Accutane's mechanism of action explained

I believe that I have discovered Accutane’s mechanism of action and I will lay my evidence on the table and the reader be the judge. This specific information about the mechanism of action might someday lead to a treatment for Accutane induced cellular damage. After all, it’s much more difficult to fix something when you do not know what is wrong. I’ve provided the scientific studies to back up my hypothesis and used analogies in order to make the biological concepts easier to understand. I’ve explained everything in such a way that it’s very straightforward, even for people without a background in molecular biology.

Today, most people that are scientifically savvy about Accutane know that it decreases cell proliferation (in the bone, skin, gut, mucous membranes, and areas of the brain), which is why it’s used in chemotherapy, but up until now, nobody knows exactly how it does this. All throughout the history of Accutane, Hoffman-La Roche has always used the lame excuse in the Physician’s Desk Reference that “the exact mechanism of action is unknown.” Liam Grant, the chairperson of the Roaccutane Action Group, said it best at the FDA Meeting of the Dermatologic and Ophthalmic Drugs Advisory Committee held on September 19, 2000,

“Roche have stated publicly for the past 17 years in every country -- because we followed the PR statements from Roche and they're all the same, and they haven't changed, by the way, since 1983 -- we do not know the mechanism by which this drug works. Therefore, there's no proof that Accutane causes depression or psychiatric disorders. And they have no shortage of medical people and others who will go up with this statement. So, here we have a product. We know it causes the side effects, but why do they cause them? Well, that's not our problem. We don't know how it works. Therefore, don't ask me about the psychiatric side effects and don't ask me about all the many, many, many physical side effects. The Roaccutane Action Group as an organization now have to go out and are now spending our money because we know, of course, that the mechanism can be determined.”

http://www.fda.gov/ohrms/dockets/ac/00/transc...

As Liam Grant just said, the mechanism of action can be determined. Roche has possessed this technological capability for quite a long time, and it is entirely possible that they already know the mechanism but they just aren’t telling anybody because it would incriminate them. There are a few other organizations besides Roche that have the technology needed to decipher Accutane’s mechanism of action such as the Life Extension Foundation in Ft Lauderdale, FL and the Linus Pauling Institute at Oregon State University. But their services might not be needed because I believe that I have already discovered the mechanism of action.

Below, I’m going to include two quotes from the scientific section of www.accutaneaction.com that hint at Accutane’s mechanism of action, but don’t specifically say the actual mechanism because the group doesn’t know about the telomere (pronounced TEE-LOW-MEER) research that I have discovered. I’m convinced Roche has known about this research for the past 25 years, they've known ever since they developed different retinoids (like Accutane) to be used in chemotherapy, they’ve just been keeping it hushed up, because if this information ever got out, you’d have several million people around the world that are now pissed off because they unknowingly took a dangerous chemotherapy drug (for their benign/harmless condition of acne) that has inflicted serious damage to their body at the cellular level. Do you think that Roche wants people to know that Accutane reduces cell division / proliferation in several different areas all over the human body? Not a chance, because then nobody would ever want to take Accutane and they'd be out billions of dollars.

This information about telomeres definitely offers an explanation for why the terrain inside my nasal passage, my skin, my eyes, my cracked lips, and even my genitalia have resembled the surface of a desert for the past 9 years ever since my senior year of high school when I finished my one and only 5 month course (80 mg/day) of Accutane in December of 1998, which ended up being the worst mistake of my entire life. I didn’t have severe cystic acne or pancreatic cancer or leukemia. I had a bad case of teenage acne. For years I’ve suffered from agonizing body-wide dryness and dehydration all because of Accutane. As a result of what happened to me, I’ve become a reluctant expert on Hoffman-La Roche’s criminal history and Accutane’s history and pharmacology. What’s amazing is that the research about telomeres was published back in 2001, so basically it has taken six years for somebody like me to come along, discover it buried in the chemotherapy archives, and put two and two together. Once you understand the concepts behind telomere biology, you’ll better understand the quotes below from the scientific section of www.accutaneaction.com and how Accutane causes programmed cell death and inhibits the proliferation of rapidly dividing cells.

