussion in 'Scientific Studies' started by haidut, Mar 29, 2016.

  1. haidut

    haidut Member

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    Ray has written so many articles on how "autoimmune conditions" like MS, rheumatoid arthritis (RA), lupus, psoriasis, etc are all metabolic diseases mostly driven by estrogen. After decades of denial by mainstream medicine, a study was just published by a team at Stanford that shows RA to be indeed a metabolic disease. More importantly, RA was found to be a disease caused by excessive reductive stress caused by excessive metabolism of glucose through the pentose phosphate pathway (PPP), and accumulation of NAPDH and reduced glutathione, accompanied by reductions in oxidative phosphorylation. The PPP is a parallel pathway to glycolysis and exists primarily as a defense mechanism against the so-called reactive oxygen species (ROS). The excessive reductive stress apparently not only neutralizes the ROS but it also inhibits oxidative metabolism in the electron transport chain.
    Ray has written about how these ROS are crucial biomarkers of proper mitochondrial respiration, and how cancer cells do everything possible to inhibit the generation of these ROS by surrounding themselves with reduced glutathione and NADPH. When supplements that inhibit the PPP pathway OR restore mitochondrial activity and thus ROS production were administered, the pathology reverted to normal. The in vivo model to treat the disease by restoring oxidative metabolism used menadione, which is vitamin K3. Menadione metabolizes to vitamin K2 (MK-4) in the body but menadione itself happens to be fairly toxic, so supplementing vitamin K2 directly is a much better approach. The human equivalent dose of menadione was 0.85mg/kg and treatment duration was just 9 days. This is very close to the 45mg daily (1mg/kg) of vitamin K2 (MK-4) used as an osteoporosis drug in Japan.
    The second treatment option was with 6-aminonicotinamide, which is a close relative of niacinamide / nicotinamide and is a specific inhibitor of G6PD. Plain nicinamide is also a potent inhibitor of G6PD and raises NAD/NADH ratio, which has additional benefits for conditions like RA.
    The effective concentration of 6-AN was 50uM. Assuming niacinamide has the same/similar effects, this concentration is achievable in humans by ingesting about 250mg - 300mg niacinamide. Also, as the study hints, combining niacinamide and vitamin K2 may be even more effective than using either one alone.
    Another possible therapeutic agent is methylene blue, since it can both oxidize NADPH and reduced glutathione AND also stimulate mitochondrial activity and thus the generation of ROS. Thus, methylene blue can combine the effects of both vitamin K and niacinamide.
    Finally, the study emphasizes the reversibility of RA, in light of it being a metabolic disease. Given that the same metabolic pathology is also present in conditions like diabetes, MS, and cancer, I wonder what the implications of this study are for those conditions as well.

    Important Metabolic Defect Identified In Immune Cells Of Rheumatoid Arthritis Patients | Scope Blog
    Restoring oxidant signaling suppresses proarthritogenic T cell effector functions in rheumatoid arthritis | Science Translational Medicine

    "...The cardinal feature of naïve CD4 T cells is the ability to massively proliferate when encountering antigen. When transitioning from naïve to effector status, T cells expand 40- to 100-fold within days (5), making them highly dependent on energy and biosynthetic precursors (6). Resting lymphocytes rely on oxidative phosphorylation and fatty acid breakdown, but upon activation switch to aerobic glycolysis and tricarboxylic acid flux, designating glucose as the primary source for ATP generation in activated lymphocyte. Anabolic metabolism of glucose provides not only energy but also macromolecular building blocks for the exponentially expanding biomass, typically by shunting glucose into the pentose phosphate pathway (PPP) (7). In the first rate-limiting step of the PPP, glucose-6-phosphate dehydrogenase (G6PD) oxidizes G6P to 6-phosphogluconolactone to generate five-carbon sugars (pentoses), ribose 5-phosphate, a precursor for nucleotide synthesis, and NADPH (reduced form of nicotinamide adenine dinucleotide phosphate), one of the cell’s principal reductants. As an electron carrier, NADPH provides reducing equivalents for biosynthetic reactions and by regenerating reduced glutathione, protects against reactive oxygen species (ROS) toxicity. Cytoplasmic NADPH is an absolute requirement to convert oxidized glutathione to its reduced form (GSH), which is converted back when hydrogen peroxide is reduced to water."

