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On 1/3/2016 at 8:11 AM, guitarman01 said:I have had liver blood test from time to time that came back normal. but based on what im reading im not sure if this is a tell all for nonalcoholic fatty liver.
would sure like to talk to josef pitha. wonder what hes up to these days?
damn. This is all related.
http://www.patentbuddy.com/Inventor/Pitha-Josef/11881333
OMFG... This JosefPitha, was kind of a big deal.
[Edited link out]
From what we understand, this will be thesecondtime in the United States that cyclodextrin alone has been used in an attempt treat a fatal disease. Over 20 years ago, cyclodextrin was used in a medical case involving a boy with severe hypervitaminosis A and cyclodextrin saved the childs life. InAddi and Cassiscase, we aretrying to save them from Niemann Pick Type C disease,afatal cholesterol metabolism disorder that is oftenreferred to as the Childhood Alzheimers. There is no cure for NPC and only one experimentaldrugtreatment. Now this promising sugar compoundthat is not a considered a drug provides us with a glimmer of hope. - See more at: [Edited link out]
I am Lajos Szente co-founder and CEO of a cyclodextrin company in Budapest, Hungary. In 1981 I worked at NIH, in Baltimore with Dr. Josef Pitha. We tried to save life of mice having a toxic lipophile in their bloodstream. We used a kind of cyclodextrin to help the animals body distribute and eliminate this toxic comopund. We succeded! Years later in Boston Childrens Hospital, Thomas Carpenter M.D. saved the life of a tween boy suffered from A-hypervitaminosis, by the same mode of administration of hydroxypropylbetacyclodextrin. Again a success! The working principle is the very same, and I am personally convinced that this, finally FDA-approved, treatment will help! My very best wishes to the little ladies and the family. If somebody knows how powerful cyclodextrins can be, it is myself. I am not only touched and amazed about everything you have done in this matter.
very truly yours,
Lajos Szente,Ph.D., D.Sc. - See more at: [Edited link out]
This Josef Pitha was a developer??????
http://www.google.com/patents/WO2004084883A1?cl=en
The studies dealing with the use of CDs with retinoids has been focused mainly on tretinoin, the all-trans form of retinoic acid. Pitha (1981) showed first that natural CDs and CD derivatives increase the aqueous solubility of retinoids, e.g. , retinol and retinoic acid. Amdidouche et al. (1989) developed a method to prepare solid tretinoin/natural -CD inclusion complexes by using a mixture of water and isopropanol. However, only 20 % of the tretinoin was in complexed form after 16 days equilibration time and evaporation of the solvent. Lin et al. have recently shown that HP--CD increases the aqueous solubility, photo-stability and oral bioavailability of tretoinin (Lin et al. 2000a,b). In addition, Wacker-Chemie has patented and sells a powder containing retinol/-CD complex for nutritional, cosmetic etc. purposes (Moldenhauer et al. 1998).
!!!!!!!!
http://www.ncbi.nlm.nih.gov/pubmed/3655980
A 2-year-old boy had signs and symptoms of chronic hypervitaminosis A. A course of increasing severity led to eventual death. A younger brother later had similar clinical features. Chicken liver spread containing up to 420 IU/g vitamin A was the likely source of intoxication. Markedly elevated circulating retinyl ester levels have persisted in the surviving sibling for 3 subsequent years despite severe restriction of vitamin A intake. A therapeutic trial of the carbohydrate-derived complexing agent 2-hydroxypropyl-beta-cyclodextrin was initiated. Circulating retinyl esters transiently increased during the infusion (from 407 to 4791 micrograms/dL), and urinary total vitamin A excretion, undetectable before infusion, increased to 23 micrograms/dL after infusion. The frequency of hypervitaminotic episodes has decreased somewhat in the 2 years since the infusion, probably related to dietary vitamin A restriction. The occurrence of this syndrome in two brothers, while a sister ingesting the same diet remains completely healthy, suggests an inherited variance in tolerance to vitamin A intake.
yikes More JosefPitha credits at the end.
http://www.sciencedirect.com/science/article/pii/0024320583903041
Rescue from hypervitaminosis A or potentiation or retinoid toxicity by different modes of cyclodextrin administration
by our guy 1983
and so I just bought some of that beta cyclodextrin on ebay. dont plan on using it till i can read about it extensively. its kind of like pushing the red button. (and il see if it even makes it here,not sure about the legality)
def going to try meth first. so much safer these days
update: maybe its not I might be reading l-methionine raises homocysteine levels by quite alot, which would not be good.
this a little off topic atm but what the hell is this?
http://www.ncbi.nlm.nih.gov/pubmed/25081735
Claritin Decreased accutane side effects?
also just read as little as 1500mg of l methionine per day can significantly raise homocysteine levels. that is kind of a bummer.
