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Repairing the long-term damage from Accutane

 
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157
(@chico-esposito)

Posted : 06/16/2013 2:55 pm

 

chico what specific foods cause this retinol reaction, and which do not? i'm skeptical but open to convincing.

For example, shrimp has 4% vit A RDA and yet causes no ill effects for me.

Regardless of the side effect you have if you take retinol post accutane it will aggravate it.

I have hard evidence the problem extends way beyond this. On my second course of Accutane my doctor prescribed 60mgs a day - that was double my first dose. At that second dosage, I couldn't even leave the house because the entire portion of my chin area was scabbing up and bleeding. I went through the extreme sensitivity to food issue for about 3 years after the crash with beta-carotene (the body uses only what it needs is more bullshit).

When the sensitivity issue passed I became incredibly intrigued. I began experimenting based on the notions of perhaps resetting receptor expression (androgen, RAR, retinoid X, etc). Well guess what, at doses of 100mgs+ of brand name Accutane; I had no classic signs whatsoever. I even had nocturnal erections on that dose, which I dont even have when I am clean. I hope you finally concede that things change, but the condition persists unwaveringly.

 

chico what specific foods cause this retinol reaction, and which do not? i'm skeptical but open to convincing.

For example, shrimp has 4% vit A RDA and yet causes no ill effects for me.

Regardless of the side effect you have if you take retinol post accutane it will aggravate it.

I have hard evidence the problem extends way beyond this. On my second course of Accutane my doctor prescribed 60mgs a day - that was double my first dose. At that second dosage, I couldn't even leave the house because the entire portion of my chin area was scabbing up and bleeding. I went through the extreme sensitivity to food issue for about 3 years after the crash with beta-carotene (the body uses only what it needs is more bullshit).

When the sensitivity issue passed I became incredibly intrigued. I began experimenting based on the notions of perhaps resetting receptor expression (androgen, RAR, retinoid X, etc). Well guess what, at doses of 100mgs+ of brand name Accutane; I had no classic signs whatsoever. I even had nocturnal erections on that dose, which I dont even have when I am clean. I hope you finally concede that things change, but the condition persists unwaveringly.

I have a story of my own, and this is the truth unabated. After i went off accutane the first time i developed a skin condition over my cheeks and temples, my skin grew much quicker in these areas, it would shed uncontrollably, now i had no idea what it was, at 18 years old i never even thought it could be accutane that was responsible, i didn't put the pieces together or anything. After a couple of years i started travelling around the country paying to see private consultant dermatologist's because i was so afraid of what was happening to my skin. I was first diagnosed with a fungal infection of the skin and put on months of oral anti fungals, then i was diagnosed with seb derm, psoriasis, eczema, etc it went on and on the different dermatologists i saw. I had skin biopsy's done, i had blood tests, i had colonoscopies to check whether it was digestive. I was in a place were i genuinely wanted to die and had no reason left to go on. My skin condition caused scarring of my face in the areas in grew. A doctor prescribed PUVA therapy to me, i've talked about this in the past on here, and my skin cleared up, i also got a good tan from it. The drug they used was psoralen it makes you sensitive to light so the light from the tanning bed can penetrate the skin deeper, and slow down skin cell production. Thats how it works, it stops the skin cell differentiation being so quick, so the condition clears up, and it did.

I was reading a lot on the internet at the time and read accutane also helps PUVA therapy, because it too increases your sensitivity to light. At this stage i still didn't blame accutane for my predicament in the first instance. So this is what i did (and i'll regret this for the rest of my life) i found some accutane on the black market from a european pharmacy, it was from Turkey and it was legit. I bought it and started taking it, going on the sunbed's hoping it would have the same effect. 20 mg once a day. This was for about 2-3 months, i consumed the whole packet of 20mg accutane in that time. As soon as i stopped taking this accutane my nose, forehead, scalp and ears developed exactly the same skin condition that was on my cheeks and temples. Now it's all over my face and has been ever since.

Originally before i took it the second time, the skin on my nose, forehead and scalp was perfect, 100% normal it was just my cheeks and temples that were shedding and scarring, i called it 'the growth' because it was a thick white plaque that would grow only in those areas. But after stopping that 2nd cycle of accutane my whole face and scalp was covered with the same thick white plaque. That second cycle ruined me, and my life has never been the same since.

I'm telling you with 100% certainty, that it was accutane that caused my skin condition, and it is a form of hypervitaminosis A that i have, and most of us exhibit only at varying levels of toxicity and with various different symptoms. It's got absolutely nothing to do with DHT inhibitors, nothing whatsoever.

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26
(@camaroz28)

Posted : 06/16/2013 10:20 pm

It's got absolutely nothing to do with DHT inhibitors, nothing whatsoever.

