tryingtohelp2014

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  1. Repairing the long-term damage from Accutane

    Dysautonomia brought me this.... I think we have an acquired form of this that produces so many different symptoms. Moreover we cannot detoxify. Not unlike the women who develop POTS after getting the Gardasil vaccine. High dose Thiamine has been recommended as a treatment. Thiamine is needed for NADPH (the first step is isotretinoin catabolism) 60% comes from the pentose pathway Thiamine is needed to produce stomach Acid (think SIBO , bacterial imbalance, Chrons etc) Thiamine is needed for collagen formation Thiamine is needed to produce ATP (think ER dysfunction/ROS/detoxification) Thiamine is needed for estrogen clearance in the liver (along with riboflavin) estrogen dominance, low T LH FSH etc. Thiamine is needed to recycle GSH. Thiamine is needed in steroid formation Thiamne deficiency is noted in low ceruloplasim results. The test needed for this is an erythrocyte transketolase test. normal blood tests are not accurate. ALLTHIAMINE is preferred. i have been using the topical. I tested high for estrogen last summer. I believe i had an estrogen induced form of cholestasis. Ive had high bilirubin for 20 years since accutane. In the past 2 weeks, the whites of my eys have been totally clear, and ill be getting a confirming blood test. Taurine did this for a few days..but it was hit and miss. We could have downregulated receptors, and the full effect could take a while to fix. Magnesium and B1 should be taken together Could accutane be the trigger like Gardisal? something very very interesting here , and it related to P53 and FOX01 Bodo Melnik published something last month.... p53: key conductor of all anti-acne therapies Bodo C. Melnik https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5606086/ This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin’s sebum-suppressive effect. Anti-androgens attenuate the expression of miRNA-125b, a key negative regulator of p53. It can thus be concluded that all anti-acne therapies have a common mode of action, i.e., upregulation of the guardian of the genome p53. Immortalized p53-inactivated sebocyte cultures are unfortunate models for studying acne pathogenesis and treatment. Keywords: Acne therapy, Apoptosis, Immortalized sebocytes, p53, SV40, TRAIL THIAMINE...... In contrast, an increased number of thiamine transporters are observed in cells that overexpress thiamine transport genes (mTHTR-1) and in cells that are exposed to conditions that induce DNA damage or p53 activation.56 Thiamine diphosphate inhibits p53 binding, and thiamine inhibits intracellular p53 activity.57 Thiamine treatment significantly decreases p53 expression in the cultured retinal neurons from diabetic rats.58 These observations suggest that the pro-apoptotic transcription factor p53 is activated by cellular damage in HIV infection and that thiamine ameliorates these effects. Go to: Abstract This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin’s sebum-suppressive effect. Anti-androgens attenuate the expression of miRNA-125b, a key negative regulator of p53. It can thus be concluded that all anti-acne therapies have a common mode of action, i.e., upregulation of the guardian of the genome p53. Immortalized p53-inactivated sebocyte cultures are unfortunate models for studying acne pathogenesis and treatment. Thiamine antagonists trigger p53-dependent apoptosis in differentiated SH-SY5Y cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5587765/ Go to: Abstract This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53. p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin’s sebum-suppressive effect. Anti-androgens attenuate the expression of miRNA-125b, a key negative regulator of p53. It can thus be concluded that all anti-acne therapies have a common mode of action, i.e., upregulation of the guardian of the genome p53. Immortalized p53-inactivated sebocyte cultures are unfortunate models for studying acne pathogenesis and treatment.
  2. Repairing the long-term damage from Accutane

    I've think ive made a breakthru! I've solved my intrahepatic cholestasis problem. 20+ years of jaundice solved almost overnight with combination of two supplements. My eyes are white, and continue to remain for a few weeks now. give me some time to write it up. MARIO.... NADPH, ATP, ESTROGEN INDUCED CHOLESTASIS CLEARANCE.
  3. Repairing the long-term damage from Accutane

    Again, another detox program that has nothing to do with what accutane actually does in the body. LOOK at this chart: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2634674/figure/fig4/ this is literally what accutane does inside your cells. it decreases copper, not increase. its very simple. for those of you who dont understand what "effluxed" means... Efflux is defined as something that is defined as flowing out or the process of flowing out. When water is flowing out of a river inlet and into a larger stream that is nearby, this is an example of efflux. The water that is flowing out of a river and into a larger body of water is an example of efflux. ATRA "effluxes" copper out of the cell.
  4. Repairing the long-term damage from Accutane

