Acne.org Products
Having too much vitamin A can also cause hair loss, I am suffering from the same too, I have a receding hairline at 18 caused by Accutane, my hair on my crown is thinning out, but my sides and back are not affected.
I am also losing hair on my eyebrow and eyelashes, at a slow rate which is now becoming noticeable.
I have been to see a GP countless number of times and they cant do anymore because my B12 came back as normal.
I might go back and ask for them to check my Iron and Vitamin A levels.
Has anybody here been off accutane for a fair amount of years, how did you end up?
1 hour ago, Owen2000 said:Having too much vitamin A can also cause hair loss, I am suffering from the same too, I have a receding hairline at 18 caused by Accutane, my hair on my crown is thinning out, but my sides and back are not affected.
I am also losing hair on my eyebrow and eyelashes, at a slow rate which is now becoming noticeable.
I have been to see a GP countless number of times and they cant do anymore because my B12 came back as normal.
I might go back and ask for them to check my Iron and Vitamin A levels.
Has anybody here been off accutane for a fair amount of years, how did you end up?
Been off it for 26 years, mpb runs in my family but folliculitis does not, still have eyebrows and eyelashes. Your thyroid ok?
Do you have scalp inflammation?
Just an update for anyone interested in the kinesiologist approach
currently on a select ratio of Iron and Vit C, another bacteria has been discovered that although I dont have is associated with MS and Alzheimers
My specialist said to look up Fenton Reaction its to do with oxidative stress amongst other things. I think it has Copper implications too, finally might have some answers on the Copper overload detected 400 years ago.....
For me its 3 drops of Iron with a Pharmaceutical grade Vit C - 2 times per day.
After a week - hair noticeably softer and facial skin softer too.
We work on clearing fungus next after this bacteria clearing
2 hours ago, TrueJustice said:Just an update for anyone interested in the kinesiologist approach
currently on a select ratio of Iron and Vit C, another bacteria has been discovered that although I dont have is associated with MS and Alzheimers
My specialist said to look up Fenton Reaction its to do with oxidative stress amongst other things. I think it has Copper implications too, finally might have some answers on the Copper overload detected 400 years ago.....
For me its 3 drops of Iron with a Pharmaceutical grade Vit C - 2 times per day.
After a week - hair noticeably softer and facial skin softer too.
We work on clearing fungus next after this bacteria clearing
Thanks for update sounds promising.
On 5/29/2019 at 4:40 PM, jellyy said:Someone commented in this link [removed]
"Astudy about vitamin a depletion in a old man who had hypervitaminosis A. It showed that RBP was greatly inhibited by protein deficiency and that eating 120 grams a protein a day causes RBP and vitamin a serum to rise. While on the high protein diet (58 days) they estimated the daily vitamin a being depleted was 226,000 iu daily.
https://www.gastrojournal.org/article/0016-5085(82)90132-9/pdf "
do you guys think this can help?
This is evidence that, even for someone with compromised vitamin A metabolism, tissue levels of vitamin A in the liver were able to be more than halved in 71 days. The hypothesis that persistent Accutane side effects stem from excess vitamin A has no merit whatsoever considering the clearance rates @guitarman01 cited.
You will be trying to get rid of a problem that isn't there with a vitamin A depletion diet.
My last dose of Accutane was taken 20 years ago and I began speaking with someone 12 years off recently. We are both generally in the same condition we were in shortly after stopping. I am actually in better shape physically, with back pain, knee pain, and constant fatigue ameliorating over the past few years, while sexual and mental/cognitive side effects are worse than they were a few months off the drug. I believe most of us participating in this thread are more than 5 years out.
12 hours ago, Calcified said:Been off it for 26 years, mpb runs in my family but folliculitis does not, still have eyebrows and eyelashes. Your thyroid ok?
Do you have scalp inflammation?
Thyroid came back normal, as of now I still have eyebrow and and eyelashes, but its more noticeable on the eyelashes that I am losing hair.
How have you got on 26 years after, do you still have hair on your face?
6 hours ago, Dubya_B said:
This is evidence that, even for someone with compromised vitamin A metabolism, tissue levels of vitamin A in the liver were able to be more than halved in 71 days. The hypothesis that persistent Accutane side effects stem from excess vitamin A has no merit whatsoever considering the clearance rates @guitarman01 cited.
