Acne.org Products
2 hours ago, MovingOnMusicGal said:I'm sure it has been brought up before, can anyone explain the science behind producing more sebum, or collagen after a night of ingesting alcohol. I know someone here has brought this up in the past . My skin is completely smooth the day after having even the smallest bit of alcohol....I feel normal for a day afterward and then it slowly goes away. I read an article that alcohol interferes with retinoic acid in the liver by blocking it's absorption. Perhaps alcohol may discharge it as well? Anyone? Shall we all get together and binge drink? Just kidding...
try some redbull and vodka.. then youll get the full effect:)
http://onlinelibrary.wiley.com/doi/10.1002/hep.510280321/pdf
Study re: retinoic acid and alcohol consumption in rats
"A previous in vitro study has demonstrated that acetaldehyde, which is an oxidative metabolite of ethanol, increased procollagen I and fibronectin gene transcription in fat-storing cells"
Boom
On 12/16/2015 at 9:18 AM, yetanotheraccutanevictim said:Can you guys/girls list some of your favorite podcasts youlisten to (health related)
My eyes are so dry that I cannot use a computer for very long so I rely on audio to learn, mainly.
Here are some that I listen to currently or have listened to in the past: [Edited link out]
Few of my favorites: ReWild Yourself with Daniel Vitalis, Revolution Health Radio, Ben Greenfield Fitness Podcast, High Intensity Health Radio, Underground Wellness Radio, Methylation Support, The Cutting Edge of Health and Wellness Today
My eye condition got so bad that I went to doctor. My nasolacrimal duct looked OK-ish, but my eyelids were all bumpy from the inside so they can't moisturize the eye properly. I got some allergy eyedrops and they helped alot, but now I'm on square one when I stopped using them. I don't know how to deal with it and it would be nice if people suffering from dry eyes would check their inner side of the eyelids so we could know if it's Accutane related.
What about trying Increlex or Igf lr3. I know that there is a cure but we get our eyes only on amino acids and things like this. Natural thingsdon't work for US I think (with natural things i mean amino acids, herbs...) accutane changed our genes remember that. My cure would be igf 1 (our Main Problem, because high igf 1 is what cause acne, and witch would be lowered to fight acne). Igf 1 works even like an antidepressant in studys upregulates dht production and downregulates foxo very potent. So why Not give it a try?!
1.your genes dont change!!!! or you would be growing a horn or a tail by now if they did. the expressions change, and that is altered by everything from smoking to accutane to diet. you still have all of your normal genes, and they still have all of the ability to express normally.
2. we have absorption problems.. and that leads to every other side effect. none of the supplements will work until this is fixed. To the people complaining about looking like methheads and gaunt... this fits that complaint as well. WE'RE WASTING AWAY! fat absorption problems!
3. amino acids work.. i can already see it physically . so take all of the natural IGF-1 promoters. its going to take at least 6 weeks imo.
45 minutes ago, tryingtohelp2014 said:
1.your genes dont change!!!! or you would be growing a horn or a tail by now if they did. the expressions change, and that is altered by everything from smoking to accutane to diet. you still have all of your normal genes, and they still have all of the ability to express normally.
2. we have absorption problems.. and that leads to every other side effect. none of the supplements will work until this is fixed. To the people complaining about looking like methheads and gaunt... this fits that complaint as well. WE'RE WASTING AWAY! fat absorption problems!
3. amino acids work.. i can already see it physically . so take all of the natural IGF-1 promoters. its going to take at least 6 weeks imo.
can you list the things that will promote natural igf. thanks
tryingtohelp2014
You're right, my english is bad I don't wanted to sayx that it has changed our genes in an irreversible manner... Amino acids work but if this little changes from natural things would range?. Know what I mean? Do you consume Methionine (I heard that it is a IGF-1 promoter) But also read bad things about it things like causing cancer I don't know exactly..
14 hours ago, MovingOnMusicGal said:http://onlinelibrary.wiley.com/doi/10.1002/hep.510280321/pdf
Study re: retinoic acid and alcohol consumption in rats
"A previous in vitro study has demonstrated that acetaldehyde, which is an oxidative metabolite of ethanol, increased procollagen I and fibronectin gene transcription in fat-storing cells"
Thanks for posting! I don't touch alcohol but that study might explain why people are relieved of their accutane symptoms after a night of drinking.
