Acne.org Products
I haven™t seen the senolytic Fisetin brought up here yet. Has anybody here tried it?
Senolytic: targets senescent cells (dead/no good cells), preventing them from building up as quickly and slows down the aging process on a cellular level within the body.
Now that definition sounds familiar.. We all know already that accutane can cause damage at the cellular level. Here™s where fisetin comes into play. Out of all the senolytics Fisetin appears to be the most potent:
Fisetin is a senotherapeutic that extends health and lifespan
This seems to be promising as far as it™s mechanism of action. But I won™t skip to any conclusions yet until I try it myself or if anybody else has. Any experiences? I™ll be giving it a test run soon since it™s the next supplement on my list to try.
17 hours ago, Accudonia said:Hey guy, so Iwanted to touch on the hair growth dysfunction topic.
Besides the obvious fact that it causes hair loss/hair thinning, has anybody noticed randomlong hair growing on your chest/face? (Not sure if anybody here brought it up yet).Im a 23 year old male with healthy hair just around the chin area and a healthy head of hair as well.
But beyond that, every week or so I randomly find abnormally long/single pieces of hair sprouting onthe cheek area. This same hair dysfunction is also oddly seen on my chest. I just wanted to comment this here tosee if this could be (very well seems to be) an accutane related problem.
I'm very hairy which I link to isotretinoin. I took isotretinoin when I was 12 and end of the course I started to get thick hair on my thighs etc. Then already in my early teens I had full chest hair etc. The hairs grow really long and thick and in uncommon places. My androgen levels are on the low end so I thing that isotretinoin made my hair follicles more sensitive to them.
6 hours ago, Moks said:Maybe someone knows what to do with post accutane headaches? They started right after i finished full course of accutane 10+ years ago and never ends.
Hows your lymphatic system?
my persistent head pressure looks like is due to lymphatic blockage in the head
Really not surprising that this could happen after Tane, if it dries the skin out, what do you think it might also do to lymphatic....hmmm
On 2/9/2021 at 7:48 PM, Gunnersup said:I'm under the impression that vitamins, and most supplements, won't do a thing for these variety of symptoms people still have
As the name implies, a supplement is just that: the tip of the iceberg in what you need to do to fix your health. People need to supplement because you can't eat over 4 pounds daily just to get enough D-3, or 100, 200 grams of raisins every single day to get your boron daily intake... or 1.5 pound of salmon to get your astaxanthin. (note: these figures are not exact, yetyou get my point).
I'd say 30% of the results come from supplements, while 20% would be getting rid of toxins (BPA and other endocrine disruptors, EMF radiation, which may also cause BRAIN FOG, among other issues, and more), and 50% all these: diet + sleep + exercise.Supplementswon't do shit if these people have a bad diet/workout routine (because being inactive, spending many hours sitting in a chair (and a bad one, with a wrong posture), looking at a smartphone all the time, etc.is awful for you, more than you think, long term), bad sleep, etc.and even more important than taking in my opinion is...doing all blood tests (and other exams) to diagnose what is your real condition.
You need to do the tests BEFORE and after you take the pills, and after you change all the rest. Wait for a few months then do this 2nd test.
Back when I did the Accutane treatment in 2011 I didn't test for B-vitamins (some examsare not available easily where I live even now, so that harms a lot the chances of finding what kind of damage isotretinoin did in terms of deficiency. If there aren't enough people doing supplementsand fixing all the rest (the 50% part), and testing for dozens of stuff then what kind of hope do we have to fix what this poison did?
If there are not enough studies then YOU NEED TO CONDUCT YOUR OWN INVESTIGATION.
Some blood tests if you do in a private lab (I don't pay for mine, in my health plan)you will spend a lot of $$$$, for example, B-6 costs more than D and common B-vitamins). Have you ever thought about the possibility thebest diet still isn't going to suffice and you'llneed a greater dose of a specific vitamin? So you would need a multivitamin or a compounding pharmacy to build the pillsbased on your needs (because, you know, some multivitamins offer very low doses which won't do some people any good).
There are supplements to ease headaches, too:
https://howtocure.com/best-supplements-for-headache/
https://nationalheadacheinstitute.com/blog/vitamin-deficiencies-can-cause-headaches/
B-Vitamin deficiencies andD-3 may account for these symptoms. Nosurprise this headache symptom could be another sign of deficiency induced by Accutane, in the end.
Note: low sodium may be among the reasons.
You don't really know if you have some deficiency unless you do many tests (and some can't be detected by the usual blood tests, I believe ZINC and magnesium). There was a moment I did more than 40 one day. And that wasn't even enough in my opinion. It was, however, very revealing since I discovered multiple deficiencies: DHT, Estradiol, LH, free testosterone and in the past TOTAL T and vitamin D. And a slightly elevated PROLACTIN (bad for libido like the others).
Also, you may not harm your health with supplements, something I doubt it will not happen withTRT or a similar drug (think about diabetics, their medsinduce other deficiencies, including B12 and the need for COQ10, and don't fix the root causeof their condition, only make the symptoms tolerable), still you are going to spend a lot of cash. That is discouraging for many, and understandable.
Some brands are not good, too, so the bottles may not be effective. Be very careful whenchoosing.
Speaking of myself, while the depression I had looks like it was gone after a few years (and my B12 levels were showed to be OK), I am sure the only effect Accutane still has over me is low libido. This proves that any damage Accutane does may not be permanent or the side effect may be lessened with a lot of effort.