You will be trying to get rid of a problem that isn't there with a vitamin A depletion diet.
My last dose of Accutane was taken 20 years ago and I began speaking with someone 12 years off recently. We are both generally in the same condition we were in shortly after stopping. I am actually in better shape physically, with back pain, knee pain, and constant fatigue ameliorating over the past few years, while sexual and mental/cognitive side effects are worse than they were a few months off the drug. I believe most of us participating in this thread are more than 5 years out.
How have you got on from being off this drug 20 years ago, do you still have your hair?
I just dont understand how this only affects a group of people, take Tanner Fox (Youtuber) for an example, he was placed on Accutane for 6 months, it completely cleared his acne and he had no side effects from it, apart from the common ones.
Bacterial strainspecific induction of Foxp3+T regulatory cells is protective in murine allergy models
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2222.2009.03437.x
B. longumAH1206 reduced the Peyer's patch gene expression associated with antigen presentation, TLR signalling and cytokine production while increasing the expression of genes associated with retinoic acid metabolism.
Friend or foe? i'mnot really sure.
you can see something quotedas "the promotion of retinoic acid metabolism was a key regulatoryfeature of this bacterium" not specific to Align or bifido longum 35624, but rather could be species wide.
you would maybe thinksomething toxic to the host and bacteria in the same phylum (P.acnes) would possiblybe toxic to this bacteria as well at high levels and they would do what they could to protect themselves by metabolizing toxic levels to prevent their death.
If anything had a chance to linger it seems the gi tract could be a target, that then could stop normal vitamin a synthesis and accumulate the esterifiedform in the liver through dietary intake.You could also run into a simultaneousvitamin a deficiency.
8 hours ago, guitarman01 said:Bacterial strainspecific induction of Foxp3+T regulatory cells is protective in murine allergy models
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2222.2009.03437.x
B. longumAH1206 reduced the Peyer's patch gene expression associated with antigen presentation, TLR signalling and cytokine production while increasing the expression of genes associated with retinoic acid metabolism.
Friend or foe? i'mnot really sure.
you can see something quotedas "the promotion of retinoic acid metabolism was a key regulatoryfeature of this bacterium" not specific to Align or bifido longum 35624, but rather could be species wide.
you would maybe thinksomething toxic to the host and bacteria in the same phylum (P.acnes) would possiblybe toxic to this bacteria as well at high levels and they would do what they could to protect themselves by metabolizing toxic levels to prevent their death.
If anything had a chance to linger it seems the gi tract could be a target, that then could stop normal vitamin a synthesis and accumulate the esterifiedform in the liver through dietary intake.You could also run into a simultaneousvitamin a deficiency.
Ra metabolism would depend how they mean. Retinol to Ra or Ra depletion. Basically high or low Ra can't tell from this.
It could always be a normal thing that Ra depletion speeds up with time during a lifetime of retinol intake. Or you thinking Ra depletion too slow now?
Maybe something prolonged going on right here. Its hard toimagine though a bacteria in the same class as c.diff plays such a role.
Any of you have a bout of food poisoning some time in your life before Accutane?
Commensals Suppress Intestinal Epithelial Cell Retinoic Acid Synthesis to Regulate Interleukin-22 Activity and Prevent Microbial Dysbiosis.
Abstract
Retinoic acid (RA), a vitamin A metabolite, regulates transcriptional programs that drive protective or pathogenic immune responses in the intestine, in a manner dependent on RA concentration. Vitamin A is obtained from diet and is metabolized by intestinal epithelial cells (IECs), which operate in intimate association with microbes and immune cells. Here we found that commensal bacteria belonging to class Clostridia modulate RA concentration in the gut by suppressing the expression of retinol dehydrogenase 7 (Rdh7) in IECs. Rdh7 expression and associated RA amounts were lower in the intestinal tissue of conventional mice, as compared to germ-free mice. Deletion of Rdh7 in IECs diminished RA signaling in immune cells, reduced the IL-22-dependent antimicrobial response, and enhanced resistance to colonization by Salmonella Typhimurium. Our findings define a regulatory circuit wherein bacterial regulation of IEC-intrinsic RA synthesis protects microbial communities in the gut from excessive immune activity, achieving a balance that prevents colonization by enteric pathogens.
On 5/30/2019 at 4:42 PM, Owen2000 said:Thyroid came back normal, as of now I still have eyebrow and and eyelashes, but its more noticeable on the eyelashes that I am losing hair.