As I currently understand it, when we ingest 13-cis-retinoic acid (13CRA/accutane)it is isomerized to all-trans retinoic acid (ATRA) which has the capacity to bind to cis retinoic acid-binding proteins (CRABPs) which go on to activate nuclear retinoid receptors (RARs) to form RAR-RXR heterodimers which bind to DNA and initiatetransactivation of retinoid responsive elements (RAREs) which induce the teratogenicity within the nucleus of cells. This also leads to a deficiency of FoxO proteins via FoxO-mediated transcriptional regulation.
On pg 749. Figure 4 of the study on alcohol & retinoic acid, it appears that ingestion of alcohol inhibitsretinoic acid biosynthesis,increases retinoic acid catabolism, and mobilizes vitamin A from the liver to other organs, which CREATES A LOCAL RETINOIC ACID DEFICIENCY IN THE LIVER.
AP-1 nuclear complex causes cell proliferation BUT if you'll read part of the study, it says that in the presence of ATRA, RARsact as negative regulators of that nuclear complex, which inhibits their cell proliferation.
But, if ATRA becomes deficient in the liver due to ingesting alcohol, the AP-1 nuclear complex can continue to function which leads to cell proliferation.
I don't think I explained it well enough but IJust thought that was interesting how alcohol can help usersget rid of some of the retinoic acid in our livers and we start to become less symptomatic, even if temporarily. Another +1 for accutane liver toxicity being a major cause of our illness.
Been taking taurine since Saturday and I've definitely been feeling even more drained that usual. I've also noticed some really inflamed bumps (nothing in them, just super inflamed and sore)around some hairs on my legs and scalp, which also happened when I came off accutane, so I'm hoping it's just a sign of more of it leaving my system.
23 hours ago, manalesenicola said:relentless1k what do you think was most important for treating erectile dysfunction?
What you other guys do for erectile dysfunction? Best supplements in your opinoin?
Raising testosterone levels which also elevated DHT levels i assume. I dont think accutane permanently inhibits the 5ar enzyme.. I took up smoking because of depression and i still regained my erections, so it was moslty hormonal.
It fixed itself with getting all my nutrients in and eating a good diet.. Took 2,5 years but i might have been lucky..
6 hours ago, Mike San said:Wouldn't igf1 be expensive though? And how would you even get it prescribed?
First it would be good to test your levels though.
There are 3 issues: Its extremely expensive
Doctors dont prescribe it unless there is some serious disease that requires it (ive never seen it used medically)
It acts locally where you inject it. Bodybuilders inject IGF1 into the muscle they train that day. For example if they train arms they inject it into biceps and triceps..
If you want to raise IGF1 through pharma, its best to take HGH. Which you wont get from a doc either + its also extremely expensive..
increasing mTOR increases IGF1 though..
The main activator of mTOR is a variety of amino acids and the hormone insulin. Testosterone also is capable of activating mTOR (R,R2).
- Protein, especially leucine
- Excess calories
- Excess carbs
- Exercise (R,R2) activated in brain, muscle and heart.Inhibited in liver and fat cells. All good
- Orexin (R)
- IGF-1 (R)
- Insulin
- Testosterone(R)
- Ghrelin (R) in hypothalamus
- Leptin (R) in the hypothalamus
- Thyroid hormone (R) in the hypothalamusand other cells(R)
- Oxygen
- Ketamine (R). (In the brain produces antidepressant effect.)
- IL-6(R) in muscle and fat
Potential long-term impact of 5-alpha reductase inhibition:
Effects of Subchronic Finasteride Treatment and Withdrawal on Neuroactive Steroid Levels and their Receptors in the Male Rat Brain., Neuroendocrinology, Dec. 2015.