Yeah that is why you failed to comment at ALL when we were discussing this. Just give to research, please. You don't have this and Joe does not have this. ALSO, I AM SURE THE RESEARCHERS ARE FEVERISHLY TRYING TO WORK OUT HOW TO CLEAR THE RETINOIDS FROM YOUR RECEPTORS. If storage issues are at work, they play a small role, not the principle role as you always allude to. The problem is the drug inhibiting it's own metabolism., amongst other things.

 

 

" to begin with you are accusing the lead doctor running the study of rigorously and premeditatedly expediting his patients death by not following previously established dosing determinations set by the FDA"
Nope, you're lying, or quote the refernce.
"So why act hastily, Dr. Death? "
You seem to be under the mistaken impression that I recommend UDCA for people with blocked bile ducts. I have no idea how you came by that impression, since I repeatedly pointed out that this is a terrible idea.

You don't even know how to use the quote function.

Those TWO articles were way above your comprehension level - clearly. You said that those people in the first article were given UDCA because it would improve their life quality. You implied that they were going to die anyway, so it was fine to proceed. You implied that the doctors knew the end outcome - THEY DID NOT. This all happened recently. AND, YES IT HAS BEEN USED IN CHILD CASES OF DRUG INDUCED INTRAHEPATIC BILIARY TREE DAMAGE. I could show you proof, but I still dont think you would understand.

You obviously couldn't digest my post, hence this meager offering. Here is some more shocking information: All cholestatsis refers to bile blockage. You cannot escape dealing with blockage. Hence, there are always risks of flooding. Why dont you officially get diagnosed, instead of thinking Dr. Joe knows best? Next time have more tapioca before trying to dissect basic articles. And, yes your ass would have exploded just like cells do when they can't clear the bile. The toilet or plumbing are other stages of the problem.

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26
(@camaroz28)

Posted : 06/16/2013 10:52 pm

 

" The nomenclature can refer to toxic bile acid build-up causing injury to hepatocytes or biliary tree damage, or both at once. Have you had a professional rule out the latter?"
Of course. Ultrasound and blood tests. if I had biliary tree damage taking UDCA would shorten my lifespan, as I have repeatedly pointed out.
"The wording used was mildly overweight males. It helped them a little, but was comparable to placebo for the majority."
In America, mildly overweight is not mildly overweight. Anyhow obesity induced liver failure is really SAD induced liver failure, not something UDCA can solve. It doesn't affect the point either way, so I didn't go into it.

I can have a field day with you. If you had a real case of drug induced cholestatsis, you would have serious obvious problems including intrahepatic biliary tree obstructions after all these years. You don't have shit; you don't labs proving anything, and you shouldn't be making recommendations to others without proper diagnosis. For the love of God, you only recently came to grips with the dehydration component.

You can't read. Not all the people in the test group were obese, only some were. Again read the literature. You miss the point continuously.

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91
(@josephbuchignani)

Posted : 06/16/2013 11:08 pm

I don't doubt that hypervitaminosis A caused your condition, Chico. And the nature of it is interesting support for your Vit A recycling hypothesis - rapid skin shedding seems more like ongoing hypervitaminosis A, than a one-off incident.
I assume the skin shedding accelerates whenever you eat foods containing retinoids?
But again, my question was whether you actually tested that shrimp affects you, or you merely theorize that it would.
" ALSO, I AM SURE THE RESEARCHERS ARE FEVERISHLY TRYING TO WORK OUT HOW TO CLEAR THE RETINOIDS FROM YOUR RECEPTORS."
Sarcasm?
"If storage issues are at work, they play a small role, not the principle role as you always elude to. The problem is the drug inhibiting it's own metabolism., amongst other things."
Sounds right.
"Those TWO articles were way above your comprehension level - clearly. You said that those people in the first article were given UDCA because it would improve their life quality. You implied that they were going to die anyway, so it was fine to proceed. You implied that the doctors knew the end outcome - THEY DID NOT. This all happened recently. AND, YES IT HAS BEEN USED IN CHILD CASES OF DRUG INDUCED INTRAHEPATIC BILIARY TREE DAMAGE. I could show you proof, but I still dont think you would understand."
Your error in reading comprehension was in assuming I was addressing those two articles specifically rather than UDCA treatment in general. I don't particularly care about the two articles, I just glanced at them to verify they did not contain any info new to me that was relevant to my decision. They did not.
Of course I'm aware it has been used in child cases of biliary tree damage. How else could I have written about biliary atresia and this quote: "The ridiculous thing is that UDCA is so good for you there is even a DEBATE about whether people with BLOCKED BILE DUCTS should STILL take it."
"All choleostatsis refers to bile blockage."
False. From Wikipedia:
"The two basic distinctions are an obstructive type of cholestasis where there is a mechanical blockage in the duct system such as can occur from a gallstone or malignancy, and metabolic types of cholestasis which are disturbances in bile formation that can occur because of genetic defects or acquired as a side effect of many medications."
Non-production of bile != obstruction of bile ducts. 2 types of cholestasis.
You are still boring me and still not saying anything new that is useful.
Granted it is a self diagnosis based on:
History of Accutane, timing of symptom onset coinciding with others here
Well-known cholestatic reactions to steroids, etc
Pale stool
Steatorrhea
Major digestive limitation
Massively positive response to UDCA, and positive response to almost nothing else. Response accompanied by darkening stool and immediate major energy/mood boost, a rate of propagation consistent only with improved blood detoxification.
Blood tests did not reveal out of range liver levels, so formal medical investigation stopped there. I seem to recall some sort of "gold standard" test that would be the next step in diagnosing cholestasis - feel free to remind me what it's called.
In fact, blood tests revealed nothing out of range, and extraordinarily low inflammation markers in general, a testament to the design of my elimination diet. Yet I was still non-functional.
Ultimately I am not concerned about whether or not I get a formal diagnosis; I am concerned about performance. I've ruled out the likely alternative life-threatening conditions, and am left with cholestasis as a negative hypothesis. If you think negative hypotheses aren't legitimate medical science, you obviously aren't familiar with the majority of digestive dysfunction diagnoses.
My reasoning is consistent with the http://en.wikipedia.org/wiki/Analysis_of_competing_hypotheses analysis of competing methods and has a high sensitivity on multiple conclusions.
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26
(@camaroz28)