How have you got on 26 years after, do you still have hair on your face?
How have you got on from being off this drug 20 years ago, do you still have your hair?
I just dont understand how this only affects a group of people, take Tanner Fox (Youtuber) for an example, he was placed on Accutane for 6 months, it completely cleared his acne and he had no side effects from it, apart from the common ones.
I have never experienced hair loss and have normal facial and body hair growth. It's strange, my beard growth didn't become "adult-like" until I crashed, then it really took off, while I lost my manly body odor completely at the same time. Not sure if the change in beard growth is coincidence or something to do with what Accutane did to me.
I have gotten along horribly in life. Everything has been a struggle. Constant fatigue and hypersomnia lead to lost jobs and a dull social life, anhedonia mixed with depression and anxiety has made waking up every day an existential nightmare, and ED and loss of libido has lead to chaotic relationships with insecure cheating women who I would not have bothered with if I was healthy. This garbage even ruined my fertility (verified by semen analysis) and I will probably never have a child; although, that is probably for the best, given my condition and the bleak view of the world and human nature that has resulted from it.
Never heard of this Tanner Fox, but he is likely of the lucky vast majority who are not genetically predisposed to developing PAS or weren't exposed to some other confounding factor that contributes to developing awful side effects. There are some youtube videos of people who developed serious issues and there are a few people I know of IRL who had severe side effects from Accutane, leading me to believe the incidence of them occurring is downplayed.
.
its funny what a good day might be for some of us compared to most.
I like to post some things as soon as I come across them so I dont lose it.
Retinoic acid suppresses intestinal mucus production and exacerbates experimental enterocolitis.
https://www.ncbi.nlm.nih.gov/pubmed/22563081
This study illustrates a direct effect of retinoid administration on intestinal mucus physiology and, subsequently, on the progression of intestinal inflammation
On 5/30/2019 at 11:39 PM, Calcified said:Ra metabolism would depend how they mean. Retinol to Ra or Ra depletion. Basically high or low Ra can't tell from this.
This is something I like to do or how I see things sometimes. Still a true statement?
Commensals Suppress Intestinal Epithelial Cell Retinoic Acid Synthesis to Regulate Interleukin-22 Activity and Prevent Microbial Dysbiosis.
Commensal Bacteria RegulateIntestinalRetinoic Acid to Prevent Microbial Dysbiosis.
1 hour ago, guitarman01 said:its funny what a good day might be for some of us compared to most.
I like to post some things as soon as I come across them so I dont lose it.
Retinoic acid suppresses intestinal mucus production and exacerbates experimental enterocolitis.
https://www.ncbi.nlm.nih.gov/pubmed/22563081
This study illustrates a direct effect of retinoid administration on intestinal mucus physiology and, subsequently, on the progression of intestinal inflammation
This is something I like to do or how I see things sometimes. Still a true statement?
Commensals Suppress Intestinal Epithelial Cell Retinoic Acid Synthesis to Regulate Interleukin-22 Activity and Prevent Microbial Dysbiosis.
Commensal Bacteria RegulateIntestinalRetinoic Acid to Prevent Microbial Dysbiosis.
I came across a study done this year Feb 2019 says isotretinoin caused increased rbp4 and triglycerides.
Fasting reduces both, so that makes sense but we may run out of Ra.
Maybe a bacteria beneficial to lowering triglycerides is key, rather than basically starving.
Really good article right here.
Here are some concepts and thoughts that are so new they are from yesterday. (at least when the article was published)
https://www.the-scientist.com/features/do-commensal-microbes-stoke-the-fire-of-autoimmunity--65871
Do Commensal Microbes Stoke the Fire of Autoimmunity?
Jun 1, 2019
AMANDA B. KEENER
Some key takeaways.
Balancing Act
Even if commensal bacteria do trigger immune attacks on our own bodies, researchers agree that eliminating the microbiome is not the answer to treating autoimmune disease. Resident bacteria are essential for developing an immune system, and in some cases are responsible for keeping potentially damaging immune responses at bay. We are much worse without our commensals than with them, saysRachel Caspi, an immunologist at the National Eye Institute in Bethesda, Maryland.