I am currently taking: Magnesium MALATE,Magnesium Bisglycinate, awhole-food multivitamin,Astaxanthin,Lutein and Zeaxanthin,Boron,Ashwagandha,Collagen,Creatine,Fish oil OR Krill OIL and Vitamin C. I was thinking of adding Coq10.
I am planning to add to this stack (for libido purposes):
- Peruvian MACA, Tribulus Terrestris, Fenugreek, Tongkat Ali, D-Aspartic Acid...
https://examine.com/supplements/maca/
https://examine.com/supplements/d-aspartic-acid/
https://men-elite.com/2018/10/23/46-ways-to-increase-dht/
it may also be a good idea to reintroduce carbs (so targeted keto). The real challenge here is to try everything in the book and find out I don't need a specific drug, or doing TRT,for real improvement. I hope this is not the case, because I hate drugs/meds.Big Pharma isn't our friend.
https://www.scoop.co.nz/stories/HL0609/S00042/roche-puts-accutane-profit-over-lives-of-consumers.htm
https://www.itv.com/news/central/2013-01-03/teen-blames-acne-drug-for-severe-depression
(Eventually Emma was treated for depression at a hospital in Staffordshire, there specialists told her that the part of her brain that produces serotonin, a hormone that regulates moods had been destroyed. So conventional anti-depressants were making her more suicidal.)
Hi All, we know that most people only come to this thread when it is too late but still, we should keep puttingout the warning to stop others from taking this drug. I could post hundreds of aticle like those aboveand it is important that we keep diggingthem up and circulating them.
If anyone hasn't completed the survey please do so now - there is only two more days left. This is also an opportunity to call for a ban and toask the MHRA to fund reasearch into finding a cure and compensation.
You can email the Isotretinoin EWG(review panel)directly [email protected]
For the UK group visit Twitter [removed] DM me for email address
Derek Jones, Doug Bremner, Prof David Healy, Prof McCaferry are just a few who advocate for us.
Remeber as much as protecting young acne kids going forward we want to find a cure for the injured.
RXisk have reached their target 100.000 Prize fund for anyone who can find a cure.
PLEASE COMPLETE THE SURVEY:
Have a look at all the side effects reported in the UK, Isotretinoin
https://yellowcard.mhra.gov.uk/iDAP/
and FAERS dashboard in the US
The more I learn about this drug, the more mind boggled I become about it can described to kids to treat pimples. The condition would heal by time in most cases and many would could cure it with positive life changes. I was 12 when I was described it. My acne barely even bothered me then and I had horrible diet and life style in general, but these things weren't discussed at all. It was my first attempt to deal with acne. I feel isotretinoin has very little do with helping patients, it's just about making money. Taking isotretinoin is likeplayingRussian roulette, you can end up with far worse condition than acne. Every time when I see somebody in internet talking about planning to start taking isotretinoin, I try to talk them out of it.
On 2/11/2021 at 7:42 AM, Pido said:I'm very hairy which I link to isotretinoin. I took isotretinoin when I was 12 and end of the course I started to get thick hair on my thighs etc. Then already in my early teens I had full chest hair etc. The hairs grow really long and thick and in uncommon places. My androgen levels are on the low end so I thing that isotretinoin made my hair follicles more sensitive to them.
Wow, consider yourself lucky man. Hair loss is like one of, if not, the most common side effect of accutane. Considering it metaphorically drops a nuke on androgen receptors, its not a secret here that it does cause hair loss lol. Sounds like you jumped the bullet on that topic.
Also you did say that you finished accutane at 12? I wonder if its possible that you were able to avoid the side effects since you havent hit puberty yet. How long have you taken it for btw? Any other side effects youve noticed?
21 hours ago, Pido said:The more I learn about this drug, the more mind boggled I become about it can described to kids to treat pimples. The condition would heal by time in most cases and many would could cure it with positive life changes. I was 12 when I was described it. My acne barely even bothered me then and I had horrible diet and life style in general, but these things weren't discussed at all. It was my first attempt to deal with acne. I feel isotretinoin has very little do with helping patients, it's just about making money. Taking isotretinoin is likeplayingRussian roulette, you can end up with far worse condition than acne. Every time when I see somebody in internet talking about planning to start taking isotretinoin, I try to talk them out of it.
Damn12 years old!! did you fill out the survey- last chance to do it today. Call for a ban, it will save lives.
https://www.surveys.mhra.gov.uk/5fa2caf33414eb1dd21958ad
On 2/15/2021 at 11:40 AM, Accudonia said:Wow, consider yourself lucky man. Hair loss is like one of, if not, the most common side effect of accutane. Considering it metaphorically drops a nuke on androgen receptors, its not a secret here that it does cause hair loss lol. Sounds like you jumped the bullet on that topic.
Also you did say that you finished accutane at 12? I wonder if its possible that you were able to avoid the side effects since you havent hit puberty yet. How long have you taken it for btw? Any other side effects youve noticed?
IIRC my course was pretty standard and I finished it like a month before turning 13. I think it messed up my body development. That's something that can't be fixed anymore, but I wish I could fix my skin, it being thin and fragile. I wonder could I have growth hormone deficiency? Years ago I got it tested and my levels were basically undetectable, but one test doesn't tell anything, you need a stress test and then doctor commented that there isn't a problem, because my IGF1 levels were good, but I don't think it means that you can't have low GH.
