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Started testosterone last Saturday, front loaded 400mg Saturday, 300mg Monday, 300mg Tuesday.
I feel slightly more awake, joint pain is already feeling a bit better, inflammation hasn't changed though, even seems a little worse. I've gotten like 10 new pimples already, and my face is getting hella oily already. Still haven't noticed any extra pump in the gym yet, but I'm sure it will come. No gyno sides yet either. My HCG should be here tomorrow and I'll start that right away keep my balls working.
Epigenetic side-effects of common pharmaceuticals: a potential new field in medicine and pharmacology.
Abstract
The term "Epigenetics" refers to DNA and chromatin modifications that persist from one cell division to the next, despite a lack of change in the underlying DNA sequence. The "epigenome" refers to the overall epigenetic state of a cell, and serves as an interface between the environment and the genome. The epigenome is dynamic and responsive to environmental signals not only during development, but also throughout life; and it is becoming increasingly apparent that chemicals can cause changes in gene expression that persist long after exposure has ceased. Here we present the hypothesis that commonly-used pharmaceutical drugs can cause such persistent epigenetic changes. Drugs may alter epigenetic homeostasis by direct or indirect mechanisms. Direct effects may be caused by drugs which affect chromatin architecture or DNA methylation. For example the antihypertensive hydralazine inhibits DNA methylation. An example of an indirectly acting drug is isotretinoin, which has transcription factor activity. A two-tier mechanism is postulated for indirect effects in which acute exposure to a drug influences signaling pathways that may lead to an alteration of transcription factor activity at gene promoters. This stimulation results in the altered expression of receptors, signaling molecules, and other proteins necessary to alter genetic regulatory circuits. With more chronic exposure, cells adapt by an unknown hypothetical process that results in more permanent modifications to DNA methylation and chromatin structure, leading to enduring alteration of a given epigenetic network. Therefore, any epigenetic side-effect caused by a drug may persist after the drug is discontinued. It is further proposed that some iatrogenic diseases such as tardive dyskinesia and drug-induced SLE are epigenetic in nature. If this hypothesis is correct the consequences for modern medicine are profound, since it would imply that our current understanding of pharmacology is an oversimplification. We propose that epigenetic side-effects of pharmaceuticals may be involved in the etiology of heart disease, cancer, neurological and cognitive disorders, obesity, diabetes, infertility, and sexual dysfunction. It is suggested that a systems biology approach employing microarray analyses of gene expression and methylation patterns can lead to a better understanding of long-term side-effects of drugs, and that in the future, epigenetic assays should be incorporated into the safety assessment of all pharmaceutical drugs. This new approach to pharmacology has been termed "phamacoepigenomics", the impact of which may be equal to or greater than that of pharmacogenetics. We provide here an overview of this potentially major new field in pharmacology and medicine
3 hours ago, TrueJustice said:Yeah meditation is definitely something we could all benefit from, use to do a fair bit of it when I practiced yoga. I need to get back into it again which hopefully will lead to meditation practice - being consistent is key with this practice.You listed supplements many of which I've taken and currently still do esp a quality fish oil BUT theres still no relief to dryness coupled with the excess sweating, basically my sebaceous glands are altered still to this day 20 years after tane - how is this for you??
I use to drip sweat in yoga like I'd been out on the piss the night before, skin has lost its fullness and sweat just pours out of me!!
I don™t notice sweat all that much, the things that still bother me are dry skin/lips¦ But I™m not sure whether that is something that can easily be fixed or reversed, but at the same time it doesn™t affect my quality of life so I guess I don™t worry about it too much.
I™m planning to start massage with Coconut Oil because there have been overwhelmingly positive scientific reviews for that against any form of dermatis, but I can™t say how this will help your skin condition in particular. https://www.ncbi.nlm.nih.gov/pubmed/15724344
œCoconut oil and mineral oil have comparable effects. Both oils showed effectivity through significant improvement in skin hydration and increase in skin surface lipid levels. Safety was demonstrated through no significant difference in TEWL and skin pH. Subjective grading of xerosis by the investigators and visual analogue scales used by the patients showed a general trend toward better (though not statistically evident) improvement with coconut oil than with mineral oil.
Just looking for a moment this is something that may help your skin. œSunflower seed oil preserved stratum corneum integrity, did not cause erythema, and improved hydration in the same volunteers
I™m not sure if that interests you, feel free to read the full study below 
https://www.ncbi.nlm.nih.gov/pubmed/22995032
If this works for you or you do find something let me know!
10 hours ago, ehohel said:Started testosterone last Saturday, front loaded 400mg Saturday, 300mg Monday, 300mg Tuesday.