Accutane has been on the market for 25 years and for that entire time Hoffman-La Roche has specifically stated in the Physician’s Desk Reference that the exact mechanism of action of Accutane is unknown. They don’t mention that Accutane is a systemic chemotherapy agent that reduces cellular proliferation of the sebaceous glands in the skin all over the body (which is why it’s so effective against acne), and also does the same thing to the cells lining the digestive tract and mucous membranes (causing a lot of dryness). To corroborate my previous statement, take a look at what scientist James Crandall says in a study that can be found on PubMed. He is stating point blank this is how Accutane works and this is what’s causing the side effects.

"Retinoic acid (active form of Accutane) induces differentiation and reduces proliferation of stem and progenitor cells. It works on acne by inducing similar events in basal sebocytes. These same actions also lead to 13-cis-retinoic's (Accutane’s) side effects, and these are directed towards proliferating cells in the adult such as in the skin, gut and bone."

"A wide ranging effect of retinoic acid is to inhibit proliferation in dividing cells, and this accounts for its frequent consideration as an anti-cancer agent."

http://www.pnas.org/cgi/content/abstract/101/...

Crandall is hinting at Accutane’s mechanism of action but he doesn’t specifically say the actual mechanism because I don’t think he knows about the telomere (pronounced TEE-LA-MEER) research that I have discovered. Recently, I’ve discovered research that shows that all-trans retinoic acid (abbreviated ATRA which is the final biologically active metabolite that Accutane turns into) down-regulates the telomerase enzyme (pronounced TEE-LA-MER-AZE) and induces telomere shortening and cell death. This I believe is the mechanism of action. Accutane causes telomere shortening leading to permanently arrested cell division / proliferation.

So why is telomere shortening a bad thing to have? Here’s a quick rundown of telomere biology. Cells all over the body are replaced by means of cell division, and there is a limit on the number of times that they may successfully divide. This is known as the Hayflick Limit. Most cells in the body divide about 50 times before they stop dividing and die a natural death. The mechanism that controls this cell division lies within the telomere / telomerase, which is a cap like structure on the end of all the different twenty three pairs of chromosomes. Chromosomes are the helical structures of DNA that are found inside the nucleus of all cells in our body which carry our genetic code. The telomere chain and its length can be thought of as a string of beads (repeating code at the end of every DNA strand), with one bead falling off the string each time a cell divides. Therefore, the telomere shortens up a little bit every time a cell divides, and again this places a limit on the number of times a cell can replicate itself, known as the Hayflick Limit. Once these beads run out and disappear, the cell stops dividing and undergoes programmed cell death (AKA apoptosis). The constant process of telomeres getting shorter eventually leads to the death of the cell and over time this cumulative cell death leads to one of the major components of the aging process. However, there exists a specialized enzyme called telomerase which acts to repair damage to the telomere, maintain its stability, and extend the length of the telomere beads, thereby overcoming the Hayflick Limit. Germ line cells (bacteria) and cancerous cells continually express telomerase in such a way that they never run out of telomere beads and therefore remain immortal. Telomerase is naturally expressed more in cells in the body that are the most rapidly dividing (the immune system, skin, bone, digestive tract, mucous membranes), because these cells undergo more cell division throughout a person’s lifetime and therefore need to have their string of beads repaired and relengthened more often. Right now I’d like to include a relevant quote from Dr. Aubrey De Grey’s new book titled Ending Aging, that can be found at Amazon.com or any major bookstore. Dr. De Grey is a world famous Biogerontologist, which in a nutshell means he studies the aging process,