@timetobanYes, I filled the survey and recommend everyoneto do it.It doesn't take a long time and it's very important.
This drug should be banned for all ages, this doesn't happen because the manufacturers have deep pocket$$$$$. Some like sexual dysfunction were not included in the leaflet for that reason, not because they didn't know. No, this has been known for DECADES. And depression was always there, it's not like this has only been found yesterday.
BTW, I just found out a forum that has some good scientific info about how Accutane works to cause some persistent side effects:
[removed]
About my previous advices in terms of libido, I found some studies that indicate they may be effective in raising libido and/or testosterone. The problem is, like I said before, that supplements are only the tip of the iceberg in the changes we need to do and they all combined make us spend too much money. Also we need to be very careful about the brands and bottles we choose, because there are too many fakes/ineffective options out there. Be careful to notbuy cheap junk.
I wonder if even with a good supplement stack people that suffer from low libido/not enough testosterone are going to have tangible results, since the changes in the body were too deep. Before I talk about that, I want to ask a noob question: if isotretinoin works by doing this:
https://pubmed.ncbi.nlm.nih.gov/29447628/
https://pubmed.ncbi.nlm.nih.gov/21418145/
https://pubmed.ncbi.nlm.nih.gov/29675596/
And I quote:
******
These drugs are effective at reducing levels of dihydrotestosterone, the primary androgen responsible for the pathogenesis of both these conditions. However, finasteride and dutasteride have also been shown to produce an increase in the incidence of sexual dysfunction, namely, impotence, decreased libido, and ejaculation disorder. The purpose of this study is to review the existing medical literature with regard to the sexual side effects of 5--reductase inhibitor therapy
***
Then that explains why my DHT, LH, FSH, prolactin, estradiol, free T (total T higher thanks to D-3 supplementation, but not high enough) are all messed up. And:
https://www.drugs.com/drug-class/5-alpha-reductase-inhibitors.html
*
5-alpha-reductase inhibitors are a group of medicines that block the action of 5-alpha-reductase, the enzyme that converts testosterone into dihydrotestosterone. This results in increased levels of testosterone and decreased levels of dihydrotestosterone; an overabundance of dihydrotestosterone has been implicated in benign prostatic hyperplasia (BPH) and prostate cancer. The scalp of men with androgenetic alopecia (male-pattern baldness) has also been found to contain increased amounts of dihydrotestosterone and miniaturized hair follicles compared with men who have a lot of hair.
Currently, two 5-alpha-reductase inhibitors are available, finasteride and dutasteride. The 5-alpha-reductase enzyme exists in two forms: type 1 and type 2. Finasteride inhibits type 2 only, whereas dutasteride inhibits both. Although dutasteride provides greater suppression of dihydrotestosterone, it is not known if this provides a significant advantage clinically. Rates of side effects such as impotence, decreased libido, ejaculation disorder, and gynecomastia are similar.
5-alpha-reductase inhibitors may be used in the treatment of benign prostatic hyperplasia (enlarged prostate gland) and male-pattern hair loss (androgenic alopecia). They are not approved for the prevention of prostate cancer.
*
Yeah, but Accutane inhibits everything: DHT, testosterone, LH, FSH, estradiol, increases prolactin... I find hard to believe only other factors such as lifestyle, diet, sleep, lack of exercise, etc. account for all my levels. If a man has low DHT he also has low libido. Listen to this:
https://howtoliveyounger.com/low-libido-is-it-low-dht/
******
If your mojo is in park and you just cant seem to kick it into high gear, it may be due to low levels of a metabolite of testosterone called 5 alpha-dihydrotestosterone or DHT.
DHT is one of the major hormones that regulate libido in men and women.
DHT is a stronger testosterone because it has a greater affinity for, and preferentially binds to, the androgen receptor to produce its effects. Increasing libido is one of the most well-known effects but there is more to this hormone.
DHT affects libido because it regulates
- Male sexual development
- Development and growth of the prostate gland, epididymis, vas deference and seminal vesicles
In men and women, DHT regulates libido and more, including:
- Growth of hair on the body
- Sebaceous and sweat gland activity
- Libido or sexual desire and sexual function
Testosterone can convert into DHT and enhance libido through activation of the enzyme 5 alpha reductase. Testosterone also converts to estrogen through the enzyme aromatase.
If estrogen is too high in relation to testosterone and DHT in men, it may lead to the development of breasts and enlargement of the prostate gland. Some estrogen is necessary to maintain bone mass and reduce fat inside the abdomen. Finding the right balance of all of the hormones is key to overall health.
Men and women like how they feel when they have adequate levels of DHT they have a greater feeling of self-confidence, motivation, and libido. However, too much DHT can have unwanted side effects.
Side effects of high DHT include high libido, as well as:
- Loss of scalp hair at the temples and on the crown
- Increased facial and body hair
- Acne and sweating
- Aggressive behavior
- High sexual desire (libido)
- Sleep apnea
- High red blood cell count
- Increased risk of high blood pressure, abnormal lipids, insulin resistance and diabetes.