I feel slightly more awake, joint pain is already feeling a bit better, inflammation hasn't changed though, even seems a little worse. I've gotten like 10 new pimples already, and my face is getting hella oily already. Still haven't noticed any extra pump in the gym yet, but I'm sure it will come. No gyno sides yet either. My HCG should be here tomorrow and I'll start that right away keep my balls working.
Keep us posted
12 hours ago, Fchawk said:Are you self prescribing?
Sorry, messaging is playing up.
@Ehohel - Are you self prescribing?
On 3/9/2017 at 8:43 AM, hatetane said:
Speaking of antibiotics, I wonder if something like doxy would "cure" people of long standing mental sides. Unlike something like amoxicillin, it crosses the blood brain barrier. Its been used by neurologist to treat chronic headaches.
Doxycycline and Singulair for NDPH
[Edited image out] It seems like a strange combination of medications to take to attempt to get rid of New Daily Persistent Headache, I know. Im trying it out now, at the recommendation of my new neurologist. If you would like to read up on some of the research that supports this treatment, take a look atElevation of CSF Tumor Necrosis Factor Levels in New Daily Persistent Headache.
Im warning you, it isnt crystal clear why this would work just by reading the research. Well, maybe if you are a doctor it would make sense. The author (Dr. Rozen) explained it all to me at length and I fully understood it in the moment. It was fascinating really, and I wish I could explain it back to you as well. I cant! If I had on my reporters hat, I would have taken notes. Honestly, as I was sitting there listening, it was all about me.
When I mentioned the magic wordcureto my doctor with hopeful eyes, he smiled. He s not using that word. It may not be a cure, and the science behind it may not be black and white or clear as day to someone like me, but there is good reason to give it a shot.
Ok, this is my oversimplified interpretation:Doxycylineis an antibiotic. NDPH is often triggered initially by a virus or an infection and there is some suspicion that this is more of an immune system issue. So, treating it with Doxy and Singulair targets the inflammation in a different way then other migraine specific medications.
Here's a study basically showing Finasteride altered the expression of copper /zinc in the testes of rats and lowered sperm count.
Zinc has been shown to increase sperm count.
Expression of E-SOD, GPX5 mRNAs and immunoexpression of Cu/ZnSOD in epididymal epithelial cells of finasteride-treated rats.
Abstract
We studied the immunoexpression of Cu/Zn superoxide dismutase (Cu/ZnSOD) and mRNAs expression of extracellular superoxide dismutase (E-SOD), and epididymal specific glutathione peroxidase 5 (GPX5), in epithelial cells of caput and cauda epididymis of rats treated with finasteride, a steroid-based inhibitor of 5alpha-reductase. The 5alpha-reductase is known to exist in two isoforms. Both 5alpha-red1 and 5alpha-red2 catalyse the irreversible conversion of T into DHT. Formation of DHT in the epididymis is mostly due to the action of 5alpha-red2 and finasteride is more potent inhibitor of this isoform. Rats were treated with finasteride for 56 days covering the duration of one spermatogenesis (four cycles of the seminiferous epithelium). Although E-SOD mRNA is normally expressed in cells of cauda but not of caput epididymis, treatment with finasteride produced the E-SOD transcript in cells of caput epididymis too. The GPX5 transcript was detected in cells of caput epididymis of control and experimental rats, but the level of expression measured densitometrically was significantly lower in finasteride-treated rats. The immunoexpression of Cu/ZnSOD was also changed in epididymis of finasteride-treated rats. Finasteride appears to change the pattern of expression of antioxidant enzymes and may alter the protective function of the epididymis in relation to spermatozoa.
http://www.nytimes.com/health/guides/disease/amebiasis/overview.html
As per PFS guy: can be induced by
Use of corticosteroid medication to suppress the immune system.
Remember a couple off other guys claiming to be cured by antibotics. (i don't think this is the same case)
14 minutes ago, TrueJustice said:Is tane a corticosteroid medication?
Nobody knows what is in tane except Merck remember!
I was looking to see how PFS guy may have acquired said infection.
Getting back to FCHAWK's theory:
http://vitalitymagazine.com/article/healing-brain-injuries-naturally/
I know a lot of guys have taken these mentioned supplements but for anyone who hasn't they are a safe place to start.
Curcumin keeps coming up and they recommend a specific type here.
I suspect everyone who takes accutane is likely to be suffering from PTSD - just my personal opinion!
I just don't get it guys. Somehow my inflammation/joint pain is estrogen related. I've added an AI to my T cycle and the next day both those symptoms are gone.
12 hours ago, hatetane said:Sorry, messaging is playing up.
@Ehohel - Are you self prescribing?
Yes
13 hours ago, hatetane said:
remember that guy who commited suicide because of hisexfoliative cheilitis from accutane
2 hours ago, ehohel said:I just don't get it guys. Somehow my inflammation/joint pain is estrogen related. I've added an AI to my T cycle and the next day both those symptoms are gone.