12 hours ago, Modeaa said:https://en.wikipedia.org/wiki/ Postural_orthostatic_tachycardia_syndrome
is a condition in which a change from the supine position to an upright position causes an abnormally large increase in heart rate, called tachycardia.......Many people with POTS exhibit low blood volume (hypovolemia), which can decrease the rate of blood flow to the heart.[1]
hypovolemia- from my last post:
https://en.wikipedia.org/wiki/ Capillary_leak_syndrome
extremely rare medical condition characterized by self-reversing episodes during which the endothelial cells which line the capillaries are thought to separate for a few days, allowing for a leakage of fluid from the circulatory system to the interstitial space, resulting in a dangerous hypotension (low blood pressure), hemoconcentration, and hypoalbuminemia.
......Acute renal failure is a risk due to acute tubular necrosis consequent to hypovolemia and rhabdomyolysis.[2][3]
http://www.ncbi.nlm.nih.gov/pubmed/21663986
Cardiac remodeling induced by 13-cis retinoic acid treatment in acne patients.
CONCLUSION: In this study, 10 weeks of 13-cis-RA therapy at a dose of 0.5 mg/kg/d was found to promote concentric-type heart remodeling due to the occurrence of two associated events: heart hypertrophy and hypovolemia.
https://en.wikipedia.org/wiki/ Hypovolemia
'' a state of decreased blood volume; more specifically, decrease in volume of blood plasma.[1][2] Hypovolemia is characterized by salt (sodium) depletion and thus differs from dehydration, which is defined as excessive loss of body water''
(i remember someone named Nathan Carr or something, someone mentioned him and that he was using some mineral sodium or something last time he checked what he was doing)
hypovolemia- from my last post /
https://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome
Another subtype, neuropathic POTS, is associated with denervation of sympathetic nerves in the lower limbs.[1] In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs.[4] Heart rate increases to compensate for this blood pooling.[9]
......Fludrocortisone, considered a first-line drug, works by reducing salt loss, which increases blood volume.[5]
https://en.wikipedia.org/wiki/Fludrocortisone
Fludrocortisone (also called 9-fluorocortisol or 9-fluorohydrocortisone) is a synthetic corticosteroid with moderate glucocorticoid potency and much greater mineralocorticoid potency. Therapeutically, it is used for its mineralocorticoid activity and not for its glucocorticoid activity.
If you like to know an update and info or contact for Nathan then pm me and yes, he had success and has done quite a bit in the accutane community! He continues to this day!
22 minutes ago, guitarman01 said:this a little off topic atm but what the hell is this?
http://www.ncbi.nlm.nih.gov/pubmed/25081735
Claritin Decreased accutane side effects?
also just read as little as 1500mg of l methionine per day can significantly raise homocysteine levels. that is kind of a bummer.
methionine with b vitamins B12 b6 folate, biotin,TMG solve this problem...turning homocysteine back into methionine.methionine will be a part of aprotocol.
This would be the sulfur part:
SAM-E 400mg up to 1600mg eventually
Taurine 3 grams
Methionine 500-1000mg
TMG
A diet high in naturally methionine and sulfur rich foods... egg whites, chicken... broccoli cauliflower etc
Tmg could also be a substitute for sam-e for those that can't afford it atm based on this article
http://www.lifeextensionvitamins.com/tmg1.html
You could probably throw in choline and inositol too, a very cheap supplement both used in that patent application.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2198910/
everything you ever wanted to know about sulfur, its the third most abundant mineral in the body.
Sulfation is a major pathway for detoxification of pharmacological agents by the liver.
1 hour ago, guitarman01 said:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2198910/
everything you ever wanted to know about sulfur, its the third most abundant mineral in the body.