Treatment for high DHT
- Lower testosterone (if youre on testosterone)
- Finesteride, a prescription medication
- Gamma Linolenic acid (GLA)
- Saw palmetto
- Green tea
- Beta-sitosterols
- Pygeum africannum
- Pumpkin seed oil (Octa Sabal Plus)
- Lipsterolic extract of Serenoa repens (Prostamol Uno)
- The combination of 5% hexane extract of C. aeruginosa and 5% minoxidil slowed hair loss and increased hair growth. However, the extract of Curcuma aeruginosa is not yet commercially available.
******
If I am understanding this right, then the only way to fix acne with a drug is by decreasing DHT, and thus becoming impotent. That's what is implied, because if having high DHT means having acne, then having low DHT means not having acne, but at the same time you will have LOW LIBIDO.
So in the end you can't have both: not having acne and high libido. At least not if you tookAccutane.
This is anoversimplification of things, of course, because not all people that took this poison had the same side effects.
In the book THE SCIENCE OF SEX by Kevin Pezzi the author said: "the persistent effects of Accutane are due to epigenetic modifications, one of which seems to partially block the ability of T to heighten libido and sensation".
About the supplements I mentioned before, here are some studies I found out:
Fenugreek: (Kevin also said hehad good results with it):
****
This study examined the effect of Testofen, a specialised Trigonella foenum-graecum seed extract on the symptoms of possible androgen deficiency, sexual function and serum androgen concentrations in healthy aging males. This was a double-blind, randomised, placebo- controlled trial involving 120 healthy men aged between 43 and 70 years of age. The active treatment was standardised Trigonella foenum-graecum seed extract at a dose of 600mg/day for 12 weeks. The primary outcome measure was the change in the Aging Male Symptom questionnaire (AMS), a measure of possible androgen deficiency symptoms; secondary outcome measures were sexual function and serum testosterone. There was a significant decrease in AMS score over time and between the active and placebo groups. Sexual function improved, including number of morning erections and frequency of sexual activity. Both total serum testosterone and free testosterone increased compared to placebo after 12 weeks of active treatment. Trigonella foenum-graecum seed extract is a safe and effective treatment for reducing symptoms of possible androgen deficiency, improves sexual function and increases serum testosterone in healthy middle-aged and older men.
****
Link for this study
2nd study (link):
Efficacy of Furosap TM , a novel Trigonella foenum-graecum seed extract, in Enhancing Testosterone Level and Improving Sperm Profile in Male Volunteers
*****************
TONGKAT ALI (or Eurycoma longifolia Jack) - perhaps the most effective T booster. In the study #3 it was also said it could boost dopamine.
Link for study #1 - Link for study #2 - Link for study #3 - Link for study #4
PANAX GINSENG - I wasn't able to find the full study that said the following:
***
Effects of Panax Ginseng C.A. Meyer saponins on male fertility.
Salvati G, Genovesi G, Marcellini L, Paolini P, De Nuccio I, Pepe M, Re M
Author information:
Panminerva Medica, 30 Nov 1996, 38(4):249-254
PMID: 9063034
Sixty-six patients have been treated with Panax Ginseng C.A. Meyer extract, of whom 30 oligoastenospermic sine causa (group A), 16 oligoastenospermic with idiopathic varicocele (group B). Twenty age-matched volunteers were used as controls (group C). Use of Panax Ginseng extract showed an increase in spermatozoa number/ml and progressive oscillating motility, an increase in plasma total and free testosterone, DHT, FSH and LH levels, but a decrease in mean PRL. It is suggested that ginsenosides may have an effect at different levels of the hypothalamus-pituitary-testis axis.
***
A decrease in prolactin and elevation in DHT, LH, FSH, free T is what we need.
**
Peruvian MACA:
******
A pilot investigation into the effect of maca supplementation on physical activity and sexual desire in sportsmen
Conclusions: 14 days ME supplementation improved 40km cycling time trial performance and sexual desire in trained male cyclists. These promising results encourage long-term clinical studies involving more volunteers, to further evaluate the efficacy of ME in athletes and normal individuals and also to explore its possible mechanisms of action.
Link for this
******
*
In summary, maca root may alleviate SSRI-induced sexual dysfunction including having a beneficial effects on libido, and there may be a dose-related effect. A replication study with a larger sample and higher maca doses is currently under development.
*
***********
About the importance of ESTRADIOL/ESTROGEN in men:
Gonadal Steroids and Body Composition, Strength, and Sexual Function in Men
by Joel S. Finkelstein, M.D., Hang Lee, Ph.D., Sherri-Ann M. Burnett-Bowie, M.D., M.P.H., J. Carl Pallais, M.D., M.P.H., Elaine W. Yu, M.D., Lawrence F. Borges, M.D., Brent F. Jones, M.D., Christopher V. Barry, M.P.H., Kendra E. Wulczyn, B.A., Bijoy J. Thomas, M.D., and Benjamin Z. Leder, M.D.
CONCLUSIONS:
The amount of testosterone required to maintain lean mass, fat mass, strength, and sexual function varied widely in men. Androgen deficiency accounted for decreases in lean mass, muscle size, and strength; estrogen deficiency primarily accounted for increases in body fat; and both contributed to the decline in sexual function. Our findings support changes in the approach to evaluation and management of hypogonadism in men.
This bit is very interesting:
******
Our finding that estrogens have a fundamental role in the regulation of body fat and sexual function, coupled with evidence from prior studies of the crucial role of estrogen in bone metabolism, indicates that estrogen deficiency is largely responsible for some of the key consequences of male hypogonadism and suggests that measuring estradiol might be helpful in assessing the risk of sexual dysfunction, bone loss, or fat accumulation in men with hypogonadism.