    "...Oxidative stress results from the action of ROS, short-lived oxygen-containing molecules with high chemical reactivity toward lipids, proteins, and nucleic acids. Until recently, ROS were regarded as merely damaging agents, but are now recognized as second messengers that regulate cellular function through oxidant signaling (8, 9). Cells can produce ROS in several of their organelles and possess specialized enzymes, such as the family of NADPH oxidases (NOX), to supply fast and controlled access. Quantitatively, mitochondria stand out as persistent ROS suppliers, with the respiratory chain complexes I and III releasing superoxide into the mitochondrial matrix and the intermembrane space (9, 10). It is incompletely understood how redox signaling affects T cell proliferation and differentiation and how cell- internal ROS relate to pathogenic T cell functions."

    "...The current study has investigated functional implications of metabolic and redox dysregulation in RA T cells. We find that RA T cells fail to properly balance mitochondrial ROS production and the cellular antioxidant machinery. Molecular studies place excessive activity of G6PD at the pinnacle of abnormal T cell regulation in RA and provide a new paradigm for the connection between metabolic activities, abnormal proliferative behavior, and proinflammatory effector functions. Mechanistically, PPP hyperactivity oversupplies RA T cells with reducing equivalents, increasing NADPH, and depleting ROS. This insufficient oxidative signaling prevents sufficient activation of the cell cycle kinase ataxia telangiectasia mutated (ATM) and allows RA T cells to bypass the G2/M cell cycle checkpoint. ATM deficiency shifts differentiation of naïve CD4 T cells toward the T helper 1 (TH1) and TH17 lineages, creating an inflammation-prone T cell pool. Several metabolic interventions are able to rebalance glucose utilization away from the PPP toward glycolytic breakdown, easing reductive stress and preventing hyperproliferation and maldifferentiation of RA T cells. Such interventions represent possible drug candidates for anti-inflammatory therapy."

    "...The PPP supplies reducing equivalents for macromolecule synthesis, the building blocks for new cells, rendering naïve CD4 T cells particularly sensitive to changes in proliferative metabolism. To examine whether excessive G6PD activity affects T cell proliferation, we treated RA T cells with the G6PD inhibitor 6-aminonicotinamide (6-AN). Preventing glucose entry into the PPP profoundly reduced cellular proliferation (Fig. 2A) and also changed intracellular ROS levels (Fig. 2B). Upon 6-AN treatment, ROS levels doubled, and in parallel, proliferative activity decreased. G6PD inhibition corrected the spontaneously elevated division indices of RA T cells (Fig. 2A). G6PD’s critical role in regulating T cell proliferation was confirmed by gene-specific RNA interference. Transfection of two distinct small interfering RNAs (siRNAs) significantly reduced G6PD protein expression (fig. S4). G6PD knockdown in RA T cells reduced intracellular NADPH and GSH concentrations, increased ROS levels, and normalized division indices (Fig. 2C)."

    "...We evaluated the synthetic naphthoquinone menadione, which is reduced into an unstable semiquinone and generates ROS when formed into a quinone. Treatment of T cells with menadione increased cellular ROS levels (Fig. 3) and resulted in ATM dimerization and pATM formation (Fig. 7, A and B). Combination of the ATM inhibitor KU-55933 with menadione treatment did not prevent ATM dimer assembly (Fig. 7B), but, as expected (15), blocked ATM phosphorylation (Fig. 7B). Menadione-induced restoration of ATM activation enabled pChk2 accumulation; this effect was disrupted when ATM phosphorylation was inhibited (Fig. 7B)."