“If it weren’t for telomerase, this gradual shortening would eventually lead to the complete loss of the telomeres in cells that replicate frequently during the lifespan, and thus the gradual erosion of the genes themselves. Telomerase periodically relengthens the telomere before it becomes critically short.”(De Grey, 294)

10% of cancer cells use an alternative process to continue their cell division known as alternative lengthening of telomeres, but 90 % of cancer cells mutate and activate the telomerase enzyme in such a way that it continually rebuilds the telomere chain so that these cells never run out of cell divisions and therefore become immortal. This is one of the major defining hallmark characteristics of cancer. Cells divide and grow out of control and don’t die off like they are supposed to. The telomere Hayflick Limit is a cellular mechanism that is in place to specifically protect us from renegade cells growing wildly out of control (AKA cancer). The following quote from Dr. Aubrey De Grey’s Ending Aging explains what would happen if cancerous cells were deprived of telomerase or alternative lengthening of telomeres,

“Either way, without a way to renew their telomeres, the single-minded multiplication of potential cancer cells rapidly grinds to a halt as it reaches the end of its telomere “rope,” and we wind up with a tiny (and generally short-lived) lump in our bodies instead of a life-threatening, malignant condition.”(De Grey, 295)

From what I’ve observed, generally, the people who suffer the latent side effects of Accutane have the OPPOSITE problem that people with cancer have. With cancer patients, there’s too much bad cell division going on, but with Accutane sufferers, there’s too little normal necessary bodily cell division or sometimes none at all because the chemotherapy drug Accutane has caused critical telomere shortening, inducing growth arrest and cell death in various areas of the body where cell division is supposed to be ongoing. The bad thing about Accutane is that there's a huge amount of individual variability when it comes to the side effects. For some people, it takes multiple courses of Accutane to induce permanent side effects, but for others all it takes is one course to put their bodies past the critical point of no return. Different people get different combinations of side effects and they are very unpredictable, because through influencing DNA transcription (which is what all retinoid/vitamin A drugs do), it causes random groups of cells all over the body to differentiate and shut-down when they are not supposed to. This is why it is used in chemotherapy. Chemotherapy drugs kill rapidly dividing/proliferating cancerous cells, but they also kill the healthy rapidly dividing/proliferating cells of the body along with the cancer. Accutane binds to the vitamin A nuclear receptors RAR and RXR on the surface of the nucleus inside every cell in the entire body and changes the cell’s gene expression and protein transcription. This is why it has an extremely long-list of side effects involving every tissue and every organ in the human body. The cells that are the most vulnerable to this effect are the ones that need to divide (undergo mitosis) more often.

I believe that the people who are suffering from chronic latent side effects are those whose individual biochemistry was the most susceptible to Accutane’s strong telomere shortening influence. The severity of Accutane long-term side effects all depends on how far the course of Accutane down-regulated the telomerase enzyme and shortened the telomere length. Here’s another quote from Dr. Aubrey De Grey’s book that explains what would happen if telomerase was completely down-regulated,

“Deleting telomere elongation capacity throughout the body would also be life-threatening, because it would mean that our regular, proliferating cells (like those in the skin or the lining of the gut) would suddenly have iron limits on their ability to reproduce themselves and thus replenish tissue. From the moment that we denuded our cells of telomerase, a clock would be ticking. With each division the telomere would shorten by a notch from whatever it had been when we took telomerase out. We would be under the specter of a rather horrible death, as our stem cells went offline one by one under replicative senescence (see Chapter 10): with each failure of a stem cell responsible for supplying key functions, the tissue would fail to be renewed and would slowly degenerate.”(De Grey, 297)

Accutane and ATRA (all-trans retinoic acid or Vesanoid) are very similar drugs, they are both retinoids, they have very similar side effect profiles and pharmacokinetics and they are almost chemically identical. Interestingly, Roche states a 14% incidence of depression for 10 mg of Vesanoid, with the knowledge that this is exactly what 40 mg of Accutane interconverts into. To clarify, here are the generic names and chemical names for these two drugs that are both manufactured by Hoffman-La Roche.