Sulfation is a major pathway for detoxification of pharmacological agents by the liver.
Good article. my takeaway from it is this
1.Methionine and SAA (sulfur amino acids) are needed to produce GAGS. GAGS are impaired when these are limited and used for protein synthesis first. Glucuronic acid is a major GAG.... and its what everyone here wants to increase to bind with accutane metabolites.
From the standpoint of the diet, methionine alone is capable of providing all the necessary body sulfur, with the exception of the two sulfur-containing vitamins, thiamin and biotin.
In light of these concerns, particularly as it relates to the unique role of the SAA in providing sulfates for GAG (glycosaminoglycans) synthesis, it seems essential to determine if the needs for sulfur are being met, in particular as it relates to GAG and GSH (glutathione) in cartilage. One could predict that GAG synthesis may not fare well during marginal intakes, and that a preference will be given to the synthesis of proteins and essential metabolic intermediates like CoA, SAM (S-Adenosyl-L-Methionine),
Sulfation is a major pathway for detoxificication of pharmacological agents by the liver. As already mentioned, certain drugs that play a key role in the treatment of cartilage anomalies, such as acetaminophen require sulfate for their excretion. Acetaminophen is given in large doses to alleviate pain, and doses of up to 4 gm/day are recommended in the label, but often more is consumed. Thirty five % is excreted conjugated with sulfate and 3% conjugated with cysteine [11]. The rest is excreted conjugated with glucuronic acid, incidentally also one of the major components of GAG.
Methionine or cysteine (0.5%) added to the diet can overcome the severe methionine deficiency induced in rats by the addition of 1% acetaminophen, (an equivalent to the 4 gm/day to a human dose) [12]. It is interesting to note that D- as well as L-methionine could restore growth, implying that depletion of sulfur was the primary defect and not one related to protein synthesis.
so yesterday I took a total of 80,000mcg of biotin. I am getting very dry skin very dry cracked lips and bloody mucus from my nose. and funny how this works but im not sure if this is a good or bad thing. lol. It could follow the whole Im pushing accutane,vitamin a back into circulation. or could it be too much sulfur? doesnt sulfur have a drying effect? trial and error or not knowing just takes way too long
On 1/3/2016 at 11:35 PM, guitarman01 said:so yesterday I took a total of 80,000mcg of biotin. I am getting very dry skin very dry cracked lips and bloody mucus from my nose. and funny how this works but im not sure if this is a good or bad thing. lol. It could follow the whole Im pushing accutane,vitamin a back into circulation. or could it be too much sulfur? doesnt sulfur have a drying effect? trial and error or not knowing just takes way too long
from ben lynch:
Keep in mind that SAMe is also a very potent detoxifier and if we can mobilizing toxins that are stimulating or toxic in any way and most are then symptoms may occur. I have a client who has a long history of meth, LSD and other drugs and they have MTHFR C677T homozygous and if I use ANY form of methyl donors, they get very bad and I suspect it is from detoxing the drugs.[Edited link out]
you could be mobilizing things without having the rest of the key supporters in place. biotin would be a role player. Methionine or SAM-E would be the superstars imo. methionine is NOT stored in the body... a constant intake is needed. i worry about the side effects if we actually get things moving fast. not enough GAGS ----> not enough glucuronic acid to bind for excretion.
Under physiological conditions, hepatic stellate cells (HSCs) within liver lobules store about 80% of the total body vitamin A in lipid droplets in their cytoplasm, and these cells show zonal heterogeneity in terms of vitamin A-storing capacity. Vitamin A is essential for the growth and differentiation of cells, and it is well known that liver cells including HSCs show a remarkable growth capacity after partial hepatectomy (PHx).
The HSCs have several important functional roles in the liver. They are the central site for retinoid storage in the liver and consequently, the body [8,9]. In the retinoid-sufficient adult rodent, as much as 9095% of hepatic retinoid is stored as retinyl ester in lipid droplets of HSCs [8,9]. For a healthy adult, the liver contains approximately 70% of the total retinoid present in the body. Thus, HSC lipid droplets are the location where the majority of the bodys retinoid stores are found.