[Edited link out]
ABSTRACT
The enzymatic conversion of http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A1702 6" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">progesterone and http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A1734 7" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">testosterone by the enzyme 5alpha-reductase exerts a crucial role in the control of nervous function. The effects in the brain of http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A506 2" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">finasteride, an inhibitor of this enzyme used for the treatment of http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=9606&lvl= 0" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">human http://europepmc.org/search/?page=1&query=%22benign%20prostatic%20hyperplasia%2 2" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">benign prostatic hyperplasia and http://europepmc.org/search/?page=1&query=%22androgenic%20alopecia%2 2" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">androgenic alopecia, have been poorly explored. Therefore, the effects of a subchronic treatment of http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A506 2" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">finasteride at low doses (3 mg/kg/day) and the consequences of its withdrawal on neuroactive steroid levels in plasma, cerebrospinal fluid and some brain regions as well as on the expression of classical and non-classical steroid receptors have been evaluated in male http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=10116&lvl= 0" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">rats. After subchronic treatment (i.e., 20 days) the following effects were detected: (i) depending on the compartment considered, alteration in the levels of neuroactive steroids, not only in 5alpha-reduced metabolites but also in its precursors and in neuroactive steroids from other steroidogenic pathways and (ii) upregulation of http://www.uniprot.org/uniprot/?query=androgen%20receptor&sort=scor e" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">androgen receptor in the cerebral cortex and beta3 subunit of GABA-A receptor in the cerebellum. One month after the last treatment (i.e., withdrawal period), some of these effects persisted (i.e., upregulation of http://www.uniprot.org/uniprot/?query=androgen%20receptor&sort=scor e" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">androgen receptor in the cerebral cortex, increase of http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A2845 3" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">dihydroprogesterone in cerebellum, decrease of http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A8527 8" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">dihydrotestosterone in plasma). Moreover, other changes in neuroactive steroid levels, steroid receptors (i.e., upregulation of http://www.uniprot.org/uniprot/?query=estrogen%20receptor&sort=scor e" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">estrogen receptor alpha and downregulation of http://www.uniprot.org/uniprot/?query=estrogen%20receptor%20beta&sort=scor e" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">estrogen receptor beta in cerebral cortex) and GABA-A receptor subunits (i.e., decrease of alpha 4 and beta 3 mRNA levels in cerebral cortex) were detected. These findings suggest that http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI%3A506 2" rel="external nofollow" style="text-decoration:none;font-weight:normal;color:#000000">finasteride treatment may have broad consequences for brain function.
There are a few of us with sexual side effects, including ED, who have tests showing reduced 5-ar activity many years after stopping Accutane. There may be nothing more that can be done except symptom management, such as Viagra. Restoring libido and other neurological and physical benefits of proper androgenic function may be next to impossible.
5 hours ago, Modeaa said:http://www.ncbi.nlm.nih.gov/pubmed/17080243
taurine could inhibit lipid peroxidation, improve lipid and glucose metabolism, decrease synthesis of TNF-alpha and TGF-beta(1),'' ''
trying to help posted a study says that tgf beta1 itself can reduce an enzyme which produce taurine, and that BCAA can prevent this TGF-beta1 effect on that enzyme and tus on taurine.
http://www.ncbi.nlm.nih.gov/pubmed/24553827
'' cysteine dioxygenase (CDO), a rate-limiting enzyme in taurine synthesis''
''BCAA, especially leucine, promoted Cdo1 gene transcription, and attenuated TGF--mediated suppression of Cdo1 gene expression.These results indicate that the low plasma level of taurine in advanced hepatic disease is due to decreased hepatic CDO expression, which can be partly attributed to suppressive effect of TGF- on Cdo1 gene transcription. Furthermore, our observation that BCAA promotes Cdo1 expression suggests that BCAA may be therapeutically useful to improve hepatic taurine metabolism and further suppress dysfunctions associated with low level of taurine in hepatic diseases
Leucine stimulates mTORC1-SREBP signaling and leucine is directly converted by sebocytes into fatty acids and sterols for sebaceous lipid synthesis. Over-activated mTORC1 increases androgen hormone secretion and most likely amplifies androgen-driven mTORC1 signaling of sebaceous follicles. Testosterone directly activates mTORC1. Future research should investigate the effects of isotretinoin on sebocyte mTORC1 activity. It is conceivable that isotretinoin may downregulate mTORC1 in sebocytes by upregulation of nuclear levels of FoxO1
http://www.ncbi.nlm.nih.gov/pubmed/23516608
Yeah, Leucine seems to be the active BCAA for us.
1 hour ago, Dubya_B said:
There are a few of us with sexual side effects, including ED, who have tests showing reduced 5-ar activity many years after stopping Accutane. There may be nothing more that can be done except symptom management, such as Viagra. Restoring libido and other neurological and physical benefits of proper androgenic function may be next to impossible.