For example, in men with serum testosterone levels of 200 to 400 ng per deciliter, sexualdesire scores decreased by 13% if estradiol levels were 10 pg per milliliter or more and by 31% if estradiol levels were below 10 pg per milliliter. Our findings also suggest that treatment with aromatizable androgens would be preferable to treatment with nonaromatizable androgens in most men with hypogonadism.
******
So that implies a modest increase in Estrogen was what I needed to improve my condition.
3rd study:
ELEVATED SERUM ESTRADIOL IS ASSOCIATED WITH HIGHER LIBIDO IN MEN ON TESTOSTERONE REPLACEMENT THERAPY
**********
(...)
RESULTS: A total of 423 men on TRT reported their sexual satisfaction. Men with serum testosterone > 300 reported a greater libido than men with testosterone < 300 (3.46 vs. 2.92, p<.01). Men with serum estradiol > 5 reported a greater libido than men with estradiol < 5 (3.70 vs. 3.23, p<.01). Men with serum testosterone > 300ng/dL and estradiol > 5 (n91) were more likely to report a score of 4 or 5 on libido (60.4%) than men with testosterone < 300 and estradiol < 5 (31.3%, p<0.01). Univariate analysis showed an association between libido and age, FSH, LH, estradiol, and total testosterone. Interestingly, on multi-variable analysis, only estradiol > 5 ng/dl (2.13, p0.001) was associated with greater libido. None of the clinical parameters evaluated were associated with erectile strength.
CONCLUSIONS: Elevated estradiol is associated with a stronger libido in men on testosterone replacement. Estradiol and testosterone levels do not appear to be associated with erectile strength.
**********
****
TRIBULUS TERRESTRIS:
Conclusions: Ninety percent of T booster supplements claimed to boost T. However, only 24.8% of these had data to support these claims. A total of 10.1% contained components with data suggesting a negative effect on T. Many had supra-therapeutic doses of vitamins and minerals, occasionally over the UL. Patients should be informed that T booster supplements may not have ingredients to support their claims.
*******
*******
(...)
Plasma total testosterone (TT), luteinizing hormone (LH) and estradiol (E2) were measured via ELISA and the urinary TIE ratio was measured by way of GCMS at the Australian Sports Drug Testing Laboratory. Tests were conducted pre and post supplementation (days 0 and 14). Statistical analysis was conducted by way of a repeated measures analysis of variance. No statistically significant between group effects were noted for plasma total testosterone, luteinizing hormone or the urinary testosterone/epitestosterone ratio (P>.05). A statistically significant increase in estradiol between days 0 and 14 was noted in the Tribulus group (P<.05). The present results suggest that Tribulus terrestris use is not detected via the urinary testosterone/epitestosterone ratio. Furthermore, it appears that the aromatisation pathway is stimulated to increase blood estradiol when ingested by healthy young male subjects.
*******
****
We concluded that Tribulus terrestris may be a promising herbal medicine for the treatment of aging patients with erectile dysfunction suffering from partial androgen deficiency. However, we recommend doing further studies on a larger scale (Increase the sample size) & changing the study design to be double blind randomized placebo controlled study.
****
And a last one:
Summary
Male fertility can be evaluated through complete semen analysis. Plants belonging to the Tribulus genus are known for their role in enhancing sex hormone levels and semen quality. The aim of this study was to evaluate the effects of T. terrestris on semen quality and physiological parameters. Sixty-five men with abnormal semen evaluation were included in this study, in which they were prescribed with oral administration of Androsten (250 mg of Tribulus terrestris dried extract per capsule). Body fat percentage, lean muscle mass gain, fluctuation in steroid hormone levels and all semen parameters were analysed during the period of treatment. The results demonstrated that decrease in the percentage of body fat and increase in lean mass were significant, as well as increase in dihydrotestosterone levels.
Complete semen analysis evaluated at the end of treatment showed significant enhancement in sperm concentration, motility and liquefaction time. Protodioscin, the main phytochemical agent of the Tribulus genus, acts on sertoli cells, germ cell proliferation and growth of seminiferous tubules. This component is known to convert testosterone into dihydrotestosterone, which plays important roles in male attributes. Our results indicate the therapeutic use of Tribulus terrestris by men presenting altered semen parameters, and/or undergoing infertility treatment.
***********
An increase in DHT? That's interesting. Also, if I am not mistaken, this study shows prolactin is also decreased.
A final note on these libido supplements:
There are many brands out there with probably ineffective Tribulus bottles, filled with crap... like calcium carbonate (Now). I couldn't find one that is really clean, however at least at this moment perhaps the best one that is out there (unfortunatelly more expensive) is the "Ultra High Strength Tribulus Capsules - 95% Steroidal Saponins - 1300mg Concentrated Extract Formula - The Strongest Testosterone Booster Available - 120 Caps" from the Toniiq Store.
That's because it has 95% saponins. All others have 40, 45%, which is probably a waste of money.
TONGKAT ALI is also another supplement we need to be careful when choosing. I am between the Nootropics Depot brand and Double Wood Supplements. Nootropics Depot seems to be reliable in terms of how effective their products are.