    Title Modification of vitamin A metabolism in rats fed a copper-deficient diet. Author Rachman F; Conjat F; Carreau JP; Bleiberg-Daniel F; Amedee-Manesme O Address INSERM U 56, Universit´e Paris-Sud, H^opital d'Enfants, Bic^etre, France. Source Int J Vitam Nutr Res, 57(3):247-52 1987 Abstract The liver is the main storage site of vitamin A and copper. Inverse relationships between copper and vitamin A liver concentrations have been suggested. We have investigated the consequences of a copper-deficient diet on liver and blood vitamin A storage in Wistar rats. Animals were fed either a copper-deficient diet for 45 days from weaning, or an identical diet containing adequate amounts of copper. Concentrations of vitamin A were determined by isocratic high performance liquid chromatography using UV detection. We have observed in the liver of the rats fed a copper-deficient diet a significantly higher mean level of retinyl esters (148 +/- 37 micrograms/g of liver) and retinol (3.3 +/- 1.4 micrograms/g of liver) compared to the mean concentration of the retinyl esters (53 +/- 8.5 micrograms/g of liver) (p less than 0.01) and retinol (1.4 +/- 0.5 micrograms/g of liver) (p less than 0.01) in controls. Opposite results were observed in the serum of the group fed a copper-deficient diet as these rats had a significantly lower level of retinol (22 +/- 4 micrograms/100 ml) compared to the mean concentration in the controls (64 +/- 20 micrograms/100 ml) (p less than 0.01). These findings suggest that a copper-deficient diet may cause defective transport of vitamin A from liver to blood. This experimental model may be useful to further investigate unusual liver vitamin A and copper concentrations observed in children during various hepatobiliary diseases. again, if you feel worse on copper , this could be a confirmation of the problem...not the problem itself. http://ajcn.nutrition.org/content/22/8/1017.extract https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0007114572000066 Moore (1969, 1970) has pointed out that retinol and copper behave similarly in being stored preferentially in the liver, and being carried in blood plasma in combination with similar, but different a,-globulins (Glover & Walker, 1964; Kanai, Raz & Goodman, 1968). Otherwise the interrelationships of these two nutrients are often inverse. Physiological or pathological factors that tend to increase the concentration of one of them often decrease the concentration of the other. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2634674/figure/fig1/
  5. Repairing the long-term damage from Accutane

    He has said absolutely nothing to back up anything. His cure is all common knowledge stuff....its not going to remove accutane /ATRA from the liver or fat cells. His explanation of copper/zinc is just internet re-hash. he has no clue about the actual levels. hair mineral analysis is quackery. from every scientific paper ive read, vitamin A is antagonistic of copper. they are inversely correlated. We took shit tons of Vitamin A... how are we copper toxic? Remember accutane was a chemo therapy drug first that was shown to be much more effective when copper was limited. .... This information indicates that any factor that antagonizes copper retention can be considered as having anti-viral properties. Those that are synergistic such as vitamin D, B1, B12, and B10, which enhance copper retention, can be considered as having anti-bacterial properties (see figure 1 and 2). As an example, vitamin A, which is considered to be an anti-infectious vitamin, can specifically be categorized as anti-viral. This is also true of vitamin C and zinc. However, zinc, vitamin C, and vitamin A are mutually antagonistic to copper; if taken in excessively high dosages by individuals with a copper deficiency, they can actually promote infectious processes — especially those of bacterial origin (This could also be why many people don't get sick after taking accutane . its like taking hi doses of Zinc... accutane (hi dose vitamin A) is anti viral bby REDUCING available copper ) Nutrients Synergistic to Copper Rarely does a single nutrient deficiency develop exclusively. Other nutritional deficiencies and excess are always involved. Referring to figure 1 and 2, we can see the potential of vitamin and mineral toxicity that can develop in the presence of copper deficiency. As an example, the need for vitamin A, C, B6, B3, and B5 is reduced in a copper-deficient state. Conversely, hypervitaminosis of most of these vitamins can be reduced by supplying adequate amounts of copper. We can see particularly that the adverse effects of hyper-vitaminosis A can be decreased by copper supplementation. Synergistic vitamins, those whose requirements are increased by copper deficiency, include vitamin D, B1, B12, C, and folic acid (B10). Supplementation of synergistic vitamins can aid in reducing the effects of copper deficiency and in restoring copper balance. As an example, increased adrenal corticosteroid production decreases copper retention56 as well as antagonizes vitamin D metabolism.57 Vitamin D can antagonize the effect of excessive corticosteroid production, thereby improving copper retention.
  6. Repairing the long-term damage from Accutane