    "...To evaluate the impact of ROS restoration on the arthritogenic potential of RA T cells, we tested two ROS-inducing reagents in the human synovium chimeras. Menadione raises ROS levels (Fig. 3I) through redox cycling. Buthionine sulfoximine (BSO) inhibits gamma-glutamylcysteine synthetase, lowers tissue glutathione (GSH) concentration, and consequently elevates intracellular ROS levels (fig. S7). Synovium-engrafted NSG mice were adoptively transferred with T cells derived from untreated or high-disease activity RA patients, and mice were treated with optimized doses of either menadione or BSO. Treatment with both ROS inducers had a beneficial effect on synovitis (Fig. 7D). Transcription factors (T-bet and RORγ) driving proinflammatory T cells were effectively down-regulated, IFNγ and IL-17 were reduced, whereas FoxP3 was spared. RANKL expression responded to both treatments (Fig. 7, D and E), as did the inflammatory cytokines TNF-α, IL-1β, and IL-6. Menadione had more powerful effects than BSO. Immunohistochemical analysis of RANKL expression confirmed that tissue-infiltrating T cells were almost all RANKL+ in the control arm but lost RANKL expression after menadione and BSO treatment. Both menadione and BSO were able to correct the spontaneous hypermobility of RA T cells in Transwell migration assays (Fig. 7F). Overall, offsetting reductive stress in RA T cells effectively suppressed synovial inflammation."

    "...CD4 effector T cells are major drivers of abnormal immunity in RA by sustaining chronic synovitis and supporting autoantibody production. Deriving from infrequent naïve precursor cells, such pathogenic T cells had to clonally expand and functionally differentiate. Here, we demonstrate that proliferative behavior and functional differentiation are critically determined by metabolic adaptations of the naïve precursor cells. Specifically, naïve CD4 T cells from RA patients are metabolically reprogrammed, favoring NADPH production over ATP generation. Excess NADPH supplies the cell with excess reduced glutathione and depletes ROS, effectively exhausting the cell’s ROS pool and weakening ROS-dependent signaling. Such reductive stress fastens the T cells’ cell cycle progression, as they skip the G2/M cell cycle checkpoint because of insufficient ATM activation. Constitutive ATM insufficiency in naïve RA T cells and pharmacologic ATM insufficiency in healthy T cells accelerate their conversion into effector memory T cells. ROS loss and ATM insufficiency promote T cell maldifferentiation into IFN-γ and IL-17 effector cells. These abnormalities are reversible by replenishing the ROS pool with the naphthoquinone menadione, by disrupting synthesis of the ROS quencher glutathione, or by blocking glucose shunting into the PPP. These pharmacologic interventions not only localize the pinnacle defect to excessive PPP utilization but also provide a framework for entirely new anti-inflammatory strategies."

    "...Naïve CD4 T cells from RA donors were differentiated in a polarizing cytokine cocktail in the absence and presence of either menadione or 6-AN, two interventions able to counteract the shift toward reductive elements. Menadione corrected the bias of RA T cells to develop into IFN-γ producers (Fig. 7C). The G6PD inhibitor 6-AN provided an at least equally successful intervention to down-regulate T cell IFN-γ production (Fig. 7C). Blocking G6PD activity reduced the frequency of IFN-γ–producing T cells to less than 15%."

    "...An important notion of the current study is the reversibility of the metabolic wiring (Fig. 7), effectively preventing hyperproliferation and maldifferentiation in vitro and in vivo. ROS induction via menadione restored ATM signaling and suppressed IFN-γ induction, shifting Tcell differentiation toward an anti-inflammatory phenotype. Menadione, known as vitamin K3, is used as a nutritional supplement (40). Large doses can cause hemolytic anemia in G6PD-deficient individuals, emphasizing the mechanistic link between PPP utilization and redox balance. Interfering with production of the ROS generator BSO proved effective in inhibiting synovial inflammation. Pharmacologic and genetic G6PD inhibition confirmed that the pinnacle defect lies in the excessive induction of this rate-limiting enzyme for the PPP. 6-AN treatment was even more effective in down-regulating proinflammatory cells, opening the door to targeting autoimmune T cells by metabolic interference. Directing such intervention to naïve T cells promises a new concept of preventing autoimmunity instead of blocking terminal inflammatory pathways."