We are constantly upregulating or downregulating gene expression/enzymes every day just by what we eat. NOTHING is permanent. ive posted ourlinks to the 5AR people earlier. this will be fixed.
This is just like the movie Lorenzo's oil...except we werent born with this problem... ITS NOT GENETIC! thats a huge difference. we dont have a genetic error inside of us... we have an active metabolite repressing an expression somewhere.
On 12/12/2015, 10:02:09, Fchawk said:
This is in response to an email asking about what someone can do a year after taking a relatively small dose of Accutane (<200mg in total), and still having negative side effetcs. Primary concerns were long term sexual function, hormonal balance, and bone growth. I think we can all agree on the first paragraph
I would say the first two treatments I would take would be Taurine and Creatine, as well as BCAAs(Branched-Chain Amino Acids). I believe many of the symptoms of Isotretinoin (Accutane) are caused by
Any taurine updates ?
thanks for understanding the reason for posting it!! I don't think it's a cure-all, I was being facetious, but, I understand the science behind it. and it does suppresssymptoms temporarily...there is something to it.
" or simpler answer based on my last post. alcohol suppresses the excitability of nerves. its a depressant. ", not at all what I am talking about. Everyone knows it's a depressant.
Been learning a lot recently from Dr. Dietrich Klinghardt. He's a fantastic resource. Definitely recommend checking him out.
Includes information on chronic infection, detoxification, electromagnetic radiation exposure, effective herbal strategies, autonomic response testing, etc.. (healing from chronic disease)
If anyone has any resources they could recommend I check out, I'd appreciate a PM. Podcasts, blogs, youtube channels, scientists, etc.. Thanks
3 hours ago, tryingtohelp2014 said:
We are constantly upregulating or downregulating gene expression/enzymes every day just by what we eat. NOTHING is permanent. ive posted ourlinks to the 5AR people earlier. this will be fixed.
This is just like the movie Lorenzo's oil...except we werent born with this problem... ITS NOT GENETIC! thats a huge difference. we dont have a genetic error inside of us... we have an active metabolite repressing an expression somewhere.
I'll check back in 10 years to see if anyone has found evidence of that unidentified metabolite that seems to stay active for decades in some of us or if anyone has brushed up on their biology lessons. Good luck Augusto. Adios.
On 15.12.2015, 22:14:36, Fchawk said:Just wondering, how many people took such low doses?I mean thats cumulative 130mg, which would have been <2 days of treatment at mydose, and having permanent sides off so little...
Does that mean this med either fucks you up or it doesn't, seeing tonnes of other people don't experience hardly anything, or there are other risk factors involved? Just an observation...
I took one course of low dose (10mg)Isotretinoinand it has completely messed up my digestive system (I can't toleratefat and fructose anymore). Symptoms startedalready few hours after swallowing the first capsule (very loud stomach noises - particularlyat night and after lying down). Two weeks later I have noticed much brighter stools (common symptom of fat malabsorbtion). Myliver enzymes were in thenormal range during the whole treatment (apart from slightly elevated bilirubin). I have tried various supplements, probiotics, antibiotics,diet modifications etc.with miserable results.At this point, I am preety sure that Isotretinoin has induced some sort of allergic reaction to certain foods (i.e.fructose intolerance)via itsimmunomodulating properties. I am also consideringsmall intestinal bacterial overgrowthbecause Isotretinoincan cause variations in the microbial floras of several sites of the body.
14 hours ago, Dubya_B said:
There are a few of us with sexual side effects, including ED, who have tests showing reduced 5-ar activity many years after stopping Accutane. There may be nothing more that can be done except symptom management, such as Viagra. Restoring libido and other neurological and physical benefits of proper androgenic function may be next to impossible.
Technically you would be able to manage this, there are DHT hormones you can take orally or inject. (Proviron and masteron are pretty much DHT, or at least replaces it in terms of libido and strength, hair loss etc goes)
Cialis is a better option than viagra (it lasts longer and its safe + has health benefits + can be used all the time) Viagra has nasty side effects
Boosting libido can be done by boosting dopamine, and that can be done with food, supplements, drugs or pharma. A lot of dark chocolate and l-tyrosine or mucuna (l-dopa) can aid that..
There are also cabergoline and such drugs that work on dopamine. Pramipexole is another one
1 hour ago, kelly jones said:IT IS THE WATER!!!! Weacne prone ppl are allergic to chemicals. STOP using them!!