    Joint Pain... has anyone tried xanthine inhibitors? Allopurinol Gout and vitamin A intoxication: is there a connection? Mawson AR1, Onor GI. Author information Abstract Several lines of indirect evidence implicate vitamin A intoxication, associated mainly with impaired renal function, in the etiopathogenesis of gouty arthritis. The enzyme xanthine oxidase is involved not only in the conversion of xanthine to uric acid but also in that of retinol to its more toxic metabolite, retinoic acid. Retinoic acid should therefore be present in high concentration in hyperuricemic states. Isotretinoin use for acne vulgaris is associated with increased serum uric acid levels. Solak B1, Erdem T1, Solak Y2. Author information Abstract A few previous case reports related vitamin A and retinoid use with elevated serum uric acid (SUA) levels. Recently, a population based study showed an independent positive correlation of serum retinol with SUA levels. Despite increasing importance of SUA in a number of disease states, no study has examined the association between retinoids and SUA. We aimed to evaluate the effect of pharmacologic dose isotretinoin on SUA level. This was a cohort study in which 51 consecutive adult patients with severe acne vulgaris who were prescribed oral isotretinoin treatment (0.5 mg/kg) were included. Dermatologic examination was performed and SUA levels were measured at study inclusion for each participant, and then repeated at the first and second months of therapy. SUA levels at first month and second month were significantly higher than baseline SUA levels (p: 0.001, 0.007, respectively). SUA levels at second month were higher than SUA levels at first month, but the difference did not reach statistical significance. This study is the first to show that pharmacologic dose oral isotretinoin treatment significantly increased SUA levels. Since hyperuricemia is associated with renal disease, hypertension, atherosclerosis and metabolic syndrome as well as gout, it is important for the dermatologist to be aware of this potential adverse effect of isotretinoin particularly in vulnerable patients. Milk xanthine oxidase (xanthine: oxygen oxidore-ductase; XO; EC 1.1.3.22) was found to catalyze the conversion of retinaldehyde to retinoic acid. The ability of XO to synthesize all trans-retinoic acid efficiently was assessed by its turnover number of 31.56 min−1, determined at pH 7.0 with 1nM XO and all trans-retinaldehyde varying between 0.05 to 2μM. The determination of both retinoid and purine content in milk was also considered in order to correlate their concentrations with kinetic parameters of retinaldehyde oxidase activity. The velocity of the reaction was dependent on the isomeric form of the substrate, the all trans- and 9-cis-forms being the preferred substrates rather than 13-cis-retinaldehyde. The enzyme was able to oxidize retinaldehyde in the presence of oxygen with NAD or without NAD addition. In this latter condition the catalytic efficiency of the enzyme was higher. The synthesis of retinoic acid was inhibited 87% and 54% by 4μM and 2μM allopurinol respectively and inhibited 48% by 10 μM xanthine in enzyme assays performed at 2μM all trans-retinaldehyde. The Ki value determined for xanthine as an inhibitor of retinaldehyde oxidase activity was 4 μM.
  7. Repairing the long-term damage from Accutane

    i have gilberts syndrome as well. well, just high bilirubin. i dont believe i ever had high bilirubin before taking accutane though. so its a chicken and the egg question. if you have gilberts , you conjugate at 30% the normal rate. the same UGT enzyme that conjugates bilirubin is also responsible for the glucuronidation of accutane. PHASE 2 ... read up on NRF2 every single person who has ever reported feeling better has unknowingly promoted the NRF2 response. either from water fasting, TUDCA, CBD oil, etc etc etc. NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. https://www.ncbi.nlm.nih.gov/pubmed/18845239 accutane has been proven to shut down the NRF2 response NFE2L2 Nuclear factor (erythroid-derived 2)-like 2 Inhibited by retinoic acid via RARalpha resulting in lack of expression of Nrf2 target genes
  8. Repairing the long-term damage from Accutane