Accutane (used for Acne)
Isotretinoin
13-cis retinoic acid

Vesanoid (used for Leukemia)
Tretinoin
All-trans retinoic acid or retinoic acid

Since a certain percentage of Accutane metabolizes into ATRA (about 30%), and since the ATRA metabolite is how Accutane exerts its pharmacological actions on the body, there’s no doubt that if ATRA causes telomere shortening then Accutane also causes telomere shortening. If Accutane truly does cause telomere shortening and down regulation of the telomerase enzyme (and I believe that it does), this could mean huge significant implications for maintaining adequate cell proliferation all over the body during a person’s lifetime. Accutane, being a potent chemotherapy drug, attacks and damages the cells in our body that are supposed to remain dividing and proliferating for our entire lifetime. If cells have shorter telomere lengths (shorter telomeres), they get closer to the Hayflick Limit and can’t divide / proliferate as much or they go on to experience growth arrest and cell death (apoptosis). This is how Accutane reduces acne, and why in some cases, the acne doesn’t come back, and the patient is left with permanent dry skin, dry mucous membranes, digestive problems, and other various permanent side effects. During the course of treatment and after, Accutane has increased the cell division / turnover rate so drastically, that these cells have ran out of cell divisions and are driven into their Hayflick Limit. This can be illustrated by observing what happens when somebody eats polar bear liver (contains extremely high toxic levels of vitamin A similar to Accutane) and their skin starts to peel off all over their body in thick giant sheets from the increased cell turnover rate, also a potential side effect of Accutane. The cell division rate (beads falling off the string) has been increased so fast and telomerase has been down-regulated so much that it cannot repair the telomere chain (the beads on the string) before the cells lose all of their cell divisions (beads) and enter growth arrest (Hayflick limit). Here’s an excellent definition of the Hayflick Limit,

“Dr. Leonard Hayflick discovered that mammalian cells divide only a fixed number of times. This "Hayflick Limit" was later proven to be caused by telomeres on the ends of chromosomes that shorten with each cell-division. When the telomeres are gone, the DNA can no longer be copied, cell division ceases, and cells enter replicative senescence or old age.”

Do some research online and on Wikipedia about telomerase, telomere shortening, and the Hayflick limit, and how they play a role as one of the major components of the aging process. Another interesting observation is that people with the premature aging disorder Progeria have shortened telomeres. So imagine what is going to happen when this information gets out that Hoffman-La Roche and the American Academy of Dermatology have given a drug that causes a form of premature aging to millions of teenagers and young adults with acne? People need to understand that stopping Accutane doesn’t necessarily mean that they’re in the clear. There are several reports by people (including myself), who claim that some of their side effects, particularly the worst kinds, didn’t emerge until years after they stopped Accutane. This drug has a chronic latent effect on people’s bodies, which is also how it permanently cures some people’s acne (with lots of collateral damage of course). There’s going to be a massive backlash when this information gets out, even with people who took a low dosage and got good results from their course of Accutane and (so far) haven’t developed any complications or chronic health problems. My impression, after conducting endless hours of research, is that there are thousands of people out there with really bizarre and unusual chronic health problems as a result of their exposure to Accutane, but they just haven’t investigated and made the connection yet. As a result of taking Accutane, their bodies are now more vulnerable to injury, reduced healing ability, sickness, and disease because they have shorter telomeres. Any individual who has ever taken Accutane needs to know about this so they can take proactive steps to avoid injury, avoid eating liver or high doses of vitamin A, lead a healthy/low-stress lifestyle, get a lot of sleep, and protect the health of their body.

This discovery of mine also opens up the possibility of testing for abnormal telomere shortening in people with chronic long-term Accutane side effects. There are specialized tests that can assess telomere/telomerase shortening. One of them is called the terminal restriction fragment southern blot TTAGGG telomere length assay. But there are only a few laboratories in the country with the technology to test telomeres/telomerase, and one of them is at Roche.