Our skin and hair can't handle Free Chlorine (Cl-), Combined Chlorine (Sodium Hypochlorite), Hydrogen Sulfide (rotten egg smell) andIron Oxide (rust water)
Get a filtered shower head!!!! You will be amazed how your water is damaging your skin and hair. A filter will filter chemicals making your hard water softer. Trust me, I have tried everything before I started washing my body with only filtered water. Wash your face with combinations of honey, lemon, and coconut oil and sugar for exfoliation. Thayers Witch Hazel (No Alcohol) as toner. Use aloe Vera gel as moisturizer. Tea tree oil is great too. Stick to natural products as listed above.
Don't use lofas and do use wash cloths but oxiclean them when washing, do not bleach them
Birth Control is a Big No as is Man-Made antibiotics. Opt for natural antibiotics such as garlic and orgeano
If for some reason the moon turns purple and this does not work, get tested for food allergies ex dairy or gluten and Do educate yourself on GMO's
You all are Beautiful Best Of Luck!!
But this has nothing to do with what we are discussing in this thread.. Its not a thread about acne
12 hours ago, octopusfrog said:Any taurine updates ?
I actually haven't begun Taurine supplementation yet, because I am living at a temporary address because I am moving states.
BCAAs, Creatine, zinc, fish oil and my vitamin stack are certainly helping though, and I can only imagine Taurine will further improve my condition
2 hours ago, VanceAstro said:I took one course of low dose (10mg)Isotretinoinand it has completely messed up my digestive system (I can't toleratefat and fructose anymore). Symptoms startedalready few hours after swallowing the first capsule (very loud stomach noises - particularlyat night and after lying down). Two weeks later I have noticed much brighter stools (common symptom of fat malabsorbtion). Myliver enzymes were in thenormal range during the whole treatment (apart from slightly elevated bilirubin). I have tried various supplements, probiotics, antibiotics,diet modifications etc.with miserable results.At this point, I am preety sure that Isotretinoin has induced some sort of allergic reaction to certain foods (i.e.fructose intolerance)via itsimmunomodulating properties. I am also consideringsmall intestinal bacterial overgrowthbecause Isotretinoincan cause variations in the microbial floras of several sites of the body.
We have a pretty good "rehab" routine at the moment, though before this was about I went on several water fasts, never very long, 3-7 days, and intermittent fasted as well, and after every one I got increased hunger, found it easier to put on weight, get a bit stronger, a bit like a sling-shot effect. For example, I might lose from 92kgdown to 86kg, which aren't that heavy for 6'5, and when I begin eating again I might rebound to 96kg over the next fortnight. Important to note that I was exercising regularly and intensly, either HIIT or gym, both during the fast and rebound, so that may be why I didn't lose much strength, though while fasted a hard session may be 10x100m, some pushups and sit ups with 5 minutes recovery, and after 3 or 4 you feel wrecked, when you are properly fueled you might be able to do twice that, or shorter breaks, or running in between sets. With resistance training I could put up what I do, but what I would recommend is split body workouts, preferably with someone that has been going to the gym for quite a while, as they will help you not injure yourself
Interesting studies by the way, just another way Isotretinoin can ruin our health...
Hey Guys I have a promising new side effect to report from taruine supplementation!
Nose Bleeds! This morning I just woke up with a rather decent amount of blood in my nose and boogers. This is a side effect I had while on accutane! The accutane is being mobilized! Ahhhhhhh im getting tingly feelings in my body, trying to keep my composure and not get overly optimistic!
I would also like to note when i was trying manganese and choline my nose bleeds did return, but no where near to this extent! I am considering adding manganese and choline back into my stack. Taurine is closely bound to manganese!
After my last exam this friday I will be doing intense amounts of cardio!
If anyone has links to studies about supplementation during treatment I would gladly read them. I think if I add those certain supplements to my stack it might significantly help! Selenium maybe?
On 12/18/2015 at 2:41 AM, Accutazed said:Hey Guys I have a promising new side effect to report from taruine supplementation!
Nose Bleeds! This morning I just woke up with a rather decent amount of blood in my nose and boogers. This is a side effect I had while on accutane! The accutane is being mobilized! Ahhhhhhh im getting tingly feelings in my body, trying to keep my composure and not get overly optimistic!