Posted : 06/16/2013 11:36 pm

 

"All choleostatsis refers to bile blockage."
False. From Wikipedia:
"The two basic distinctions are an obstructive type of cholestasis where there is a mechanical blockage in the duct system such as can occur from a gallstone or malignancy, and metabolic types of cholestasis which are disturbances in bile formation that can occur because of genetic defects or acquired as a side effect of many medications."
Non-production of bile != obstruction of bile ducts. 2 types of cholestasis.
Ultimately I am not concerned about whether or not I get a formal diagnosis; I am concerned about performance.
Obviously, absent bile production deserves it only distinct nomenclature, and that does not apply to the articles, which, unless you have forgotten was OUR POINT OF DEPARTURE. We are obviously concerned with the paradoxical treatment modality of dislodging bile with bile, and the related dosing. Stay on track. And gallstone or malignancy still ends in a bile back up, so no point there. You will not see a doctor; because it will prove definitively that you go from one rubbish obsession to another aimlessly. The worst part is you make recommendations based on your experience and reviewing; and, to be honest both don't exist.

 

 

" ALSO, I AM SURE THE RESEARCHERS ARE FEVERISHLY TRYING TO WORK OUT HOW TO CLEAR THE RETINOIDS FROM YOUR RECEPTORS."
Sarcasm?

No, that is a serious statement.

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MemberMember
26
(@camaroz28)

Posted : 06/16/2013 11:52 pm

 

Your error in reading comprehension was in assuming I was addressing those two articles specifically rather than UDCA treatment in general. I don't particularly care about the two articles, I just glanced at them to verify they did not contain any info new to me that was relevant to my decision. They did not.
Of course I'm aware it has been used in child cases of biliary tree damage. How else could I have written about biliary atresia and this quote: "The ridiculous thing is that UDCA is so good for you there is even a DEBATE about whether people with BLOCKED BILE DUCTS should STILL take it."

But that is exactly where you said it's usage is extremely dubious; you simultaneously argue, that it's usage in those settings shouldn't even be debated because it so good, and it's a no-brainer decision. You completely subvert your own previous point to attempt to escape the intractability of your simplifications. In blockage cases you lament that many are scared to lift doses so they can get benefits, and that is stupid; you then go on to say that in blockage cases it shouldn't be used. That is where your glorious toilet analogy came into play. You end this train of misunderstanding; by saying that the articles don't apply when unwell people were made much more unwell with dosages that were not overly high, and the doctors were surprised. You argue that the doctors were fully aware and happy for them to descend further. No clue.