As mentioned above, the size and number of HSC lipid droplets are markedly influenced by dietary retinoid intake.
Relationship of concentration of vitamin A in the liver and rate of depletion:
The rate of vitamin A liver metabolism is proportional to its concentration in the liver.
When the liver stores are low, the rate of depletion is much slower:
[Edited link out]
https://www.ncbi.nlm.nih.gov/pubmed/1522488
"Intravenous infusion of hydroxypropyl-beta-cyclodextrin into a patient with hypervitaminosis A led to a release of liver-storedretinoidsinto serum in quantities much higher than those that could be directly solubilized by hydroxypropyl-beta-cyclodextrin.Hydroxypropylcyclodextrins may serve as artificial lipid carriers in the circulation, and because the exchanges that involve inclusion complexation occur very quickly, the presence of hydroxypropylcyclodextrins in organisms may catalytically augment the establishment of equilibria in lipid distribution."
https://www.ncbi.nlm.nih.gov/pubmed/9120816
It is clear that lipophilic agents (like retinoids), after their incorporation into hydroxypropyl beta-cyclodextrincomplexes and subsequent in vivo administration, are rapidly released and exchanged into the plasma.
"Etretinate, a highly lipophilic retinoid, is known to accumulate in the human body with a slow systemic elimination (half-life approximately 100 days) after long-term treatment. Retinoids with high lipophilicity and slow body elimination have the propensity of eliciting teratogenic effects."
On 1/4/2016 at 12:57 AM, yetanotheraccutanevictim said:Under physiological conditions, hepatic stellate cells (HSCs) within liver lobules store about 80% of the total body vitamin A in lipid droplets in their cytoplasm, and these cells show zonal heterogeneity in terms of vitamin A-storing capacity. Vitamin A is essential for the growth and differentiation of cells, and it is well known that liver cells including HSCs show a remarkable growth capacity after partial hepatectomy (PHx).
The HSCs have several important functional roles in the liver. They are the central site for retinoid storage in the liver and consequently, the body [8,9]. In the retinoid-sufficient adult rodent, as much as 9095% of hepatic retinoid is stored as retinyl ester in lipid droplets of HSCs [8,9]. For a healthy adult, the liver contains approximately 70% of the total retinoid present in the body. Thus, HSC lipid droplets are the location where the majority of the bodys retinoid stores are found.
As mentioned above, the size and number of HSC lipid droplets are markedly influenced by dietary retinoid intake.
Relationship of concentration of vitamin A in the liver and rate of depletion:
The rate of vitamin A liver metabolism is proportional to its concentration in the liver.
When the liver stores are low, the rate of depletion is much slower:
[Edited link out]
https://www.ncbi.nlm.nih.gov/pubmed/1522488
"Intravenous infusion of hydroxypropyl-beta-cyclodextrin into a patient with hypervitaminosis A led to a release of liver-storedretinoidsinto serum in quantities much higher than those that could be directly solubilized by hydroxypropyl-beta-cyclodextrin.Hydroxypropylcyclodextrins may serve as artificial lipid carriers in the circulation, and because the exchanges that involve inclusion complexation occur very quickly, the presence of hydroxypropylcyclodextrins in organisms may catalytically augment the establishment of equilibria in lipid distribution."
https://www.ncbi.nlm.nih.gov/pubmed/9120816
It is clear that lipophilic agents (like retinoids), after their incorporation into hydroxypropyl beta-cyclodextrincomplexes and subsequent in vivo administration, are rapidly released and exchanged into the plasma.
"Etretinate, a highly lipophilic retinoid, is known to accumulate in the human body with a slow systemic elimination (half-life approximately 100 days) after long-term treatment. Retinoids with high lipophilicity and slow body elimination have the propensity of eliciting teratogenic effects."
so ourfatty liver, isfilled with altered vitamin A ,that is very hard to get rid of.... unless we take an artifical lipid carrier, cyclodextrin. Notice the serum vitaim A levels increase to a ridiculous level after taking the drug?? but its seems to say its bound to this, and the toxicity is lessened?! it does mention bone pain though. i almost wish a hosptial could administer this,and then do a blood transfusion or a blood draw.
or we can do what this Joesf Pitha said and take all of these fatty liver "rescuers" naturally removing these lipid globules from the liver, and basically doing the same thing?
he basically invented and patented both ways!!!!!