    2 avocados a day making you feel better? https://www.healthaliciousness.com/articles/high-copper-fruits.php http://www.dailymail.co.uk/health/article-4109776/Could-salad-contaminated-Doctor-warns-toxic-levels-copper-lurking-kale-avocado-coconut.html The role of copper in biological phenomena that involve signal transduction is poorly understood. A cellular model of neuronal differentiation has been utilised to examine the requirement for copper during nerve growth factor (NGF) signal transduction that leads to neurite outgrowth (Birkaya and Aletta, 2005). NGF increases cellular copper content within 3 days, whereas copper chelators reduce the effects of NGF on neurite outgrowth and copper accumulation (Birkaya and Aletta, 2005). Our data supports a model of malignant neural cells requiring higher intracellular copper levels for viability, and that retinoid-induced neuritic differentiation of neuroblastoma cells causes intracellular copper depletion. In non-neuronal cells ATP7A regulates copper homeostasis by translocating copper from the trans-Golgi network to the plasma membrane, in response to an increased copper load. In Menkes disease a defect in the ATP7A protein leads to a reduced transport of copper from the intestine into the circulation and central nervous system, as well as reduced transport of copper into the Golgi apparatus. In our studies, a significant increase in copper efflux, and decrease in copper uptake occurred over 8 days of retinoid treatment. Thus, reduction in cellular copper levels directly contributes to the retinoid therapeutic effect. The retinoid anti-cancer effect is mediated by effects on ATP7A and intracellular copper We next examined the hypothesis that ATP7A mediates the effects of RARβ2 on neuroblastoma cells by its effects on intracellular copper metabolism. We measured copper efflux in neuroblastoma cells (BE(2)-C and SH-SY5Y) which were pre-treated with 10 μm aRA over a time course of 8 days, then loaded with radioactive 64Cu. After 64Cu loading, cells were washed, then incubated in normal growth media to allow copper efflux over a short 4 h time course. In both cell lines there was a higher copper efflux in cells pre-treated with aRA at 4 h (Figure 4A). As the retinoid treatment affects the cell number at the end of the growth period, 64Cu uptake was standardised against cell viability, as assessed by the Alamar Blue assay (Figure 4B). Retinoid treatment resulted in a marked decrease in 64Cu accumulation in both SH-SY5Y and BE(2)-C cells. Forced downregulation of ATP7A reduced copper efflux and increased viability of retinoid-treated neuroblastoma cells. Copper supplementation enhanced cell growth and reduced retinoid-responsiveness, whereas copper chelation reduced the viability and proliferative capacity. Taken together, our data demonstrates ATP7A expression is regulated by retinoic acid receptor β and it has effects on intracellular copper levels, revealing a link between the anticancer action of retinoids and copper metabolism. http://www.nature.com/bjc/journal/v100/n1/full/6604833a.html?foxtrotcallback=true
  9. Repairing the long-term damage from Accutane

    mario.... your latest post on fm03. have you seen this? the gene upregulated the most in the skin from topical RA is FM02. OVER 50X! WHY? Upon analysing the gene array manually for genes affected more than 10-fold by RA without RA was found to upregulate 8 genes more than 10-fold. One of these was FMO, which was upregulated 50.17-fold after 24-h stimulation with RA. FMO has been found to be present in human skin [59]. It is known to metabolize xenobiotics, but to our knowledge, not known to metabolize retinoids. http://onlinelibrary.wiley.com/doi/10.1111/ics.12121/full
  10. Repairing the long-term damage from Accutane