PERUVIAN MACA - Many options, like NOW FOODS, DOUBLE WOOD, PURE ORGANIC INGREDIENTS... we need to do some research in terms of effective dose (because many companies don't put enough and that's the 1st thing we should check) and if capsules are equally as good as taking in powder form. Just like Tongkat, powder options may have a very bad taste that doesn't go away, so that's why people opt for capsules.
PANAX GINSENG - haven't looked into many brands. DOUBLE WOODS is cheaper, however it may not be good enough. NOOTROPICS DEPOT = expensive.
FENUGREEK - I am considering NOW FOODS or Nature's Way. It's a cheaper supplement, and like MACA there are many brands.
*****
My final take on all of this:
- It may be a good idea to try:
* MACA (to boost libido by increasing estrogen, if the man has very low levels)
* TONGKAT ALI - probably the most effective T booster
* TRIBULUS - same as Tongkat.
* PANAX GINSENG - same as Tongkat. Ginsengs also help with vitality, memory, energy, mood, focus.
* ASHWAGANDHA - don't take if it's not KSM-66, like Tribulus there are many useless bottles out there. It will be (for sure) effective if there's a need to decrease cortisol/stress, since these are known to be very bad for testosterone.
And... that's it.
29:10 - interesting mention about Finasteride, a 5alpha reductase inhibitor. Accutane/isotretinoin also does the same, and suppresses DHT. The problem is ED dysfunction/low libido associated with it (29:50). At 32:42 he mentions again this probably permanent side effect. During the last minutes he also talks about other supplements for improving testosterone/libido.
https://truelibido.com/supplements/maca/
https://truelibido.com/supplements/tribulus-terrestris/
https://truelibido.com/supplements/tongkat-ali/
https://truelibido.com/supplements/fenugreek/
Hi Perene,
great info youve posted above- thank you
What is your take on CBDoil?
Are there any articles on its affect on testosterone that you know of?
I dont know much about itmyself other than its gaining popularity and is more accepted amongst the medical community for helping people. Starting to be available in chemists etc which was unheard of 5-10 years ago
I mean what youve said above is very useful for sexual issues but theres everyone else who doesnt necessarily have those issues but may have chronic gut issues or chronic joint issues post Tane...
Could CBD oil be more of anholistic approach to our issues, the point being it may treat multiple issues that the injured are left with after Tane - sexual or otherwise
Hey everyone, I have scheduled my 10 day water fast at the Siddhayatan spiritual retreat. I am skeptical that it will change that much but I have it scheduled right now. The 6 day water fast that I did was unsupervised and I broke the fast half way through with one bowl of ramen noodles. I will be flying out to Texas on Monday.
I am suspicious that the mechanism of action with accutane is to lower testosterone because high testosterone levels cause large, oily pores. Scientists currently don't know why accutane works at clearing skin. I feel like I am not even a man after accutane use. I am hoping that this clears things up.
I am going to have to use Togkat Ali! Currently I am using HCG to boost testosterone.
On 2/17/2021 at 2:37 PM, DeepAcceptance said:Hey everyone, I have scheduled my 10 day water fast at the Siddhayatan spiritual retreat. I am skeptical that it will change that much but I have it scheduled right now. The 6 day water fast that I did was unsupervised and I broke the fast half way through with one bowl of ramen noodles. I will be flying out to Texas on Monday.
I am suspicious that the mechanism of action with accutane is to lower testosterone because high testosterone levels cause large, oily pores. Scientists currently don't know why accutane works at clearing skin. I feel like I am not even a man after accutane use. I am hoping that this clears things up.
I am going to have to use Togkat Ali! Currently I am using HCG to boost testosterone.
Don't know about CBD... I compiled a few studies on isotretinoin here (PDF):
https://www.dropbox.com/sh/hlck885uu1jvi52/AABkIrjGGVjmSNpjsI5m6rDMa?dl=0
Besides the others about supplements. What is said specifically in PDFs 1 and 10 is that Accutane messes with the hormones in an attempt to fix acne, the thing is,no one can be healthy if, for example, DHT is too low. Listen: it can't be too high (because that means ACNE and other known problems), but if it's too low you will have a host of other issues. That's precisely wherethis poison fails: it supresses things during the treatment and we are unable to return to normal or higher levels later. Or if this is achievable, it's too difficult. Some changes are said to be permanent. Others I believeit can be fixed over time, like depression due to low B12. My B12 levels were measured to be OK and depression ceased to be a problem after a few years.
In study #1 (from isotretinoin) the following is said, among other things:
****
The effect of low-dose isotretinoin therapy on serum androgen levels in women with acne vulgaris
*
Background: Acne vulgaris is a common dermatologic disease that causes significant social and psychological morbidity. Isotretinoin, as a vitamin A derivative, is the most effective agent in the treatment of acne. Evidence suggests that isotretinoins therapeutic function is independent of hormonal mediation; however, the effect of isotretinoin on serum androgens and precursor androgen levels in humans remains unclear.
Objective: Herein, we aim to investigate the effect of low-dose isotretinoin on androgen levels in women and postulate the role of concomitant anti-androgen therapy (e.g., spironolactone).
Methods: A total of 36 women, age 18 to 30 years, with moderate-to-severe nodulocystic acne were treated with 20 mg isotretinoin (Roaccutane) daily for 3 months. A hormone panel was obtained at baseline and after completion of the treatment course. The panel included dehydroepiandrosterone (DHEA), 17-hydroxyprogestrone, testosterone, free testosterone, dihydrotestosterone (DHT), luteinizing hormone, follicle stimulating hormone, and prolactin.