12 hours ago, guitarman01 said:Tmg could also be a substitute for sam-e for those that can't afford it atm based on this article
http://www.lifeextensionvitamins.com/tmg1.html
You could probably throw in choline and inositol too, a very cheap supplement both used in that patent application.
TMG doesnt make SAM-E initially though.
methionine + magnesium = SAM-E
SAM-E does its detoxifying thing, then by losing this detoxifying methyl group, it becomes homocysteine....
homocysteine +TMG gets recycled back into methionine starting the entire process again. other paths help this homocysteine tobecome methionine again.... includes b6, methylb12 and methylfolate. these also donate a methyl group back.
also from your article, it says we can safelytake up to 5-6 grams of methionine with adequate b vitamins before running into real homocysteine problems.
you never get the initialpool of methionine or SAM-E from TMG though...just like cysteine never gets made back into methionine.
25 minutes ago, tryingtohelp2014 said:
so ourfatty liver, isfilled with altered vitamin A ,that is very hard to get rid of.... unless we take an artifical lipid carrier, cyclodextrin. Notice the serum vitaim A levels increase to a ridiculous level after taking the drug?? but its seems to say its bound to this, and the toxicity is lessened?! it does mention bone pain though. i almost wish a hosptial could administer this,and then do a blood transfusion or a blood draw.
or we can do what this Joesf Pitha said and take all of these fatty liver "rescuers" naturally removing these lipid globules from the liver, and basically doing the same thing?
he basically invented and patented both ways!!!!!
Ok, so we have proof now we can expell the accutane withHydroxypropyl-Beta-Cyclodextrin
"It doesn't matter how beautiful your theory is, it doesn't matter how smart you are. If it doesn't agree with experiment, it's wrong." - Richard P. Feynman
I'm up for the experiment, but I cannot find any dosing.
TTH2014, are you sure it recognizes Accutane in the liver and pushes it back into circulation?
6 minutes ago, Walden Rev said:
Ok, so we have proof now we can expell the accutane withHydroxypropyl-Beta-Cyclodextrin
"It doesn't matter how beautiful your theory is, it doesn't matter how smart you are. If it doesn't agree with experiment, it's wrong." - Richard P. Feynman
I'm up for the experiment, but I cannot find any dosing.
TTH2014, are you sure it recognizes Accutane in the liver and pushes it back into circulation?
no idea... im afraid of the 100 fold serum vitamin A increase that happens after taking the drug as well. ive already emailed the maker of the drug and told him about this forum. if anyone would know its him, andhis old partner Josef Pitha.
i honestly think we already have a natural way.
On 1/4/2016 at 2:25 AM, Walden Rev said:
Ok, so we have proof now we can expell the accutane withHydroxypropyl-Beta-Cyclodextrin
"It doesn't matter how beautiful your theory is, it doesn't matter how smart you are. If it doesn't agree with experiment, it's wrong." - Richard P. Feynman
I'm up for the experiment, but I cannot find any dosing.
TTH2014, are you sure it recognizes Accutane in the liver and pushes it back into circulation?
I did buy the powdered form on ebay. but from what I have been reading doesnt sound very safe. and they were injecting it. dont know what kind of effect orally would have. or hey we could all just shoot it up. kidding. i think.
On 1/4/2016 at 2:12 AM, tryingtohelp2014 said:TMG doesnt make SAM-E initially though.
methionine + magnesium = SAM-E
SAM-E does its detoxifying thing, then by losing this detoxifying methyl group, it becomes homocysteine....
homocysteine +TMG gets recycled back into methionine starting the entire process again. other paths help this homocysteine tobecome methionine again.... includes b6, methylb12 and methylfolate. these also donate a methyl group back.
also from your article, it says we can safelytake up to 5-6 grams of methionine with adequate b vitamins before running into real homocysteine problems.
you never get the initialpool of methionine or SAM-E from TMG though...just like cysteine never gets made back into methionine.
i dont think 5-6 grams seems very safe, ive also read in another study b vitamins didnt make a difference. I got a few of these supps coming on wednesday, so I guess thats when the party starts.