Once Accutane’s mechanism of action gets out, nobody will ever want to take it, and those who have already taken it will have to live with the consequences of knowing that they‘ve exposed themselves to a powerful cell-proliferation reducing chemotherapy drug that has damaged their body at the cellular/DNA level and depending on the extent of the damage, possibly shortened their life expectancy. In these individuals like myself, the cells in certain areas of the body like the skin, nasal passage, or digestive tract have a reduced ability to divide and proliferate, which is why the mucous membranes, the nasal passage, eyes or lips become very dry, and certain areas of the digestive tract also lose this ability, so then it sustains damage and develops into inflammatory bowel disease. After all, the digestive tract can be thought of as a tube (your body is hollow) that is technically “outside of the body” because the mucosal barrier with secretory IgA is what protects us from pathogens and the harsh substances of digestive metabolism. Just like the skin, the lining of the digestive tract is a barrier that separates our bodies from the outside world. This protective barrier becomes dysfunctional and gets diminished after Accutane because the cells can’t divide as much. This is how Accutane can destroy your gut.

I always knew that Accutane’s mechanism of action would reveal itself by examining the way that retinoids are used in chemotherapy. When retinoids are used for chemotherapy, at least they make an attempt to tell patients how the stuff works and warn them about the side effects. This study below is the smoking gun for Accutane's mechanism of action, because ATRA (all-trans retinoic acid or Vesanoid) is the active metabolite that 13-cis retinoic acid (Accutane) turns into. Nobody besides me has made this connection yet. Nobody has posted any information about retinoids and how they cause telomere shortening on the Roaccutane action group forum. Here's a quote from the abstract of a study that can be found at this link,

Retinoids down-regulate telomerase and telomere length in a pathway distinct from leukemia cell differentiation

http://www.pubmedcentral.nih.gov/articlerende...

"A second pathway of hTERT regulation, identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. This pathway leads to telomere shortening, growth arrest, and cell death, all events that are overcome by ectopic expression of hTERT.”

Here's another interesting quote from the scientific abstract of a study. I’ve provided the link to this study below,

Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL

http://www.nature.com/leu/journal/vaop/ncurre...

"These results support the idea that, by hTERT targeting, retinoids can induce telomere shortening and cell death and their integration in therapy protocols for myeloid leukemias refractory to maturation should be considered."

hTERT (AKA human telomerase reverse transcriptase) is what maintains the telomeres of eukaryotic chromosomes. In the quote above, it says it right there in black and white, retinoids can induce telomere shortening and cell death. This is how Accutane reduces adult stem cell proliferation in the bone marrow, how it reduces cell division and causes severe dryness of the mucous membranes (eyes, lips, mouth, nose, GI tract, urethra), how it reduces cell proliferation in the “embryonic-like” regions of the brain (the hippocampus and subventricular zone), how it can cause necrosis or abnormalities of gastrointestinal tissue leading to inflammatory bowel disease, how it (and vitamin A toxicity) induces premature growth plate closure in the bones of adolescents, how it occasionally causes permanent hair loss, and finally how it reduces acne, sometimes permanently. Accutane has the most significant damaging effect on any group of cells in the body where cell division / proliferation needs to be constantly sustained throughout a person’s entire lifetime, which are areas where cell division is the most rapid, ongoing, and abundant.

To sum all of this up, the evidence we currently have is that long term treatment with ATRA (all-trans retinoic acid), which is almost chemically identical to Accutane, causes “telomere shortening, growth arrest, and cell death.” The cells that the researchers tested in the studies I listed above were cancerous cell lines, but if ATRA causes these effects in cancerous cell lines, then it is highly likely that it will do the same thing to our body’s own dividing/proliferating cells such as the cells in the bone, skin, digestive tract, and even the hippocampus and subventricular zone in the brain. This is the “big link” hypothesis. Besides the Crandall study on the hippocampus, to my knowledge, I don’t know of any specific studies that have been conducted on how it affects the body’s own rapidly dividing cells, but given the nature of some people’s symptoms and side effects, telomere shortening is an obvious possibility.