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91
(@josephbuchignani)

Posted : 06/17/2013 1:08 am

First of all, I absolutely don't mind being wrong as long as my health keeps improving. Below is my thoughtstream which results in admitting I was wrong on various points.
Questions: What is the name of no bile production, as opposed to cholestasis?
------------
Some additional support for my interpretation, and undermining Camaroz's assertion that drug induced cholestasis also involves obstruction at the cellular level:
"However specific diagnostic markers for drug induced liver injury are lacking, and convincing cause and effect evidence exists for few cases (The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.Destroy user interface control2). Indeed establishing causality has been a major hindrance in the understanding of drug induced liver injury"
"There is increasing evidence that drugs that are excreted by the liver into bile are prime candidates for producing cholestatic liver disease in the susceptible patient "
"Acute and chronic cholestatic liver injury results from dysfunction of the mechanisms of bile formation. However, drug induced cholestasis can present with asymptomatic disease where the only clinical manifestation is an elevation in alkaline phosphatase. Moreover, the target of injury can vary from a mixed hepatocellular cholestatic injury, to impairment of canalicular bile flow resulting in pure intrahepatic cholestasis, or to an obstructive drug induced cholangiopathy where the initial site of injury is located at various levels of the bile duct epithelium"
Hm, it appears that I should get tested for alkaline phosphatase. I'm not sure if I have or not; it's not in my records. Also, it appears Camaroz may have been right to emphasize physical blockage - but does it extend to all cases?
"Cholestatic reactions tend to be prolonged after the discontinuation of the causative agent, presumably because cholangiocyte repair and regeneration is slower than that of the hepatocyte, and because bile secretory function may be slower to recover than other hepatocyte functions. In some cases, persistence of a self-propagating immune response may play a role in prolonging drug induced cholestasis."
Interesting, http://en.wikipedia.org/wiki/Cholangiocyte cholangiocytes are epithelial, which is the tissue that Accutane targets. More evidence for the blockage hypothesis. Bad news.
"Symptoms may occur weeks or months after beginning treatment. "
" in some cases, if there is significant loss of the interlobular bile ducts (VBDS), drug induced cholestasis can lead to chronic liver disease that may progress to liver failure"
It appears the best I can hope for is mild non-specific bile duct injury - cholangiopathies.
But I thought there was some mechanism whereby drugs could shut down bile production without affecting transport? What is that called?
"Chronic Drug Induced Cholangiopathies
These drug induced cholestatic disorders vary from asymptomatic patients with isolated elevations in alkaline phosphatase or gammaglutamyl transferase and liver histology showing only mild bile duct disarray or ductopenia, to progressive forms of the VBDS (The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.Destroy user interface control24). While some reports of asymptomatic idiopathic adulthood ductopenia fail to identify a causative agent (The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.Destroy user interface control25) others suggest that these cases may originate from overlooked drug induced bile duct injury (The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.Destroy user interface control26, The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.Destroy user interface control27). The common drugs known to cause the various drug induced cholestasis syndromes are enumerated in Table 3."
Ok, so apparently Camaroz is right that it's all about transport. The distinction is that UDCA is good for micro transport but bad if macro transport is already fucked. Then you get lakes. But UDCA supports and protects the micro network.
[Edited link out]
[Edited link out]
That second image is quite anti-UDCA. I was surprised to find a toxic dose listed: (28 mg/kg/day)
This directly contradicts this paper:
"In conclusion, biliary enrichment of UDCA increases with increasing dose and reaches a plateau at 22-25 mg/kg"
[Edited link out]
Another pro-UDCA article:
[Edited link out]
Crucially, the above article states the UDCA may ASSIST hepatocyte cell excretion of bile. So this is the production/transport distinction. Since I am not getting "lakes", it's a fair bet that UDCA is assisting transport out of cells, in which case it is no problem, and taking it will never give me lakes.
If the problem is epithelial duct tissue damage, then I may or may not develop lakes over long term UDCA use. But generally it's viewed as a good thing, it seems, and I can see how it would be helpful in repairing and maintaining the small networks. Its anti-inflammatory effects are valuable in a variety of auto-immune disorders. My condition may be an auto-immune progressive one initiated by Accutane, or merely a one-time static injury that is non-progressive.
If the big networks are blocked, it is absolutely a bad idea to take it - despite temporary quality of life improvement, it will accelerate death.
So the situation bears monitoring, both via complete liver blood tests for phosphatase and others, and also ideally at least one biopsy. Thanks Camaroz, your dense snark proved useful after all, however unintentionally.
"The liver pathology of drug-induced liver injury covers a wide spectrum of lesions from bland cholestasis to hepatitis and mixed forms.[122,123] It occurs with many drugs through a variety of mechanisms, which might differ in their clinical presentations ranging from asymptomatic mild biochemical abnormalities to an acute illness with jaundice that resembles viral hepatitis"
"data on the incidence of cholestatic forms of DILI are scarce. Cholestatic liver injury is typically characterized by a predominant elevation in alkaline phosphatase and bilirubin levels; however, the extent of aminotransferase elevations varies upon the causative drugs and the histologic pattern of liver injury. Bland canalicular cholestasis is typically associated with minimal hepatocellular inflammation and normal or only slightly elevated aminotransferase levels and is often seen with anabolic steroids or oral contraceptives."
Bland cholestasis, the common steroid / estrogen form, is accompanied by little parenchymal injury.
Expect only modestly elevated aminotransferase levels (5x). ALP barely elevated, perhaps 2x. Cholesterol normal. Resembles cases of incomplete gallstone obstruction! Nice fit!
I only have a partial case of this, since it did not proceed to jaundice or pruritis.
Prognosis is good! Great.
Sequelae: chronic drug-induced intrahepatic cholestasis. Exactly what I said it was. Long list of drugs implicated.
Can be fatal, proceed to PBC, but that's for jaundiced cases.
"The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments. However, although pale stools and dark urine are a feature of biliary obstruction, they can occur in many intra-hepatic illnesses and are therefore not a reliable clinical feature to distinguish obstruction from hepatic causes of jaundice."
Aha, here's a way to test it:
" Bilirubin is then removed by the kidneys into the urine. Little if any, urobilinogen will be found in the urine since little or no bilirubin is reaching the intestines."
I just have to go off UDCA, drink less water, get tired, and do a urine test. If the urine has bilirubin and low urobilinogen, cholestasis.
And Camaroz was right about the transport, kind of. It's all a transport mechanism for bilirubin, but there's an alternate route - the kidneys. So I think my route was partially blocked well upstream in the tiny networks or cell excretion levels, and the kidneys were picking up the extra load. But this is testable. Sweet.
Conclusion:
Priotity 1: Get tested for any possible markers that I'm forming "lakes". Are there liver tests for this? I need a knowledgeable liver doctor to answer this.
Priority 2: Do an off-UDCA baseline liver function test, with urine and bloodwork. I may have already done this, and will request records from the US.
So yes, Believe and Camaroz are correct - this is a problem that SHOULD be monitored. Not because UDCA is bad, but because the original injury may have been very bad, or started a progressive problem.
But odds are, since I never showed jaundice, this is one of those borderline generic damage cases that UDCA will simply regenerate over time, and more is better.
It appears I experienced some form of idiosyncratic hepatoxicity. Upstream cholestasis being the most probable.
"OUR POINT OF DEPARTURE"
No, the point of departure was my decision to use UDCA.
"absent bile production deserves it only distinct nomenclature"
Bile is not produced if the cell is full, or the cell is dead. The former hepatitis, the latter cholestasis. Thus, distinction not drawn on those lines.
"because it will prove definitively that you go from one rubbish obsession to another aimlessly."
Funny then that my income and health are increasing geometrically lately. Must be just lucky.
"You end this train of misunderstanding;"
Certainly it was. Allow me to restate my point, then: past a certain point, the hepatoprotective, anti-inflammatory and blood detoxifying benefits of UDCA are outweighed by the extent of irreversible biliary tree damage or extrahepatic obstruction. When bile can no longer flow, lakes form and death is accelerated.
Note that you are also contributing to the error. It is bile caniculi -> canals of hering -> bile ductules -> intrahepatic bile ducts -> duct -> duct -> duct. In other words, the smallest upstream capillaries are not called ducts. The quote to which you objected uses the word "duct", not "biliary tree", and thus is referring only to the larger portals.
Lost in all this is whether hepatocytes can somehow stop producing bile without being blocked, as a result of drug induced injury, and yet not be dead either (hepatitis). This is what I had confused with the "upstream cholestasis" case, and it appears the former simply doesn't happen, for whatever reason.
You are a very unclear communicator, Camaroz, but you do know a few things, which is why I'm willing to engage with you.
Oh, and I knew it was sarcasm, I was more curious what your point could possibly be.
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MemberMember
91
(@josephbuchignani)