Yes
Come on - you should know better. Guesswork is not appropriate, you should at least be having bloods taken regularly.
I just hope you are one of the older guys.
55 minutes ago, hatetane said:Come on - you should know better. Guesswork is not appropriate, you should at least be having bloods taken regularly.
I just hope you are one of the older guys.
I'm aware, but I'm just gonna do bloods 2 weeks in see if my dosing is correct. Started the AI because of high E2 symptoms. Just stating my results as soon as I took it.
B2 + sunlight? thioredoxin reductase cofactors and/or inducers?
sulforaphane and selenium riboflavin, thiamine
13-cis-retinoic acid covalently binds to thioredoxin reductase in human keratinocytes.
13-cis-Retinoic acid is a stereospecific suicide inhibitor of thioredoxin reductase. [3H]-labeled 13-cis-retinoic acid has been used to covalently label thioredoxin reductase in human keratinocytes. The acid-soluble cytosol fraction of human keratinocytes contained three radioactive proteins labeled by the addition of high-specific-activity [3H]-13-cis-retinoic acid to cell cultures. One of these proteins was identified as cytosolic keratinocyte thioredoxin reductase by fast-protein liquid chromatography and SDS-gel radioautography. The inhibition of thioredoxin reductase by 13-cis-retinoic acid may explain the known cytostatic and teratogenic properties attributed to this retinoid.
https://www.ncbi.nlm.nih.gov/pubmed/2064786
some people develop TMAU(fish odor) after accutane . this is controlled by the flavin FMO3 hmmmm. more riboflavin
http://www.curezone.org/forums/am.asp?i=2217022
[Edited link out]
https://answers.yahoo.com/question/index?qid=20140429215524AAfvQCV
Selenium ameliorates isotretinoin-induced liver injury and dyslipidemia via antioxidant effect in rats.
https://www.ncbi.nlm.nih.gov/pubmed/24966012
Riboflavin is a vitamin but not at all harmless. It is therefore not surprising that riboflavin and the riboflavinogenic coenzymes flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) play a role in many fields of practical medicine. Here we report on new developments in medical flavinology focusing on the assessment of riboflavin status, medical interventions based on flavins, and current medical aspects concerning the enzymes glutathione reductase (GR) and thioredoxin reductase (TrxR) as representatives of a large family of homodimeric flavoproteins. For systematic and more specific informationparticularly on the clinical aspectswe should like to refer the reader to comprehensive reviews (14). This article cannot deal with one specific method. However, methodological details of special medical interest are included. We will keep recalling a simple rule that is often broken in practical medicine and in medical research:Drugs, B2 and light? The treatment cant be right. It implies that flavins are readily photodegraded, and that a whole range of drugs (5,6) but also biological macromolecules (3,7,8) are subject to inactivating modification in riboflavin-dependent photoreactions. As exemplified for the cytostaticVincaalkaloids vinblastine and vincristine as well as for the synthetic drug vindesine precautions have to be taken to prevent this side effect of riboflavin application (6).
https://link.springer.com/protocol/10.1385%2F1-59259-266-X%3A229
http://forums.phoenixrising.me/index.php?threads/roaccutane-caused-depression-isotretinoin.12117/
The flavoenzyme methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, which serves as a methyl group donor in the conversion of homocysteine to methionine. In rats, experimental riboflavin deficiency is associated with low MTHFR activity and reduced levels of 5-methyltetrahydrofolate. In humans, reduced enzyme activity caused by the commonly occurring 677C†’T substitution of the MTHFR gene is associated with elevated plasma homocysteine.
Maybe our bodies cant convert folate to its active form to downregulate GNMT because of a riboflavin def
Maybe people wth the MTHFR 677CT polymorphism are more prone to long term side effects?
Maybe accutane depletes something like riboflavin (FAD) and thiamine (NADPH) that are needed for MTHFR to even work correctly?
I wish richvank was still alive.
he quotes:
Glutathione (oxidized): This is a measurement of the concentration
of the oxidized form of glutathione (abbreviated GSSG) in the blood
plasma. The reference range is 0.16 to 0.50 micromoles per liter.
Normally, oxidized glutathione in the cells is recycled back to reduced glutathione by glutathione reductase, an enzyme that requires vitamin B2 and NADPH. If this reaction is overwhelmed by oxidative stress, the cells export excess GSSG to the plasma. In some (but not all) PWCs, GSSG is elevated above the normal
range, and this represents oxidative stress. It is more common in CFS to see this level in the high-normal range. This value may increase slightly under initial treatment of a partial methylation cycle block.*
.....
anecdotally one person said they spontaneously cured themselves from finasteride with these supplements. they contain folate and riboflavin.
riboflavin is an aromatase inhibitor
riboflavin is a 5AR inhibitor as well
http://propeciahelp.com/forum/viewtopic.php?f=1&t=11457
On 3/8/2017 at 8:27 AM, Justdry said:On 3/8/2017 at 1:02 AM, ehohel said:I've gotten like 10 new pimples already, and my face is getting hella oily already.