Another significant observation that can be picked up from this research is that if ATRA causes telomere shortening, and that this is also the mechanism of action for how vitamin A toxicity causes many side effects and reduces cell division, this could explain why lots of people have reported that consuming high amounts of vitamin A or foods rich in vitamin A after their course of Accutane worsens their side effects, especially the problems related to dryness. In other words, this could explain why for some people, the side effects get a lot worse after they stop Accutane, because the dietary vitamin A they need to stay alive might be slowly killing them because Accutane has shortened their telomeres too far. A search on the internet reveals an abundance of information about vitamin A and retinoid compounds being inhibitors of telomerase.

Vitamin D3, Vitamin A and The Prevention of Tumor Cell Immortality
http://grouppekurosawa.com/blog/2006/01/vitam...

Vitamin A Cancer Adjuvant Therapy from the Life Extension Foundation
http://www.lef.org/protocols/prtcl-027h.shtml

http://www.telomere.net/
http://learn.genetics.utah.edu/features/telom...

In my opinion Roche stating that “the exact mechanism of action is unknown” for the past 25 years is just a ruse to distract people from learning the information that the systemic cell division reducing effect of retinoic acid is specifically what’s responsible for making their acne go away and causing a lot of the side effects. James Crandall’s statement “A wide ranging effect of retinoic acid is to inhibit proliferation in dividing cells, and this accounts for its frequent consideration as an anti-cancer agent” is good enough for me as an explanation for the mechanism of action. Being a systemic chemotherapy agent, Accutane does NOT know the difference between cancer and your body’s own rapidly dividing cells. With the knowledge that many parts of the human body (such as the skin, digestive tract, bone, lungs, mucous membranes, bladder, urinary tract, and sexual organs) rely on rapid and plentiful cell division/proliferation to sustain their proper function throughout a person’s lifetime, this information about retinoic acid having a “chemotherapy like” cell division reducing effect becomes extremely important. Because it means that if you take too much Accutane for too long of a period of time, you are essentially slowing down or stopping cell division in areas of your body where cells are supposed to remain dividing for your entire lifetime. In my opinion this is what is causing a lot of the chronic long term side effects, these people basically have the opposite problem that people with cancer have. As I’ve talked about in depth above, a potential explanation for the mechanism of action could involve human telomerase reverse transcriptase (hTERT), the chief regulator of cell division in our rapidly dividing cells. It has already been shown that retinoic acid down-regulates hTERT in cancerous cells, which is sufficient evidence to call for an investigation of its effects on hTERT in the human leukocytes, enterocytes, keratinocytes and sebocytes. So to prove Accutane's mechanism of action, here's what you do. With skin biopsies, test telomerase and the telomere lengths of the basal sebocytes before and after a four month course of Accutane. Roche is going to have a cow when they read this.

NCC.

This information about telomeres is facinating. It really does explain why accutane causes damage in every part of the body.

I have read this entire post and I think everyone else should read it also so they know what they are getting into.

Scary.

is this a scientific study? has any medicinal body accepted these explanations? just asking....

wow.