Posted : 06/17/2013 2:52 am

So, tl;dr here's my current best understanding:
Non-production of bile is hepatitis, liver cell death, major obvious symptoms, you will be under direct medical supervision, out of scope for me.
Cholestasis is transport issue, not cellular failure to produce bile. Can be upstream gumming or downstream macro blockages. Congenital is out of scope; autoimmune is possible; chronic is definite. Both chronic and autoimmune are in scope, can be drug induced. They are poorly studied, with ideosyncratic expression, and can be very difficult to detect.
Top of stream from exiting cell through tiny caniculi isn't called ducts, is microscopic, half chemical, half mechanical. UDCA helps a bunch here.
Downstream is bigger tubes, down to exiting liver and outside liver. UDCA helps less, but still helps quite a bit with e.g. gallstones and general anti-inflammatory, anti- auto-immune and blood detox.
Contraindications: If the blockage is total upstream (extensive severe auto-immune, hepatoxicity or congenital) or downstream (macro causes, plus previous), UDCA cannot drain, forms lakes, accelerates death. These cases are out of scope for me with 99% confidence, because would be accompanied by major obvious symptoms and direct medical supervision.
Nevertheless, monitor risk of liver damage progression to ensure no lakes eventually do form. Ask experienced liver doctor how best to do this. And confirm ideosyncratic drug induced chronic cholestasis self-diagnosis with a baseline urine+blood complete test battery.
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26
(@camaroz28)

Posted : 06/17/2013 3:42 am

Note that you are also contributing to the error. It is bile caniculi -> canals of hering -> bile ductules -> intrahepatic bile ducts -> duct -> duct -> duct. In other words, the smallest upstream capillaries are not called ducts. The quote to which you objected uses the word "duct", not "biliary tree", and thus is referring only to the larger portals.