    Nicotinamide, a glucose-6-phosphate dehydrogenase non-competitive mixed inhibitor, modifies redox balance and lipid accumulation in 3T3-L1 cells. - PubMed - NCBI
    "...KEY FINDINGS: G6PD mRNA levels increased at day 4 of adipocyte differentiation, whereas G6PD activity progressively increased at days 4 and 6 of differentiation and was reduced in adipocytes. Concomitantly, ROS, reducing power and lipid accumulation increased gradually as the preadipocytes matured into adipocytes. High glucose increased the activity of G6PD, which coincided with an increase in ROS, reducing power and lipid accumulation. All of these changes are prevented by nicotinamide, with the exception of lipid accumulation in adipocytes. Nicotinamide increased IDP activity without affecting NADPH levels. Lastly, nicotinamide inhibited G6PD in a non-competitive mixed way."

    Methylene blue directly oxidizes glutathione without the intermediate formation of hydrogen peroxide. - PubMed - NCBI
    http://www.jbc.org/content/260/28/15168.full.pdf
    "...Methylene blue stimulates the oxidation of glutathione in red blood cells in vitro and in vivo. This oxidation has been attributed to hydrogen peroxide that is generated from the autooxidation of leucomethylene blue arising from the reduction of methylene blue by NADPH. In this report we present evidence that methylene blue directly oxidizes glutathione and that oxidation of glutathione by hydrogen peroxide is a secondary reaction. Moreover, superoxide dismutase has no effect on the oxidation. Under aerobic conditions, methylene blue oxidizes glutathione 30 times faster than the spontaneous autooxidation of glutathione. Under anaerobic conditions the stoichiometry of the reaction of methylene blue with glutathione supports a direct chemical reaction. The reaction rates between glutathione and methylene blue suggest a second order reaction over the conditions tested. That neither oxygen radical formation nor significant amounts of hydrogen peroxide are produced by methylene blue, even in the presence of added glucose, is further confirmed by the failure to detect significant amounts of lipid peroxidation products, or hemolysis, in red blood cells incubated with the dye."
     
  2. jaa

    jaa Member

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    This is very interesting stuff. I don't have anything to add other than thanks for posting.
     
  3. Drareg

    Drareg Member

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    Great study ,thanks.

    What's your take on G6PD deficiency ? It can cause hemolytic anemia etc.
    G6PD deficiency can be asymptomatic, it's common enough?

    Peat speaks about hemolytic anemia in the Irons Dangers,I'm still looking if he mentions it elsewhere.







     
  4. OP
    haidut

    haidut Member

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    The only true G6PD deficiency seems to be hereditary. I think is very rare, and the doctors I have talked to have never heard of it.
     
  5. Drareg

    Drareg Member

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    If somebody had it,what angle would you take to treat baring in mind Peats views mixed with your view also?
     
  6. OP
    haidut

    haidut Member

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    I guess taking substances that increase RBC count. In males, vitamin K, testosterone, DHEA, copper, etc can do that pretty well. I think lower ferritin also raises RBC count as an adaptive measure to perceived iron deficiency and thus lower ability to carry oxygen in the blood.
     
  7. Goat-e

    Goat-e Member

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    Fascinating, thanks for posting this.

    I have so-called seronegative RA (basically all the symptoms but no raised RF in blood tests) so it will be interesting to see if I respond the same way as the test subjects. The fact that glucose is getting shunted into the wrong pathway probably goes a long way to explaining the fatigue which comes with this condition, I'd never been able to quite work out why that is such a feature of the disease (though oddly not one talked about that much).