    read what this guy says about 5AR. and reducing joint pain and for increasing testosterone. we used a 5AR1 inhibitor for so long, then went cold turkey. 1. could we be experiencing a sensitized 5AR enzyme now? 2. is that why some people experience relief from starting 5AR inhibitors again? 3. too much 5AR = low testosterone and other hormones? http://parityhedgesystemcraps.blogspot.com/2014/05/how-to-stop-losing-hair-and-regrow-it.html The Power of 5ARAlpha 5 Reductase is an enzyme that you don't have much of in your teens and early 20's but by the time you get to your late 30's, early 40's you are making a disproportionate amount of it. This is the hormone that is responsible for clearing out your testosterone and splitting it into dihydrotestosterone creating DHT. This may be all clear and fine when you don't have much of this hormone in your early 20's but when you move foward 15 years there is actual damage that occurs in your body from having too much dihydrotestosterone (DHT) circulating in your body:1. It clears too much testosterone out of your system and basically starts turning you into a balless wonder. Without testostoerone at the levels you had in your youth, you start gaining wieght. Your muscle mass starts to shrink. You aren't as confident and bold as you used to be, not such a go getter anymore. You have less energy, and are more tired. Sex becomes a chore. With low testosterone, you start developing stiffness and pains and arthritis.You are less of a man. Basically a whole bowl of wimpy middle aged flabby man suck. This is one of the reasons that a man's free testosterone in his system starts to drop off and medical issues start to arise like prostate cancer and heart attacks. With low test, you are going to need a damn good reason to get up out of your chair to walk into the kitchen to help someone calling you. With proper levels of testosterone, you will feel jacked enough to run through a wall. 2. 5AR causes a swollen prostate and prostate cancer. This is a big problem. Excessive DHT will cause your prostate gland to begin swelling up causing urineary and medical issues including the big C: Prostate Cancer. My father had this problem. In his 50s he had to start using the bathroom all the time and then in his 60's he was diagnosed with prostate cancer. He researched several options and one new treatment was radioactive seeds. He had radioactive seeds placed in his prostate in order to keep the cancer at bay. So far so good, god willing, hes still with me. But with radioactive material in his body. Frank Zappa the musician got prostate cancer and it killed him. I believe thats the same thing that also killed George Harrison. Its a serious issue that affects most men starting in their 40's. If you start having flow issues or have to go frequently overnight, this is probably whats starting to happen. See your doctor. Frank Zappa caught it too late.3. 5AR casues DHT which directly causes hair loss. And the ever increasing levels that are climbing in your bloodstream aren't doing you any favors as you get older. If you have androgen receptors (if your grandfather was bald on your mom's side) they are going to get filled up by these DHT molecules destroying your hairline. Please review the above Phase I section for the specifics on this. Without 5AR, your testosterone levels won't be a problem as it won't be creating any DHT. But as you reach your mid 30's you will begin to be swamped by larger amounts of the 5AR causing this problem.
  11. Repairing the long-term damage from Accutane

    riboflavin 5 phosphate ( active B2) is a natural 5AR inhibitor.
  12. Repairing the long-term damage from Accutane

    some guy on this thread mentioned taking Sulforaphane Accutane inhibits NrF2................. Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha http://www.pnas.org/content/104/49/19589.long NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity http://www.sciencedirect.com/science/article/pii/S0891584908005108 https://selfhacked.com/blog/about-nrf2-and-natural-ways-to-increase-it/ The UDP-glucuronosyltransferase (UGT) family catalyze the conjugation of a glucuronic acid to drugs, chemicals, and toxins, making them more water-soluble and readily excreted. Nrf2 has been shown to induce UGT1A1 and UGT1A6. Top Ways to Increase Nrf2 Exercise (R), LLLT (R) Fish oil/DHA (R), Vitamin D (R) Sulforaphane/Broccoli sprouts (R) -and other Isothiocyanates from cruciferous vegetables (R), Lipoic Acid Butyrate (R), Garlic (R), Curcumin (R) Luteolin (R) – luteolin is ideal because it inhibits Nrf2 in many cancer cells (R), PGC-1a (R) Calorie Restriction (R) Ketosis (R), Molecular Hydrogen (Machine) (R), Thyroid hormones (R) – make sure your thyroid hormones are up to par. Berberine (R) See this post for more on Berberine. PQQ (R), Cinnamaldehyde/Cinnamon (R), Anthocyanins (R, R2, R3) Carnitine (R), Interestingly, several widely used dietary components or supplements with medicinal properties have recently been shown to activate adaptive stress response pathways in cells. For example, sulforaphane (present in high amounts in the broccoli sprouts) (Juge et al., 2007), and curcumin (concentrated in the roots of the turmeric plant) each activate the transcription factor Nrf2 which binds to the antioxidant response element (ARE) of genes that encode antioxidant and phase 2 enzymes (Dinkova-Kostova and Talalay, 2008). Other adaptive stress response pathways activated by phytochemicals include the sirtuin – FOXO pathway (resveratrol) and the transient receptor potential - calcium pathway (Calixto et al., 2005). The mechanism of action of such phytochemicals can therefore be considered as a form of hormesis in which exposure to a low amount of a stressor triggers an adaptive response which increases resistance to more severe stress and disease (Calabrese et al., 2007).