I am not contributing to anything; you are thick, and the passages you have just quoted from medical texts highlighting your new found understanding aren't impressive. I never said they were, they are the canaliculi." Bile formation begins in bile canaliculi that form between two adjacent surfaces of liver cells." I just referred to the whole structure as a "tree" because it is all one big network, and, for the sake of brevity. It still took you years to consider this, despite all the classic markers that you NOW see. I will not be drawn into more discussion with this on you. Your ego cannot take constructive critique; you should really get that checked out.

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26
(@camaroz28)

Posted : 06/17/2013 3:59 am

What do you recommend as an alternative to detox the liver? So far I have only gotten similar - sometimes even better - results by doing a combination of liver flushing and colon hydro theraphy.

In the past I have used Chinese bitters, and it made me capable of standing on my own two feet. It ultimately required higher and higher doses to work. Although, my liver labs were brilliant to begin with, things began to decline in that regard. It is definitely a case of diminishing returns.

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91
(@josephbuchignani)

Posted : 06/17/2013 4:22 am

"I never said they were, they are the canaliculi."
Context, my dyspeptic fellow. Your words: "But that is exactly where you said it's usage is extremely dubious; you simultaneously argue, that it's usage in those settings shouldn't even be debated because it so good, and it's a no-brainer decision."
That is only true if blocked bile ducts = cholestasis. If caniculi are not ducts, or if formation is not blockage, the distinction works fine.
I had no need to pay attention to the liver until after I started taking a potentially dangerous liver drug, and verified that the liver was the key to my problems. Because doctors had already told me, during and after, that the liver was not the problem. Liver research was not on my critical path to greater health, until now, when I am already healthy, and want to avoid getting worse later.
If you concede that, "Bile formation begins in bile canaliculi that form between two adjacent surfaces of liver cells," then cholestasis is once again about bile formation, not just bile transport, and your central criticism of my understanding of the liver fails.
"All cholestatsis refers to bile blockage." Your words. Now refuted by your other words.
As it turns out, the actual medical terminology is contradictory, probably because the distinction between chemical and mechanical transport at that microscopic level is quite fine.
While we're at it, let's not forget your lie about "rigorously and premeditatedly expediting his patients death by not following previously established dosing determinations set by the FDA".
It must irk you tremendously that I've been able to provoke your ego into shortcutting my research process. What a fantastic way to make you shut up!
Anyhow, I found a great website that explains drug induced liver injuries - FINALLY:
"Liver injury can be categorized by a number of systems. Some systems are based on the histologic lesion produced (i.e., inflammation, necrosis, cholestasis), others the type of injury (i.e., cytotoxic, cholestatic, mixed),"
"Mechanisms of liver injury.
Disruption of calcium homeostasis leading to cell surface blebbing and lysis
Canalicular injury
Metabolic bioactivation of chemicals via cytochrome P450 to reactive species
Stimulation of autoimmunity
Stimulation of apoptosis
Mitochondrial injury"
"Cholestasis can be produced by chemicals that damage the structure and function of the bile canaliculi. "
This is the most likely cause, given that steroids and estrogen do this, and we know Accutane targets epithelial tissue, which the caniculi are made of.
"A key component of bile secretion involves a series of ATP-dependant export pumps such as the canalicular bile salt transporter, that moves bile salts and other transporters that export other bile constituents from the hepatocyte cytoplasm to the lumen of the canaliculus."
This is what I meant by tiny tubes are as much chemical as mechanical.
"Some drugs bind these canalicular transporter molecules and lead to the arrest of bile formation or movement within the lumen of the canalicular system (Trauner et al., 1998). In rare circumstances affected individuals (~1%) develop progressive destruction of cholangiocytes leading to vanishing bile duct syndrome "
"Secondary injury can result as bile salts have a detergent action that can damage cell membranes and injure biliary epithelium or hepatocytes in areas of cholestasis."
"Another mechanism leading to cholestasis involves disruption of actin filaments situated around the bile canaliculi preventing the normal pulsatile contractions that move bile through the canalicular system to the bile ducts."
Accutane does bad things to hairs and villi as well, so this could also be it.
This form of injury is consistent with a long term, slow appearing effect of the sort Accutane is famous for. And UDCA is perfect for combating this kind of problem - as long as the blockage is not already complete.
The next one, "Metabolic Bioactivation by Cytochrome P450 Enzymes", is harsh, severe and immediate. Can be ruled out.
Next, "Stimulation of Autoimmunity", is also possible, and UDCA helps moderate this.
"It should be remembered that the liver is more than just hepatocytes and that liver injury can occur when other cell types are damaged. The biliary epithelium, Kupffer cells, endothelial cells, and the hepatic stellate cells can all suffer chemical-induced damage and contribute to liver injury and fibrosis"
In general, the Accutane-likely stuff sounds like things UDCA is very good at reversing. The exception would be if it's progressive, in which case use UDCA unless/until it progresses to the point where UDCA starts doing more harm than good. Then get a transplant.
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26
(@camaroz28)