One recent study even found that mimicry can play a role in commensals immunosuppressive activities. An antigen made by several species of the gut microbe genus Bacteroides looks like the pancreatic protein IGRP and activates a subset of cytotoxic IGRP-specific T cells. Those T cells travel to the intestines and protect mice from colitis by killing other immune cells known to cause gut inflammation (Cell, 171:65567, 2017).
Still, removing certain microbes could be a strategy to consider for patients with a high risk of developing autoimmunity or in the earliest stages of disease, says Yale University immunologist Martin Kriegel. Its theoretically feasible to select those patients, identify the cross-reactive triggers, and remove the inciting agent, he says. The hard part is how do you remove them? In the case of lupus, he says, it might be possible to use a topical antibiotic to remove the source of Ro60 mimics in the skin microbiota.
Caspi is somewhat skeptical of targeting commensals to treat a disease thats already underway. A lot of these things are inductive events, she says. They trigger something. That doesnt mean that by eliminating the inductive event you can stop it. Instead of removing bacteria from the body, Caspi suggests that adding them in the form of probiotics to, for example, manipulate abundances of gut bacteria that display antigen mimics. By using the appropriate probiotics, we still might be able to affect the progression of disease, she says.
Mireia Sospedra Ramos [Edited link out], an immunologist at the University of Zurich, says there is already some evidence that altering the gut microbial assemblage could benefit multiple sclerosis patients, pointing to studies that have shown that taking probiotics can reduce markers of inflammation and some symptoms of the disease. She adds that the same commensals may not benefit all patients, however, because people are likely to carry immune cells that react to different antigens.
The solution is unlikely to be as simple as eradicating or altering a single species of bacteria, says Caspi. I dont think that we can draw a straight line to treatment from [our findings on molecular mimicry]. We may need to call upon other methods of restoration of immune balance rather than trying to eliminate what caused it in the first place.
I think I may have figured out the final puzzle piece to my problems. I've had really good results fighting MMP-9 which is involved in inflammatory processes, but I know that it's just part of something larger. I think I now have a much clearer picture of the whole.
So before tackling MMP-9, I was taking a slew of things to fight Helicobacter Pylori. I've long wondered if I was infected because I fit a lot of the symptoms and I believe the bacteria runs in my family - history of ulcers and Rosacea etc.
But fighting Pylori didn't seem to have much of an effect, or was actually making things worse. I immediately dropped almost all the anti-H. Pylori supps and went right into inhibiting MMP-9 and all my symptoms suddenly improved by about 80%. But then things backslid a bit so that my symptoms were stuck at about 50% better than normal. I was pissed. I didn't understand why. But then I tried adding a couple anti-H. Pylori supplements back to my MMP-9 inhibitors and things went back to 80% improved. This sort of confirmed to me that H. Pylori is likely involved.
I think when I took only anti-H. Pylori supps maybe I was getting hit with some herxheimer reflex or some of the herbs and oils were irritating to my gut and I wasn't taking much to fight the resulting inflammation. Then when I switched to fighting MMP-9 it worked so well because I was finally taking on the inflammation while the H. Pylori were still suppressed from my prior use of anti Pylori supps. Then the H. Pylori started to come back and I was stuck in a tug of war between the bacteria creating inflammation 24/7 and me taking anti inflammatories to fight it. By adding back a couple anti-H. Pylori supps I started fighting both.
So if I have H. Pylori and a lot of MMP-9 going on, the question is what's the middle man between them? And I'm now pretty sure it's the Epidermal Growth Factor Receptor (EGFR). Pylori damage the gut walls which leads to EGFR upregulation. Increased EGFR correlates with hightened MMP-9 according to studies. I studied EGFR and its ligand EGF in the past because L-Glutamine, which helps my symptoms a lot, is supposed to heal the gut through an EGF mechanism.