Results: Serum levels of testosterone (p = .015), prolactin (p = .001), and DHT (p = .001) were significantly decreased, while serum levels of DHEA (p = .001) significantly increased after isotretinoin treatment. No significant change was found in the other hormones evaluated. Limitations: The distribution of acne was not assessed in our patient population. We did not directly evaluate for associations between elevated DHEA levels and clinical response rates.
Conclusion: Isotretinoin alone can decrease androgen levels, but increase an important driver of acne pathogenesis (i.e., DHEA). The co-administration of an anti-androgenic agent (e.g., spironolactone) may optimize the therapeutic efficacy of isotretinoin by limiting iatrogenic increases in DHEA and perhaps allow for more widespread use of low-dose isotretinoin.
*****
A few more passages from that PDF:
Isotretinoin has a profound inhibitory effect on the size and function of sebaceous glands, resulting in reduction of acne lesions.
Evidence suggests that isotretinoins therapeutic function is independent of hormonal mediation (Farrell et al., 1980); however, the effect of isotretinoin on serum androgens and precursor androgen levels in humans remains unclear (Feily and Namazi, 2011; Gomez and Moskowitz, 1980; Lookingbill et al., 1988; Marynick et al., 1983). Herein, we investigate the effect of low-dose isotretinoin on androgen levels in women and postulate the role of concomitant anti-androgen therapy.
***
RESULTS:
Serum hormone levels before and after isotretinoin therapy are summarized in Table 1. Serum levels of testosterone (p = .015), prolactin (p = .001), and DHT (p = .001) were significantly decreased after isotretinoin treatment. In contrast, serum levels of DHEA (p = .001) significantly increased after isotretinoin treatment. Luteinizing hormone, follicle stimulating hormone, free testosterone, and 17-hydroxyprogesterone showed no significant change after treatment (p > .05 for all).
***
This 2019 paper also said:
*********************
To date, few studies have explored the effect of isotretinoin on androgen levels, and the results of published studies are inconclusive and at times conflicting. We identified that 3 months of therapy with low-dose isotretinoin resulted in significant decreases in levels of serum total testosterone, prolactin, and DHT but increased DHEA levels. The remaining fold changes in serum hormone levels were not significant.
Our results are relatively concordant with those of Lookingbill et al. (1988) and Karadag et al. (2015). Lookingbill et al. (1988) found that isotretinoin caused elevation of free testosterone and depression of DHT. Karadag et al. (2011) found that isotretinoin therapy resulted in decreased prolactin and total testosterone levels but increased DHEA levels. In another clinical trial, total testosterone and prolactin levels were significantly decreased in patients treated with isotretinoin, with no change in free testosterone and DHEA levels (Karadag et al., 2011).
Together, these reports suggest that isotretinoin therapy decreases total testosterone, prolactin, and DHT, while increasing free testosterone and DHEA. Although the mechanism of these changes is not well understood, we hypothesize that isotretinoin induces the separation of testosterone from sex hormone-binding globulin, thereby increasing free testosterone levels and inhibiting the transformation of testosterone to DHT.
Isotretinoin alone can decrease androgen levels, but in prior reports (including our own), isotretinoin increased DHEA levels. DHEA is an important driver in the acne pathogenesis of hyperandrogenic patients; 72% of acneic women have been found to have clinical and/or biochemical hyperandrogenemia (Lookingbill et al., 1988). Hence, it is important to address androgen-derived pathogenesis during acne treatment. At our institution, we find that co-administration of isotretinoin with spironolactone achieves superior therapeutic efficacy. We postulate that sprinolactone decreases the level of DHEA and other androgens that are further increased by isotretinoin, thereby improving and optimizing the therapeutic efficacy of isotretinoin.
Perhaps this therapeutic optimization with the addition of spironolactione may allow for more widespread use of low-dose isotretinoin. Taken together, our data indicate that isotretinoin has an effect on certain serum androgen levels (Feily and Namazi, 2011). Given the conflicting results in current studies, a randomized, controlled, and adequately powered study is needed to elucidate the effects of isotretinoin on serum hormone levels and the clinical benefit of treating acne with oral isotretinoin alone versus oral isotretinoin with spironolactone.
*********************
I was able to find the 1988 paper "Effect of Isotretinoin on Serum Levels of Precursor and Peripherally Derived Androgens in Patients With Acne". This one is even more interesting. It's study #10 (PDF)
Take note of what this one says about DHT. I said earlier my levels have showed to be low in multiple blood tests. Not only them: estradiol was also low (it needs to be in the middle of the lab range, otherwise this means low libido, and low T). Also my SHBG is in the 40's, from a range up to 50's. High SHBG if I am not mistaken is bad for testosterone.
My free T is insufficient and not even in the middle of the lab range. And finally my prolactin needs to be half what the tests say (instead of 20's, should be in the 10's). High PRL is another sign of low libido.