On 1/4/2016 at 2:32 AM, tryingtohelp2014 said:no idea... im afraid of the 100 fold serum vitamin A increase that happens after taking the drug as well. ive already emailed the maker of the drug and told him about this forum. if anyone would know its him, andhis old partner Josef Pitha.
i honestly think we already have a natural way.
that sure would be something if they emailed you back. I would think by now they would be aware of some long term affects. or they already knew...
we should keep emailing them and links to peoples stories like this one.
[Edited link out]
I dont even like reading it. sounds alot like me.
"The best tool available to make nasal and sublingual steroids are derivatives of beta cyclodextrins. The one that is most readily available is hydroxypropyl-beta cyclodextrin (HPBCD). (Note: Plain beta-cyclodextrin is of little use) In case you have not heard of these, cyclodextrins are cyclic oligosaccarides (sugars) that have a hydrophilic outer surface and a hydrophobic inner surface.(3) They can be thought of as a doughnut, with the center capable of having a steroid molecule stuck inside it. The hydrophilic outer surface makes the cyclodextrin soluble in water, and when it is combined with a steroid, it can make the poorly water soluble steroid soluble as well.(3) In addition to making steroids soluble, cyclodextrins have very other important properties that make them ideal for our purpose. Cyclodextrins are known to enhance steroid delivery through biological membranes.(3) The large CDs themselves are very bad at permeating biological membranes, but they deliver the steroid to the membrane, where it partitions into the membrane, leaving the CD on the outside of the membrane.(3) The conventional penetration enhancers like alcohols or polyethylene glycol act by disrupting the lipid layers of membranes.(3) That is a big source of irritation from the old formula, and this irritation can thus be avoided by the use of CDs. Another advantage is, once administered, the steroid is rapidly absorbed. Nearly 95% of the steroid will be absorbed within 20 minutes. This also causes the need for multiple doses throughout the day.
It seems that hardly anyone out there knows how to complex a steroid with a cyclodextrin. One procedure I saw on a different companys steroid column was laughable. It was pretty obvious that whoever wrote that procedure knew very little about cyclodextrins. It is really fairly easy to do. There are multiple ways to do it, but I will tell you three methods to try, depending on what resources you have available. In all instances, you need a ratio of 9g of HPBCD to 1g of steroid. Complexation occurs because the steroid is more energetically stable inside the CD than outside of it. It is an equilibrium process, but the equilibrium lies much more on the side of complexation.(3) Water is essential for complexation to occur. It is removed from the inner cavity to allow for the steroid to enter, but even normal room humidity is sufficient for complexation if the mix is given sufficient time.(4)"
The bodybuilding community already knows this substance.
On 1/4/2016 at 12:57 AM, yetanotheraccutanevictim said:Under physiological conditions, hepatic stellate cells (HSCs) within liver lobules store about 80% of the total body vitamin A in lipid droplets in their cytoplasm, and these cells show zonal heterogeneity in terms of vitamin A-storing capacity. Vitamin A is essential for the growth and differentiation of cells, and it is well known that liver cells including HSCs show a remarkable growth capacity after partial hepatectomy (PHx).
The HSCs have several important functional roles in the liver. They are the central site for retinoid storage in the liver and consequently, the body [8,9]. In the retinoid-sufficient adult rodent, as much as 9095% of hepatic retinoid is stored as retinyl ester in lipid droplets of HSCs [8,9]. For a healthy adult, the liver contains approximately 70% of the total retinoid present in the body. Thus, HSC lipid droplets are the location where the majority of the bodys retinoid stores are found.
As mentioned above, the size and number of HSC lipid droplets are markedly influenced by dietary retinoid intake.
Relationship of concentration of vitamin A in the liver and rate of depletion:
The rate of vitamin A liver metabolism is proportional to its concentration in the liver.
When the liver stores are low, the rate of depletion is much slower:
[Edited link out]
https://www.ncbi.nlm.nih.gov/pubmed/1522488
"Intravenous infusion of hydroxypropyl-beta-cyclodextrin into a patient with hypervitaminosis A led to a release of liver-storedretinoidsinto serum in quantities much higher than those that could be directly solubilized by hydroxypropyl-beta-cyclodextrin.Hydroxypropylcyclodextrins may serve as artificial lipid carriers in the circulation, and because the exchanges that involve inclusion complexation occur very quickly, the presence of hydroxypropylcyclodextrins in organisms may catalytically augment the establishment of equilibria in lipid distribution."
https://www.ncbi.nlm.nih.gov/pubmed/9120816
It is clear that lipophilic agents (like retinoids), after their incorporation into hydroxypropyl beta-cyclodextrincomplexes and subsequent in vivo administration, are rapidly released and exchanged into the plasma.