So I now have a theory of how everything's gone down for me:
As a teenager I believe I had an H. Pylori infection that was asymptomatic (maybe it contributed to my acne though). When I took 2 courses of Accutane I believe it changed the physical environment of my digestive tract somehow, either allowing H. Pylori to flourish or become pathogenic toward me or both. The resulting damage from the Pylori infection led to my stomach etc. producing a vast upregulation of EGFR in an effort to have EGF bind to it and heal me. I believe this then led to the permanent food allergies that Accutane gave me because EGF is not the only thing that can bind to EGF receptors. Lectins from wheat, dairy, corn, soy, beans, eggs etc. can also bind to them and some end up in circulation and can bind to keratinocyte EGFR, causing proliferation and inflammation. Here's an interesting study that sheds light on this phenomenon:
"The clue to the role that diet may play in the etiology of rosacea comes from the observation that pharmaceutical eradication of the bacteria, Helicobacter pylori, improves or ameliorates symptoms in rosacea patients (1-3). H. pylori is the bacteria that causes gastric and duodenal ulcers. Although the physiological basis for the curative effect of H. pylori eradication is unknown, we believe that a mechanism in the human gut, the epidermal growth factor receptor (EGF-R) likely plays a crucial role in the etiology of rosacea. The EGF-R is unusual in that it is expressed luminally in the gut (4,5). The primary role of the luminally expressed gut EGF-R is to provide a healing mechanism for damaged epithelial cells in the gut. One of the endogenous ligands for the EGF-R is EGF which is found in saliva and when swallowed promotes healing in damaged epithelial cells lining the gut (5). Additionally, salivary EGF may also finds its way into circulation through this pathway based upon the observation that surgical removal of the salivary and parotid glands in experimental animals reduces blood concentrations of EGF.
Infection of the GI tract with H. pylori leading to ulcers causes an upregulation (increase in density) of the EGF-R (6). Hence any substance in the gut capable of binding the EGF-R will have increased access to the peripheral circulation. We believe the reason why eradication of H. pylori reduces rosacea symptoms is because it downregulates (or reduces the numbers of) the EGF-R. Hence gut borne substances which would have gained entry to the circulation through the EGF-R and which may cause rosacea are partially denied access into the circulation.
In support of the notion that the EGF-R is central to the development of rosacea is the observation that EGF-R blocking pharmaceuticals elicit erythematous papules and follicular pustules (7-9) that likely occur because of an overexpression of the EGF-R in keratinocytes (8).
In regard to diet, the following substances also bind the gut EGF-R and gain access to circulation:
1. Wheat germ agglutinin (WGA) a dietary lectin which is found in both whole and refined wheat products (10).
2. Peanut agglutinin (PNA) a dietary lectin which is found in peanuts (11).
3. Tomato lectin (TL), a dietary lectin which is found in tomatoes (12)
4. Phytohemmagglutinin (PHA) a dietary lectin which is found in kidney beans and all other Phaseolus vugaris bean varieties (13, 14)
5. Soybean agglutinin (SBA) a dietary lectin which is found in all soybeans and soy products, whose specifity is to one of the sugars in the EGF-R (15)
6. Betacellulin (BTC) a hormone found in milk and cheese which is a natural ligand for the EGF (16, 17).
7. Egg white lysozyme, a lectin found in the whites of eggs (18)
Hence, once these dietary ligands for the EGF-R bind the gut EGF-R, some eventually escape destruction in gut epithelial cell lysozomes and reach circulation intact where they can bind the keratinocyte EGF-R and cause increased proliferation and inflammation (19). Dietary factors which can bind the EGF-R should be strongly implicated in the etiology of rosacea. Randomized controlled clinical trials will be needed needed to test the efficacy of elimination diets using known dietary ligands for the EGF-R."
EGFR is also involved in cancer progression, and EGFR inhibitors are used to fight it. One of the curious side effects of EGFR inhibitors is, for some reason, keratinocyte EGFR ends up becoming overexpressed and leads to bad skin and hair problems in up to 90% of patients:
"DISCUSSION: EGFR inhibitors act by inhibiting mechanisms of tumour proliferation in certain cancers at advanced stages or refractory to other treatments. Our findings in these four patients are similar to the published cases in terms of rapid onset of monomorphous, papulopustular, follicular eruption without comedons. Rapid response to tetracyclines and benzoyl peroxide is also reported in literature. This treatment must be instituted rapidly and patients must be informed about the cutaneous side-effects of EGFR inhibitors before the start of therapy. The pathophysiology of these eruptions is still unknown. Skin signs are probably due to interaction with EGFR functions, including overexpression of EGFR in keratinocytes and hair follicles."
"Wide range dermatologic adverse events can be found. The common findings are papulopustules and xerosis. Less common side effects are paronychia, regulatory abnormalities of hair growth, maculopapular rash, mucositis, and postinflammatory hyperpigmentation."
This all sounds like it describes what happened to me pretty well. It could even explain why all the hair on my head thinned out and changed texture.