    I originally came across Ray Peat (and this forum) when I was trying to work out what had gone so wrong that four years ago at age 36 I was waking up not able to make a fist with either hand, so inflamed and painful were my joints. And it was spreading to other joints so I needed to do something fast. But in investigating it turned out my daytime temps peaked at 35.7, so, figuring I wasn’t going to be able to achieve anything until my body was working better, I cast aside my focus on the RA and concentrated on raising my metabolism which I’ve finally managed to some extent by going T3 only in three largish doses a day (anything less than 12.5mcg at a time has zero effect). With that side of things working better now I’m wanting to get to the bottom of the RA again so this post is timely!

    Interestingly there are people who treat RA with lose dose Minocycline as they believe it’s a Mycoplasma infection, but maybe given that Mino is a similar molecule to vitamin K (IIRC) that’s why it seems to work for some (worked for me for a bit but then stopped). One thing which did give me complete (and I really mean complete) remission of symptoms for a few months before it also stopped working was 3-5g of Taurine at night.

    I’ve also had a mitochondrial function test which showed I had poor NADH/NAD+ recycling so this study is looking more relevant all the time.

    So I'm going to try this. The dosage, given I’m 80kg would be 50 drops of Kuinone - is that right as it seems a lot? Is there anything I potnetially need to be aware of taking that much K?
     
  8. OP
    haidut

    haidut Member

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    Have you looked into pregnenolone? It was used for rheumatoid arthritis before cortisol stole the show. The vitamin K given was through the GI tract. So using Kuinone you should be getting much better absorption something to the effects of 1 drop Kuinone = 4-5 drops Thorne. So you should be able to get away with 10 drops Kuinone daily.
     
  9. jaa

    jaa Member

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    Do you think there's much of a difference between applying thorne and then applying a DMSO based supplement like Pansterone on top vs applying Kuinone? Or is that inadvisable for reasons I'm not aware of?
     
  10. OP
    haidut

    haidut Member

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    I think that approach would help increase absorption. Still, it probably won't come close to Kuinone since the Thorne vitamin K is dissolved in oil and the DMSO mixes with oil but does not solve it. No harm in trying though.
     
  11. jaa

    jaa Member

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    Good to know. Thanks.
     
  12. Goat-e

    Goat-e Member

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    Thanks for the info.

    Yes, I've tried Pregenenolone but whilst it helped with stress and raised temps a bit it sadly didn't do anything for joint stiffness. Ray also wrote about Progesterone for various types of arthritis but, other than knocking me out (which is fun in itself;)), it again didn't seem to have any effect.

    I've also tried Niacinamide, there was a doctor in the 50's I think who treated RA with small doses spread throughout the day and clearly had a lot of success - I found that it just gave me really annoying headaches, even with extra sugar.

    So I'm all poised to try the Kuinone, just waiting for it to arrive. Will reoprt back.
     
  13. OP
    haidut

    haidut Member

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    The human studies with RA and niacinamide did not use low doses. They used 3g - 5g a day. That dose may be needed to raise NAD, which very low in RA patients and is kept low by the enzyme PARP, which the body used to try to repair the joint damage and that enzyme potently depletes NAD. Higher doses niacinamide not only server as precursor to NAD but also inhibit PARP and thus prevent its depletion. So, not sure how much you are taking but you may want to revisit this.
    How much pregnenolone did you try? The arthritis trials were again using higher doses. The minimum effective doses was 200mg and the maximum was 500mg beyond which no benefit was observed. It also took about a month for benefits to manifest. This is unlike cortisol's effects, which are uncontrollably potent and quick, and the reason is that pregnenolone actually repairs some of the damage done by RA and that takes time to see. Cortisol simply shuts down the symptomatic pathways. That, and it melts your muscles, brain, skin, and thymus.
     