"Etretinate, a highly lipophilic retinoid, is known to accumulate in the human body with a slow systemic elimination (half-life approximately 100 days) after long-term treatment. Retinoids with high lipophilicity and slow body elimination have the propensity of eliciting teratogenic effects."
Yes, but you should finish posting the paragraph!
Etretinate, a highly lipophilic retinoid, is known to accumulate in the human body with a slow systemic elimination (half-life approximately 100 days) after long-term treatment. Retinoids with high lipophilicity and slow body elimination have the propensity of eliciting teratogenic effects. Therefore, synthetic retinoids with reduced systemic retention are desired.
Etretinate is not Isotretinoin!
42 minutes ago, vianello said:Yes, but you should finish posting the paragraph!
Etretinate, a highly lipophilic retinoid, is known to accumulate in the human body with a slow systemic elimination (half-life approximately 100 days) after long-term treatment. Retinoids with high lipophilicity and slow body elimination have the propensity of eliciting teratogenic effects. Therefore, synthetic retinoids with reduced systemic retention are desired.Etretinate is not Isotretinoin!
I think you need to go back a few post.
http://www.google.com/patents/US4649040 check this link out. its a mind blown kind of moment.
its like tryingtohelp went back in time and talked to his other self. its from 1984 and this guy was working on the same thing. finding a way to eliminate all retinoids from the body. all types.
its like in 1981 he found a way to deliver retinoids more effectively, inthe same way these bodybuilders use cyclodextrin to deliver steriods with 95% efficiency.. then in 1984,, three years later, he started messing with the sulfurs to get rid of it...and he patented it!!, almostknowing/seeing after these three years, this enhanced retinoid therapy would run into problems like a fatty liver?!
accutane is an extremely lipophilic retinoid! thats why they tell you to eat a high fat meal when taking it. and...they dont know with any certainty what gets left behind, what unknown metabolite gets made, or how it even works(supposedly)! they couldnt possibly know about polymorphisms yet...fast or slow methylators, or something we havent even discovered yet, that makes accutane stay around for 20+ years after in some people, while others need multiple courses with no effect.
what we do know is.... a lot of us ARE suffering teratogenic effects multiple years after this drug shouldve been totally eliminated. theres just no other explanation.
so bodybuilders add a steriod to this donut to enhance delivery.
But they also discovered this donut administered by itself draws retinoids out. Like a super chelator.
related to the same methionine depletion theory... http://www.acne.org/messageboard/topic/353098-crazy-hair-loss-after-5-days-on-accutane-help-me/#entry3497618
look at this poor girl... only 5 days on accutane , and she is losing all of her hair andeyebrows.... even after having stopped accutane.
how many times have we seen these stories ofpeople, only on this drug a week or less, and having years of problems??!
but then if you read her posts something interesting is seen,
1. she suffered anorexia prior
2. she is a vegan.
both are related to methionine/taurine depletion even before taking accutane. maybe accutane totally pushed her off of a cliff, and now shes stuck like the rest of us?
1 hour ago, guitarman01 said:I did buy the powdered form on ebay. but from what I have been reading doesnt sound very safe. and they were injecting it. dont know what kind of effect orally would have. or hey we could all just shoot it up. kidding. i think.
i dont think 5-6 grams seems very safe, ive also read in another study b vitamins didnt make a difference. I got a few of these supps coming on wednesday, so I guess thats when the party starts.
that sure would be something if they emailed you back. I would think by now they would be aware of some long term affects. or they already knew...
we should keep emailing them and links to peoples stories like this one.
http://www.allthingsmale.com/community/threads/accutane-changed-me.24094/
I dont even like reading it. sounds alot like me.
Do you plan on using it shortly?