Posted : 06/17/2013 5:01 am

YOU ARE A MORON. I have paddled your ass and you are still trying to save face. From Wikipedia: In anatomy, a canaliculus is a small passageway. In other words it is a smaller duct than the others.

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26
(@camaroz28)

Posted : 06/17/2013 5:19 am

 

In general, the Accutane-likely stuff sounds like things UDCA is very good at reversing. The exception would be if it's progressive, in which case use UDCA unless/until it progresses to the point where UDCA starts doing more harm than good. Then get a transplant.

Now he is saying use it until you need a transplant. What a moron, indeed.

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(@josephbuchignani)

Posted : 06/17/2013 6:26 am

On the contrary, none of your self-contradictory quibbles change any of my recommendations, except at the below 1% probability range, and even then, not materially, since medical supervision would commence before they became relevant. The real payoff is a better understanding of how Accutane may induce long term cholestasis and related problems. So my satisficing heuristics proved perfectly reliable, andyour predictable ego has managed to serve the greater good.

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(@josephbuchignani)

Posted : 06/17/2013 6:59 am

In sum, if you have general fatigue and digestive issues with fat, go to a doctor and get your blood and urine tested for liver issues.
If nothing comes up, give UDCA 1.5-2g /d a shot for 3 days anyway. It might be ideosyncratic, poorly understood, hard to detect, chronic drug induced cholestasis. Possibly by Accutane performing its intended function on the epithelial tissue of your liver. If no big change after 3 days, drop it or continue, won't matter much either way.
Or, if the liver tests find something, the doctor will almost certainly put you on long-term UDCA anyway.
If you're jaundiced, have pruritis, or other major liver symptoms, you'll be seeing a doctor regularly anyway. And he may take you off UDCA at some point, rightly so, but that'll be the least of your worries because there'll be a liver transplant on your horizon.
So for us, UDCA is about as safe as trying hyaluronic acid if your eyes are dry and your joints cracking. A no brainer.
And if you do try UDCA, or if you're suffering from Accutane sides in general, make sure to drink lots of water and get essential salts from e.g. concentrated shrimp broth. I drink water between every portion of food. Dehydration is an obvious mechanism of Accutane's action, and UDCA alone didn't fully solve my problem until I doubled or tripled water intake.
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(@camaroz28)

Posted : 06/17/2013 7:41 am

 

It might be ideosyncratic, poorly understood, hard to detect, chronic drug induced cholestasis.

Or it may just be that you are insane. If you mean poorly understood by you - you sure proved that.

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(@and1)

Posted : 06/17/2013 7:55 am

It seems that aside from Jospeh, who I really thank for having made me aware of UDCA, I am the only one who has tried it.

What it basically boils down to is you go to the doctor and he will assess whether or not the drug is safe for you. I hope that the discussion between Joseph and Camaroz doesn't scare people, whom UDCA may have helped, away from trying it.

Looking at your discussion it is obvious that you guys are at opposite ends of a spectrum. On the one end of the spectrum we have Joseph who essentially claims that UDCA is one of the best things that ever happened to him and that it is virtually completely safe, on the other end we have Camaroz who thinks UDCA is a very scary drug that is potentially life threatening.

The truth probably lies somewhere in between. In my case not much if any liver testing was done before I got the presription. I take the drug and I would see a doctor as soon as I would feel something is not going according to plan.

I personally would enourage anybody who suspects the underlying problem to be rooted in the liver to give UDCA a shot and do some research on their own.

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(@josephbuchignani)

Posted : 06/17/2013 8:09 am

"ideosyncratic, poorly understood, hard to detect, chronic drug induced cholestasis"

All of those words are quotes from the papers I linked which you obviously haven't read, Camaroz.

Cheers Believe. Of course there's nothing wrong with getting a doctor's opinion, but just because he won't prescribe it doesn't mean you shouldn't try it.