  14. narouz

    narouz Member

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    Very interesting stuff, haidut. Thanks!
    I'm gonna have to order some Kuinone and give it a test drive. :>)
     
  15. Goat-e

    Goat-e Member

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    I tried 200mg pregnenonlone a day split into two doses for a three weeks. So it looks like it fell a bit short. With the niacinamide I did work up to 4g but I just couldn't get past the headache which became near constant, and which only went away when I stopped (I could revist this now that I seem to have my t3 dosage dialed in a bit better).

    My Kuinone arrived today so I've got to decide whether to revist the Preg at higher dose for a month or start in with the Kuinone. Or I could do my usual trick of barrelling in with everything all at once and confusing the issue;).
     
  16. Amazoniac

    Amazoniac Member

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    I wonder if casein's fame of triggering autoimmune conditions is because of its ability to stimulate anabolism, and for that to happen the problematic parts are being deconstructed too rapidly and so inflammation occurs..
     
  17. Centsmom

    Centsmom Member

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    How have these worked for you
     
  18. Simba1992

    Simba1992 Member

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    Hello Goat-e,
    So curious to hear if you had any help from kuinone:) I am seronegative RA too and am taking Preg and just ordered Methyl blue. Did you ever try that? Funny with B3 I got a headache from that too. I am taking LDN and am on AIP diet and aspirin, Vit A and Hemp oil. Have you found anything that really helps?I haven't been using any RA meds so far. Diagnosed Dec. 2015. Very thankful for any help, Simba
     
  19. Goat-e

    Goat-e Member

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    Hi Simba,

    I've managed to get rid of symptoms completely, no inflammation or morning stiffness at all. It's hard to say specifically what helped, other than the broader goal of getting my metabolism to work properly again. That was a long road, trying the various strategies Peat recommends. I also no longer believe in the 'autoimmune' classification, what I think was happening with me was that my body was stressed, the stress hormones were breaking down muscle to get enough glucose and then my immune system was reacting to the cellular debris causing the inflammation and stiffness (search the forum for Cunliffe for more on this view of the immune system, and listen to this A Bioenergetic View Of Autoimmunity [Generative Energy #12]).

    You say you're doing AIP by which you mean Auto Immune Paleo? My troubles actually started whilst doing Paleo, and although this doesn't prove anything, the first dr who diagnosed my RA had another patient, similar age to me, who was also doing Paleo and then got RA... Basically Paleo will stress your system, and whilst that can initially seem to improve things, it very quickly ends up going downhill.

    That's the long answer, the short answer is that by taking the right level of thyroid, making sure I have ample sugars in my diet and a good amount of protein has worked wonders. It can take awhile to get it all dialed in though, but it can be done! And it all starts with forgetting about 'RA' as much as possible to begin with assessing your basic metabolic function (temp and pulse) to know where you are. From there you can work out a strategy, test it for a few weeks and then reassess. You'll get quite skilled at this as you go on, and although it will seem slow at the start things will pick up as parts of the puzzle gradually fall into place.
     
  20. Simba1992

    Simba1992 Member

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    Thank you so much Jake
    I am so very happy to hear that you in fact have gone through exactly the same process as I have (it has been a lonely hard journey)and true enough I came to a point where I was going downhill fast, but I was hard set on not taking the toxic meds. Then I found Ray Peat and everything started to make sense. I was in fact hypoglycemic and hypothyroid. My liver did not store glucose and cortisol was eating up my tissues. At last I can really follow the needs of my body and know when carbs are needed. My body temperature slowly reaching a normal state. For one month now I have adjusted my diet, actally possible to keep some good things from AIP, taking aspirin in the morning and evening, supplementing with Vit A, K2, B3 calcium, copper, preg, progesterone, hempoil and did order Methyl blue. Actually I am quite excited with how much better I feel! It is not an easy task to start from zero trying to make sense of all Mr. Google has to offer. Thank you again
     
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