Was your skin dry before you started this? Oil returned immediately?
9 hours ago, tryingtohelp2014 said:
http://forums.phoenixrising.me/index.php?threads/roaccutane-caused-depression-isotretinoin.12117/
The flavoenzyme methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, which serves as a methyl group donor in the conversion of homocysteine to methionine. In rats, experimental riboflavin deficiency is associated with low MTHFR activity and reduced levels of 5-methyltetrahydrofolate. In humans, reduced enzyme activity caused by the commonly occurring 677C†’T substitution of the MTHFR gene is associated with elevated plasma homocysteine.
Maybe our bodies cant convert folate to its active form to downregulate GNMT because of a riboflavin def
Maybe people wth the MTHFR 677CT polymorphism are more prone to long term side effects?
Maybe accutane depletes something like riboflavin (FAD) and thiamine (NADPH) that are needed for MTHFR to even work correctly?
I wish richvank was still alive.
he quotes:
Glutathione (oxidized): This is a measurement of the concentration
of the oxidized form of glutathione (abbreviated GSSG) in the blood
plasma. The reference range is 0.16 to 0.50 micromoles per liter.
Normally, oxidized glutathione in the cells is recycled back to reduced glutathione by glutathione reductase, an enzyme that requires vitamin B2 and NADPH. If this reaction is overwhelmed by oxidative stress, the cells export excess GSSG to the plasma. In some (but not all) PWCs, GSSG is elevated above the normal
range, and this represents oxidative stress. It is more common in CFS to see this level in the high-normal range. This value may increase slightly under initial treatment of a partial methylation cycle block.*.....
anecdotally one person said they spontaneously cured themselves from finasteride with these supplements. they contain folate and riboflavin.riboflavin is an aromatase inhibitor
riboflavin is a 5AR inhibitor as wellhttp://propeciahelp.com/forum/viewtopic.php?f=1&t=11457
He then posted some results a couple of weeks later.
Look at his Vitamin D levels.
Another thing I can say I take everyday is about 100mg of edible cannibas, not sure if this lead to any improvements but I have been taking it for a few years to help with depression and anxiety. I used to come here years ago but stayed away for 3 years because it made my anxiety worsen. I've been feeling my PFS effects everyday for 6 years and this 4 day span I had was more emotions and the most I've felt alive since the day I took saw palmetto and fin. Anyway I wonder if I hadn't stopped taking my vitamin regimen if I would still be recovered? Does it sound like I've had a "crash"?
after a few weeks following the recovery period I had, things are weird again. It seems as if I am more hyperthyroid now than hypothyroid, not sure if that is a good thing at all. Getting really nervous like I used to but it's visibly affecting me worse now. Here's my blood work I got back and would appreciate any input:
Testosterone: 295.20 NG/dl (175 - 781 NG/dL)
Free Testosterone: 49.6 pg/mL (6.0 - 224.0 pg/mL)
T3 Free: 3.88 PG/mL (2.5 - 3.9 PG/mL)
TSH: 0.96 ulu/mL (0.34 - 5.60 uIu/mL)
Vitamin B12: >1500 (200 - 914 PG/mL)
Vitamin D 25 Hydroxy: 43 ng/mL (30 - 100 ng/mL)
D2: >4 ng/mL (no range)
D3: 43 ng/mL (no range)
15 hours ago, hatetane said:
Studies have shown that the activity of 5-alpha-reductase is higher in the scalp and facial skin than in other areas, so that testosterone and dihydrotestosterone stimulate more sebaceous gland proliferation in these areas. Estrogens have been found to decrease sebaceous gland secretion.
Here's something I've been talking about with references to medscape to go along with it. if accutane was somehow able to alter stomach acid production and lead to a chronic hyperacidity state this could lead to a host of problems including a paradox of poor digestion and even decreased liver function. Just using Zollinger-Ellison as a example but there are other similar conditions.
Just going to paste some key possibilities here
http://www.medscape.com/viewarticle/407944_4
gastric acid hypersecretion and subsequent activation of pepsinogens by the acid (which causes mucosal injury of the small intestine), but also from acid inactivation of pancreatic enzymes and the acid damage to enterocytes.
inactivation of pancreatic lipase by intraluminal acid in the upper small intestine and the low pH environment render some primary bile acids insoluble, and thereby reduce the formation of micelles (which are necessary for fatty acid and monoglyceride absorption). In addition, patients often have blunted villi and, in rare cases, totally flat mucosa with resultant malabsorption.