This is also an interesting study about retinoids and EGFR:
"Retinoid-induced epidermal hyperplasia is mediated by epidermal growth factor receptor activation via specific induction of its ligands heparin-binding EGF and amphiregulin in human skin in vivo.
Rittie L1, Varani J, Kang S, Voorhees JJ, Fisher GJ.
Author information
Abstract
Retinoids are widely used in the treatment of photoaging to stimulate dermal repair. However, retinoids also induce epidermal hyperplasia, which can lead to excessive scaling. Scaling is the major deterrent to topical retinoid therapy. Keratinocyte growth is strongly stimulated via ligand activation of EGFR. We examined regulation of EGFR ligands by retinoids and the role of EGFR in retinoid-induced hyperplasia in human skin in vivo. Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Laser capture microdissection-coupled real-time reverse transcription-PCR reveals that tRA increases HB-EGF mRNA throughout the epidermis, whereas AR induction is limited to basal keratinocytes. Topical tRA activates extracellular signal-regulated kinase 1/2 (Erk1/2) downstream EGFR effectors in human skin in vivo. tRA increases the soluble forms of AR and HB-EGF proteins, and induces epidermal hyperplasia, in human skin organ culture. Neutralization of HB-EGF or AR with specific antibodies strongly reduces tRA-induced epidermal hyperplasia. Finally, inhibition of EGFR activation by genistein reduces epidermal hyperplasia caused by topical retinoid treatment. These data demonstrate the central role of EGFR activation in retinoid-induced epidermal hyperplasia, and suggest that EGFR inhibitors can mitigate retinoid-induced scaling."
Anyway, I've now ordered the natural EGFR inhibitors Genistein, EGCG, and Quercetin. If I'm right about my theory, then once I add these supps so that I'm fighting H. Pylori, EGFR overexpression, and MMP-9, I should see a further decrease of symptoms.
Ive successfully cleared both H PylorIand Mycoplasma bacteria
Ill stay on the Iron and Vit C to get through winter, minimise getting flu etc
Now clearing Fungus which is stubborn
Zinc, Zinc, Zinc is the key plus Molybdenum- my body is screaming for that to get rid of Fungus
My body cant get enough of Taurine either which is interesting. It definitely aids bile flow but Kinesiologist cant say for sure if its ridding excess Vit A too.Hes good but he cant pinpoint exactly why my body wants these large amounts of Taurine daily....
At this stage its best I dont question it and just get on with taking it.
4 hours ago, TrueJustice said:Ive successfully cleared both H PylorIand Mycoplasma bacteria
Ill stay on the Iron and Vit C to get through winter, minimise getting flu etc
Now clearing Fungus which is stubborn
Zinc, Zinc, Zinc is the key plus Molybdenum- my body is screaming for that to get rid of Fungus
My body cant get enough of Taurine either which is interesting. It definitely aids bile flow but Kinesiologist cant say for sure if its ridding excess Vit A too.Hes good but he cant pinpoint exactly why my body wants these large amounts of Taurine daily....
At this stage its best I dont question it and just get on with taking it.
Seems very pro vitamin A.
Honestly I'm still on the fence here regarding A.
He likens excess Vit A to those who suffer heavy metal toxicity - why doesone person suffer whilstanother person is fine?......
You could put 2 people on exactly the same diet, one could get heavy metal toxicity while the other has no issues - a lot of it comes down to your genetics.
Like us on Accutane- some are fine whilst others get affected - is it because of the liver and bad bile flow?....maybe but no one can say for sure.
All we can do is treat what comes up, one step at a time - calm nervous system, treat adrenals, break down biofilms, treat bacteria and fungus issues etc etc rebuild the body. Who knows maybe as my body continues to get stronger itll just kick into action and the liver will start working properly again unassisted....
In case anyone wants to know, hes treating Fungus with Pau Darco herb. I cant be specific on the fungus I have but regardless hed still use this herb to knock them all out. Its probably Candida amongst other things
He said Fungus sucks up our Zinc reserves.
11 hours ago, TrueJustice said:Zinc, Zinc, Zinc is the key plus Molybdenum- my body is screaming for that to get rid of Fungus
My body cant get enough of Taurine either which is interesting. It definitely aids bile flow but Kinesiologist cant say for sure if its ridding excess Vit A too.Hes good but he cant pinpoint exactly why my body wants these large amounts of Taurine daily....