I'm willing to do a supplement vacation (except Taurine) and testcyclodextrin, but if you plan on using it I'll hold off the buying.
16 minutes ago, guitarman01 said:
Yes, but still its in the "acute phase", where all retinoids (isotretinoin, etrinate etc.) are still present in the body. Isotretinoin has a short half-life.
Yes, an administration of these agents during the toxic phase will speed up the elimination.
"lipophilic" does not say too much about systemic retention.
Plus this girl, is "the proof" that it is not stored... after only 5 days?!!
There is a lot of vegetables and grains that have enough methionine, this can't be the problem with her. ( Mushrooms, rice, spinach, broccoli, nuts are really high etc)
Over the years we have certainly got enough methionine...
I'm not saying supplementing won't have an effect - maybe it would jump-start something / shift...
1 hour ago, vianello said:Yes, but still its in the "acute phase", where all retinoids (isotretinoin, etrinate etc.) are still present in the body. Isotretinoin has a short half-life.
Yes, an administration of these agents during the toxic phase will speed up the elimination."lipophilic" does not say too much about systemic retention.
Plus this girl, is "the proof" that it is not stored... after only 5 days?!!
There is a lot of vegetables and grains that have enough methionine, this can't be the problem with her. ( Mushrooms, rice, spinach, broccoli, nuts are really high etc)
Over the years we have certainly got enough methionine...I'm not saying supplementing won't have an effect - maybe it would jump-start something / shift...
Lipophilic literally means "Fat loving"... it stands to reason if you develop a fatty liver while on accutane... its from the accutane/and or filled with an accutane metabolite.
And vegetables arent a high source of methionine...vegetables contain organic sulfur. BIG difference. unless shes eating a ton of Brazil nuts. hence......
The low-methionine content of vegan diets may make methionine restriction feasible as a life extension strategy.
http://www.ncbi.nlm.nih.gov/pubmed/18789600
Accutane was a chemo drug first... why? how? Oh i know.. upregulate GNMT and kill methionine.
http://nutritionfacts.org/2014/07/08/a-low-methionine-diet-may-help-starve-cancer-cells/
So, where is methionine found? In my video,Starving Cancer with Methionine Restriction, you can see a graph of foods with their respective methionine levels. Chicken and fish have the highest levels. Milk, red meat, and eggs have less, but if we really want to stick with lower methionine foods, fruits, nuts, veggies, grains, and beans are the best. In other words, In humans, methionine restriction may be achieved using a predominately vegan diet.
think of us on this scale of methionine restriction heh meat lovers------>vegans--------------------GNMT------------------->long term accutane sufferers. We might have to take a ton just to get back to where the vegans are. As long as theres an active or even passive metabolite causing a GNMT expression... we never get out.
http://www.google.com/patents/US4649040
It has been reported that although various retinoids may differ in relative bioeffectiveness, their toxic symptoms are quite similar. For example, a natural compound, 13-trans retinoic acid, and its synthetic aromatic analog, etretinate, differ in the dose required to induce pathological changes, but do not differ in the pathological changes induced (Bolag, supra). It has been suggested that the similarity of toxic effects may be based at least in part on metabolic interconversion of these compounds (McCormick, et al., Biochemistry 22: 3933-3940, 1983).
On the upside, long term sufferers should be cancer resistant.
I PRAY that her only being on the drug 5 days is THE PROOF, that its not stored. then it will be simple... turn the autophagy off/downregulate FOX01 ... and turn everything back on like a light switch. but after 20 years, sadly, i dont think this will be the case. She might respond SUPER quick to a protocol showing this can be reversed though... and that would be the proof. ive already msgd her.
9 minutes ago, Walden Rev said:
Do you plan on using it shortly?
I'm willing to do a supplement vacation (except Taurine) and testcyclodextrin, but if you plan on using it I'll hold off the buying.
From reading up, it sounds like beta-cyclodextrin is basically used to make insoluble drug compounds soluble in water, so the insoluble drug molecule will sit inside the structure of the sugar (the beta-cyclodextrin) and hence the drug has become water soluble.
I'm not sure supplementing this orally would be of any benefit to removing retinoids from the liver, however I'm not suggesting it's not worth trying. Also it looks pretty safe, and is FDA approved (although that evidently doesn't mean much..)