My hypothesis about Accutane’s mechanism of action is very controversial, but there’s lots of evidence to back it up, everything can be found up above in the scientific studies I’ve provided. Basically I just connected the dots on a few things. I discovered how the retinoid ATRA (also known as all-trans retinoic acid or Vesanoid) works against cancer, and given the fact that Accutane converts into ATRA (which is the biologically active form), therefore whatever ATRA does to the body Accutane’s effect is very similar. Both drugs are used in chemotherapy against cancer, they are almost chemically identical and have very similar side effect profiles. The core of my hypothesis is that since ATRA and probably Accutane both cause telomere shortening of cancer cells, then it is highly likely that they will have the same effect on our bodies own rapidly dividing cells (skin, lungs, digestive system, bone, hair) which is how it works to reduce acne and also how it causes so many side effects all over the body. Today it has become obvious to all of the scientific community that Accutane induces apoptosis (programmed cell death) causing reduced cell division/proliferation, but they haven’t arrived at a consensus about how it does this. I believe that I have discovered the mechanism of action for how it reduces acne and causes a lot of the side effects. It down-regulates the telomerase enzyme and shortens the telomere length so the cells can divide as much anymore. You cannot count on Roche being truthful about anything related to Accutane’s mechanism of action. For the past 25 years they’ve stated in the Physician’s Desk Reference that the mechanism of action is unknown. This is their way of sidestepping issues regarding all of the harm Accutane causes to the human body and to distract people from learning more about how Accutane does what it does.

A full copy of the Crandall study I listed above can be found at this link,

http://www.accutaneaction.com/Studies/2004_Cr...

There's a typo in my recent post above. It says "so the cells can divide as much anymore" but it should say "so the cells CAN'T divide as much anymore."

It is an impressive explanation, hard to follow sometimes for a non-scientific person like myself, but I do get the bottom line.

I'm (almost) happy that hair loss is my only side effect, until now at least.

NCC, you don't say much about duration of course and side effects. I did see that you said that for some persons the side effects can last very long or even be permanent, depending on how your vulnerable or not you body is to this treatment.
In your theory, how bad/permanent can side effects get after a two week treatment?

Thank you so much for sharing your knowledge with us, and good luck with your health.

I've read hundreds, maybe even over a thousand testimonials and while it is less likely to get permanent side effects from two weeks of Accutane, it is still possible. The only way to find out is to never take it again and see what happens. From what I've read, the people who are a lot more likely to get permanent side effects (especially side effects related to dryness) are the ones who take Accutane for an extended period of time (over several months or multiple courses) The side effects are identical to what would happen if you took very high doses of vitamin A for a long period of time, inducing a condition called chronic hypervitaminosis A. The threshold for dose and duration of Accutane causing permanent side effects is different depending on the individual. I took it 10 years ago at 80 mg per day for five months and stopping the treatment did little to alleviate my side effects (painful dry and irritated eyes, dry nasal passage, dryness all over my body). These side effects are still with me today, including several others that manifested in the years after finishing Accutane (to name a few would be Type 1 Diabetes diagnosed a year and a half ago, problems with digestion and circulation, urinary discomfort and pain of varying degrees aka interstitial cystitis, dryness and hypersensitivity of my genitalia to the point where I can’t wear boxers anymore and sexual experiences with the ladies have become very rare) Some of my side effects wax and wane, but they never completely go away. I don’t have the time to go into detail about everything right now, but I will in the future.

thx for your answer, I definitely won't EVER take it again!!

I'm really sorry to hear all the worries you have, I hope that you have the necessary support of people around you

hugs from Belgium

The question when taking any drug is: Does the benefits outweigh the side effects? So why would it be any different with accutane? If you put up with acne like this: http://www.medscape.com/content/1997/00/40/88... a large portion of you life, you tried everything and nothing worked, would it be worth it to take accutane and be relieved of this nightmare for the side effects?... I think it would be...

Living life with sh!t all over you face isnt living. I have an aunt that took accutane back in 87. She has no problems. She is 42 and she sometimes gets mistaken for my wife (im 28) when we go out to places. She doesnt look prematurely aged at all.

So your telling me in the 25 years accutane has been around hundreds of labs with millions of dollars in equipment, the FDA and thousands of educated doctors who have prescribed the drug don't know the mechanism of what stops the sebum production in the skin, but you, through your internet research nonetheless, has uncovered the secret? Ok.