Retinol binding protein. Vitamin E is also helpful.
here's a study. They said it was a small group size, but I also saw something similar when they were looking at different levels of effectiveness with ATRA treating Leukemia and liver metabolism, which might not be a variable factor.
Retinoic Acid 4-Hydroxylase Inducibility and Clinical Response to Isotretinoin in Acne Patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103843/
Conclusion
Factors other than CYP26 activity may determine response to isotretinoin in acne.
These results suggest that variation in CYP26 basal expression and/or induction may play only a minor role in determining therapeutic response to isotretinoin.
7 hours ago, guitarman01 said:here's a study. They said it was a small group size, but I also saw something similar when they were looking at different levels of effectiveness with ATRA treating Leukemia and liver metabolism, which might not be a variable factor.
Retinoic Acid 4-Hydroxylase Inducibility and Clinical Response to Isotretinoin in Acne Patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103843/
Conclusion
Factors other than CYP26 activity may determine response to isotretinoin in acne.
These results suggest that variation in CYP26 basal expression and/or induction may play only a minor role in determining therapeutic response to isotretinoin.
By the end of treatment their is way less peeling etc.
So cyp26 is probably altered, unfortunately they only tested post accutane patients, need to compare with controls.
In terms of responsiveness of accutane it worked for me but a B12 injection brings back cystic acne.
Dont drink the water. You can see it might be possible. Commensal bacteria that could break down retinoic acid that could maybe even be further metabolized by the host. When I say commensal bacteria im not really talking about yogurt, kefir or even vsl3. Im talking about bacteria of human origin.
Cyanobacteria blooms produce teratogenic retinoic acids
https://www.pnas.org/content/109/24/9477
Generally, 4-oxo-RAs were considered to be metabolites of RAs formed in vertebrates by cytochrome P450 enzymes such as CYP26A1 and CYP26B1, which have been cloned in human, mouse, rat, and chicken (25). The appearances of RAs and 4-oxo-RAs in natural blooms and cultured cyanobacteria and algae at relatively high concentrations first indicated that cyanobacteria and algae were able to transform RAs into their 4-oxo metabolites.
On 6/5/2019 at 4:43 AM, guitarman01 said:Dont drink the water. You can see it might be possible. Commensal bacteria that could break down retinoic acid that could maybe even be further metabolized by the host. When I say commensal bacteria im not really talking about yogurt, kefir or even vsl3. Im talking about bacteria of human origin.
Cyanobacteria blooms produce teratogenic retinoic acids
https://www.pnas.org/content/109/24/9477
Generally, 4-oxo-RAs were considered to be metabolites of RAs formed in vertebrates by cytochrome P450 enzymes such as CYP26A1 and CYP26B1, which have been cloned in human, mouse, rat, and chicken (25). The appearances of RAs and 4-oxo-RAs in natural blooms and cultured cyanobacteria and algae at relatively high concentrations first indicated that cyanobacteria and algae were able to transform RAs into their 4-oxo metabolites.
So fasting or diet changes that reduce bacteria, may therefore reduce p450 enzymes.
So maybe dairy doesn't just add vitamin A, maybe it adds bacteria promoting Ra metabolism too.
Zinc starves bacteria.
I think you may be onto something here.
4 hours ago, Calcified said:So fasting or diet changes that reduce bacteria, may therefore reduce p450 enzymes.
So maybe dairy doesn't just add vitamin A, maybe it adds bacteria promoting Ra metabolism too.
Zinc starves bacteria.
I think you may be onto something here.
I think diet and in turn the microbiome could influence p450 activity.
Zinc can actually be a nutrient for bacteria, a lot of bacteria compete for nutrients between themselves and the host.
On a different note, interesting thought right here when looking at whattruly may be a probiotic.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547204/
Oral Lactobacilli and Dental Caries
On 5/16/2019 at 8:48 PM, TrueJustice said:After stopping Accutane 17 years ago, one thing I have noticed is I have never had the cold or flu, the worst case will be, I will have the sniffles for a few hours (symptoms before a cold or flu) and then it dissapears.
I have not had e flu shot the last 17 years and I have stayed next to many people with the flu and cold plus kiss my girfriend many times while she has a cold, yet never got it. Has anyone ever experienced this ?