I would also like to note when i was trying manganese and choline my nose bleeds did return, but no where near to this extent! I am considering adding manganese and choline back into my stack. Taurine is closely bound to manganese!
After my last exam this friday I will be doing intense amounts of cardio!
If anyone has links to studies about supplementation during treatment I would gladly read them. I think if I add those certain supplements to my stack it might significantly help! Selenium maybe?
I am so jealous that you can do cardio..
Ive become so weak from accutane that my heart speeds up like i was sprinting a world championship marathon if i do some light jogging..
Not really sure if nose bleeds is a good sign though, but at least its not a side effect of the taurine itself..
---
I think im going to skim through all the pages of this thread and note down all useful studies, regimens, anecdotes and theories that has been found throughout these 311 pages so far
Ive already been through all the stuff on pubmed. Anyone else knows other study databases i can look in?
Below are my pubmed findings: (and some other stuff)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219165/
http://www.ncbi.nlm.nih.gov/pubmed/24697846
http://www.ncbi.nlm.nih.gov/pubmed/24966012
http://www.ncbi.nlm.nih.gov/pubmed/25573071
http://www.ncbi.nlm.nih.gov/pubmed/25219729
http://www.ncbi.nlm.nih.gov/pubmed/26110123
http://www.ncbi.nlm.nih.gov/pubmed/22517509
http://www.ncbi.nlm.nih.gov/pubmed/23135667
http://www.ncbi.nlm.nih.gov/pubmed/25597375
http://www.ncbi.nlm.nih.gov/pubmed/26338739
http://www.ncbi.nlm.nih.gov/pubmed/22714752
http://www.ncbi.nlm.nih.gov/pubmed/25484410
http://www.ncbi.nlm.nih.gov/pubmed/25294249
http://www.ncbi.nlm.nih.gov/pubmed/25853176
http://www.ncbi.nlm.nih.gov/pubmed/21410620
http://www.ncbi.nlm.nih.gov/pubmed/23722388
http://www.ncbi.nlm.nih.gov/pubmed/15863802
http://www.ncbi.nlm.nih.gov/pubmed/10859533
http://www.ncbi.nlm.nih.gov/pubmed/26154692
http://www.ncbi.nlm.nih.gov/pubmed/21720662
http://www.ncbi.nlm.nih.gov/pubmed/24683393
http://www.ncbi.nlm.nih.gov/pubmed/21860167
http://www.ncbi.nlm.nih.gov/pubmed/20941944
http://www.ncbi.nlm.nih.gov/pubmed/20930691
http://www.ncbi.nlm.nih.gov/pubmed/26034688
http://www.ncbi.nlm.nih.gov/pubmed/25721216
http://www.ncbi.nlm.nih.gov/pubmed/20059367
http://www.ncbi.nlm.nih.gov/pubmed/20128787
http://www.ncbi.nlm.nih.gov/pubmed/25625453
http://www.ncbi.nlm.nih.gov/pubmed/22813063
http://www.ncbi.nlm.nih.gov/pubmed/25354039
http://www.ncbi.nlm.nih.gov/pubmed/22110774
http://www.ncbi.nlm.nih.gov/pubmed/20465675
http://www.ncbi.nlm.nih.gov/pubmed/20465621
http://www.ncbi.nlm.nih.gov/pubmed/20394627
http://www.ncbi.nlm.nih.gov/pubmed/21663986
http://www.ncbi.nlm.nih.gov/pubmed/7669643
http://www.ncbi.nlm.nih.gov/pubmed/7858417
http://www.ncbi.nlm.nih.gov/pubmed/19492487
http://www.ncbi.nlm.nih.gov/pubmed/16517990
http://www.ncbi.nlm.nih.gov/pubmed/15177980
http://www.ncbi.nlm.nih.gov/pubmed/11675849
http://www.ncbi.nlm.nih.gov/pubmed/11172037
http://www.ncbi.nlm.nih.gov/pubmed/25008440
all the links are individual studies, I didnt think of adding the title to each link so you have to open each one.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219165/
In fasting state, insulin signal is weak and FoxO1 is activated by translocation into the nuclei to trigger gluconeogenesis for glucose supply. Under insulin resistance conditions, however,hyperactive FoxO1 promotes gluconeogenesis in such an uncontrolled way that it leads to hyperglycemia. It is well known that isotretinoin impairs insulin resistance.176,177 This fact can be well explained by FoxO1-mediated upregulation of phosphoenolpyruvate carboxykinase (PEPCK), the key enzyme of gluconeogenesis.19 Thus, hyperactive FoxO1 explains impaired insulin sensitivityand an increased disposition for hyperglycemia observed under isotretinoin treatment (Fig. 4).