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(@camaroz28)

Posted : 06/17/2013 8:18 am

On the one end of the spectrum we have Joseph who essentially claims that UDCA is one of the best things that ever happened to him and that it is virtually completely safe, on the other end we have Camaroz who thinks UDCA is a very scary drug that is potentially life threatening.

Joseph's suggestion are to take UDCA as, "It might be ideosyncratic, poorly understood, hard to detect, chronic drug induced cholestasis." He advises this, because he has no other current bullshit obsessions to recommend as the "cure." Or, take UDCA, if you actually have cholestasis, and don't worry about it fucking up your liver more, because you are definitely going to need a transplant." He easily has the worst comprehension skills of anyone on this thread.

 

"ideosyncratic, poorly understood, hard to detect, chronic drug induced cholestasis"

All of those words are quotes from the papers I linked which you obviously haven't read, Camaroz.

Oh, you mean the words you obviously cut and paste from knowledgeable people because you desperately want to sound intelligent and you can't on your own. I am still staggered at your inability to get the point ever.

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(@and1)

Posted : 06/17/2013 8:21 am

but just because he won't prescribe it doesn't mean you shouldn't try it.

True.

You take it UDCA before meals right, like half an hour before or with the meal?

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(@josephbuchignani)

Posted : 06/17/2013 9:48 am

"Or, take UDCA, if you actually have cholestasis, and don't worry about it fucking up your liver more, because you are definitely going to need a transplant."
Not a quote from me, liar.
"Oh, you mean the words you obviously cut and paste from knowledgeable people because you desperately want to sound intelligent and you can't on your own."
Paraphrased actually, which suggests command of the material. Also, you're projecting again. Unlike you, I speak to teach and to learn. When you were beating me, I had no problem humbly acknowledging it. But you're not anymore.
Believe, no I take it inbetween bites during a meal. Size and fattiness of meal dictates how many, within the rough daily limit.
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(@camaroz28)

Posted : 06/17/2013 10:22 am

Yeah, sorry Joseph these were your words: "In general, the Accutane-likely stuff sounds like things UDCA is very good at reversing. The exception would be if it's progressive, in which case use UDCA unless/until it progresses to the point where UDCA starts doing more harm than good. Then get a transplant." Yes, those were your exact words. If a doctor led you down this path you could sue without question for negligence. Absolute garbage.

"When you were beating me, I had no problem humbly acknowledging it." Rubbish, you elided till the end. It has not been the first time I had to reign you in and it won't be the last. I don't how many time you have claimed victory over this syndrome - all lies.

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(@josephbuchignani)

Posted : 06/17/2013 11:21 am

" unless/until it progresses to the point where UDCA starts doing more harm than good."

You wouldn't be able to sue for negligence, because the UDCA was discontinued before it started doing net harm, dummy.

"I don't how many time you have claimed victory over this syndrome - all lies."

Not at all. In earlier phases, victories constituted fluctuations between level 0 and level 1, primarily. Now I am stable at level 4, even with all-nighters.

Levels:

0 bedridden invalid

1 can do something. paid work unlikely.

2 can do part time work, with some difficulty

3 can do full time work with significant struggle

4 can do full time work with only minor struggle, if any

The problem with the word "cured" is that it is too blunt an object. Therefore I am happy to clarify my meaning.

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(@chico-esposito)

Posted : 06/17/2013 11:33 am

Yeah that is why you failed to comment at ALL when we were discussing this. Just give to research, please. You don't have this and Joe does not have this. ALSO, I AM SURE THE RESEARCHERS ARE FEVERISHLY TRYING TO WORK OUT HOW TO CLEAR THE RETINOIDS FROM YOUR RECEPTORS. If storage issues are at work, they play a small role, not the principle role as you always allude to. The problem is the drug inhibiting it's own metabolism., amongst other things.

I see no purpose in getting into a slagging match with you, your opinion is your own and it's an interesting opinion, i respect it, but i respectfully disagree. Research says a lot of things, research is why we have chemotherapy drugs being pumped into people with cancer, damaging the body much more than it heals, it's why we have hugely toxic amounts of vitamin A being given to children for their acne problems. Medicine and medical research is still in it's dark ages, people will look back in many years time and see that it was a business venture not a health promoting exercise.

What you fail to understand is the simplicity of it, pump people full of a synthetic retinoid and some people are going to get symptoms of hypervitaminosis A. Of course it isn't the same exactly, because retinoic acid is not retinol, but the symptoms are similar in certain aspects. If it was just a DHT thing, why are so many people reacting to eating retinol in foods on this thread, well after stopping accutane? if your research can explain that i'll take notice.

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(@camaroz28)

Posted : 06/17/2013 11:33 am

".....in which case use UDCA unless/until it progresses to the point where UDCA starts doing more harm than good. Then get a transplant." And you are still trying to weasel your way out.

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