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Ro)accutane induced alterations in control of micturition and urine storage suggested to be partially due to effects on the spinal cord and GABA
The micturition reflex is one of the autonomic reflexes, but the release of urine is regulated by voluntary neural mechanisms that involve centers in the brain and spinal cord. The micturition reflex is a bladder-to-bladder contraction reflex for which the reflex center is located in the rostral pontine tegmentum (pontine micturition center: PMC). There are two afferent pathways from the bladder to the brain. One is the dorsal system and the other is the spinothalamic tract. Afferents to the PMC ascend in the spinotegmental tract, which run through the lateral funiculus of the spinal cord. The efferent pathway from the PMC also runs through the lateral funiculus of the spinal cord to inhibit the thoracolumbar sympathetic nucleus and the sacral pudendal nerve nucleus, while promoting the activity of the sacral parasymapathetic nucleus. Inhibition of the sympathetic nucleus and pudendal nerve nucleus induces relaxation of the bladder neck and the external urethral sphincter, respectively. There are two centers that inhibit micturition in the pons, which are the pontine urine storage center and the rostral pontine reticular formation. In the lumbosacral cord, excitatory glutamatergic and inhibitory glycinergic/GABAergic neurons influence both the afferent and efferent limbs of the micturition reflex. The activity of these neurons is affected by the pontine activity. There are various excitatory and inhibitory areas co-existing in the brain, but the brain has an overall inhibitory effect on micturition, and thus maintains continence. For micturition to occur, the cerebrum must abate its inhibitory influence on the PMC [3].
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(Ro)accutane induced irreversible proteinuria
...(Ro)accutane is found to cause a statistically significant induction of TGF-beta1 in several independent studies. Six weeks of isotretinoin treatment caused a statistically significant 19% increase in suction blister fluid TGF-beta1 [1]. There are no measured values of the cumulative effect after 3-4 months exposure, which is common in acne-subjects. Various studies have shown that significantly increased TGF-beta1 correlate with with the amount of urinary protein excretion (proteinuria and albumineria), in adose, but also importantly time dependent manner. This due to failure in the kidney, of renal proximal tubular protein reabsorbtion. This is of major importance, because a significant failure in reabsorbtion leads to the loss of important vitamins, hormones and amino-acids [2].
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2814%2960375-5/abstract
The endothelial glycocalyx, a friable but protective lining of all blood vessels, is damaged in both atherosclerosis and kidney disease. We examined whether factors in the plasma of patients with kidney disease could damage the endothelial glycocalyx, and sought underlying mechanisms.
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Accutane, Methylation Block and Glycine N-Methyltransferase
1. "All-trans-Retinoic Acid Rapidly Induces Glycine N-methyltransferase in a Dose-Dependent Manner and Reduces Circulating Methionine and Homocysteine Levels in Rats,[Edited link out]
2. "Retinoic Acid and Glucocorticoid Treatment Induce Hepatic Glycine N-Methyltransferase and Lower Plasma Homocysteine Concentrations in Rats and Rat Hepatoma Cells," http://jn.nutrition.org/content/133/11/3392.full
3. "Activation and induction of glycine N-methyltransferase by retinoids are tissue- and gender-specific," http://www.ncbi.nlm.nih.gov/pubmed/12054489
4. "Decreased plasma folate concentration in young and elderly healthy subjects after a short-term supplementation with isotretinoin," http://onlinelibrary.wiley.com/doi/...sCustomisedMessage=&userIsAuthenticated=false
5. "Inhibition of glycine N-methyltransferase by folate derivatives: implications for regulation of methyl group metabolism," http://www.sciencedirect.com/science/article/pii/S0006291X85800061
6. "Phosphorylation modulates the activity of glycine N-methyltransferase, a folate binding protein. In vitro phosphorylation is inhibited by the natural ligand," http://www.jbc.org/content/264/16/9638.full.pdf