Finally, my LH and FSH levels have always been low. Another clear sign of a problem. Now, back to the paper:
*****
Sebaceous glands are stimulated by androgens and can convert them to more active forms. Isotretinoin, however, has a profound inhibitory effect on sebaceous gland size and function. This study evaluated the effect of isotretinoin on serum levels of precursor and tissue-derived androgens. Twenty-four subjects (15 men and nine women) were treated for 20 weeks with 1 mg/kg/d of isotretinoin. Serum samples were obtained at baseline, 8, 16, and 24 weeks, and assayed for precursor androgens\p=m-\total testosterone (TT), free testosterone (free T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone-sulfate (DHEA-S); and tissue androgens\p=m-\dihydrotestosterone (DHT), and its metabolite, 3 \g=a\-androstanediol glucuronide (3 \g=a\-diol G).
Isotretinoin had no meaningful effects on precursor androgens, except for producing an elevation of free T in women. In contrast, isotretinoin produced depressions in the serum levels of DHT and 3\g=a\-diol G in women and in 3 \g=a\-diol G in men. These decreases are believed to be the result, rather than the cause, of a reduction in the size of the sebaceous glands: The magnitude of the observed decreases may represent the amount of tissue-derived androgens that sebaceous glands normally contribute to the circulating pool.
******
This is an old paper (33 years old), so it may be wrong (or the way these testings were conducted was wrong or inadequate), so it says stuff like:
*********************
Also, no evidence suggests that isotretinoin alters serum levels of precursor androgens, although few data have been published. In one study of 13 men treated with isotretinoin at a dose of 0.5 to 1.0 mg/kg/d, no significant alterations occurred in serum TT, luteinizing hormone (LH), or follicle-stimulating hormone (FSH). In another study of eight men treated with isotretinoin at a dose of 2.0 mg/kg/d, no significant change occurred in the serum levels of DHEA-S, TT, 17-hydroxyprogesterone, LH, or FSH.Neither study evaluated women, nor did they measure serum levels of tissue-derived androgens.
Our results likewise revealed no significant effects of isotretinoin on serum levels of precursor androgens (Tables 1 and 2), with the exception of free T in women.
*********************
However, right next we read this:
*********************
We did, however, observe that isotretinoin therapy resulted in significant decreases in the serum levels of tissue-derived androgens. Serum levels of DHT were significantly decreased in women (Table 1), while the serum levels of 3a-diol G were significantly depressed in both sexes (Tables 1 and 2). The isotretinoin effect on 3a-diol G was most pronounced in women. From these observations, we asked the following question: Are these effects on tissue androgens the cause of or the effect from the dramatic decrease in sebaceous gland size induced by isotretinoin? The work of Gomez and Moskowitz would argue against a causative role. In their hamster flank organ preparation, these workers demonstrated that isotretinoin had no inhibitory effect on 5a-reductase activity: DHT and 3a-androstanediol were produced normally in the presence of the drug.
How then can we explain the decreased levels of DHT and 3a-diol G, which occurred in our patients while receiving isotretinoin therapy? It is possible that in humans, isotretinoin, or a metabolite thereof, could in fact act as a 5a-reductase inhibitor. But if this were the case, all DHT produced by peripheral tissues (including, for example, the prostate gland in men) would be affected and a decrease in serum DHT and a more profound decrease in 3a-diol G would have been expected in men.
We suggest that the decreases we observed in serum levels of tissue-derived androgens are more likely the result of the marked diminution in size of the sebaceous glands caused by the drug. This then reduces the amount of tissue available for converting precursor androgens to tissue-derived hormones. Furthermore, since isotretinoin is not known to affect any other androgen tissue, the decreases we observed in the serum levels of DHT and 3a-diol G may reflect the contribution that sebaceous glands in the skin normally make to the circulating pools of these peripherally produced androgens. Perhaps the effect is more pronounced in women because, in comparison with men, women have lower baseline levels of androgens and fewer available sources for tissue androgen conversion.
After discontinuing isotretinoin therapy, DHT and 3a-diol G values in women increased but not to baseline values. This is consistent with the observation that sebaceous gland activity (as determined by sebum excretion measurement) does not fully return to baseline status four weeks after therapy. In men, the mean 3a-diol G values returned to baseline at the 16th week of therapy and even exceeded the baseline four weeks after therapy, but the quadratic trend (which compares values during therapy with values before and after therapy) showed a statistically significant effect. We cannot easily explain why the 3a-diol G values begin to recover during therapy.
Perhaps, the glucuronidation of isotretinoin itself leads to induction of more conjugating enzyme, resulting in increased glucuronidation of 3a-diol G from sources other than sebaceous glands.
This hypothesis, however, is speculative. It is known that sebaceous glands can also convert precursor substrates to more potent androgens - specifically DHEA to T. This pathway has been implicated clinically by the finding of elevated DHEA-S levels in many patients with severe acne. It is also known that the majority of serum T in women is derived from the peripheral conversion of androgen substrates. How much of this might be derived from sebaceous glands? Our finding no decrease (in fact, a slight increase) in serum TT in women receiving isotretinoin provides circumstantial evidence that sebaceous glands do not make a major contribution to the circulating pool of testosterone.
*********************
So that last bit contradicts what DeepAcceptance just said: "high testosterone levels cause large, oily pores".
Finally:
*********************
We were somewhat surprised by the increase in free T that occurred in women during isotretinoin therapy (Table 1). Although the changes are statistically significant (P = .028), they still could have occurred by chance. Alternatively, it is possible that isotretinoin could be competing with testosterone for its binding to albumin or testosterone-binding globulinthereby making more free T available.
Since retinoic acid has been shown to compete with estrogen for binding to protein, this possibility cannot be ruled out. The lack of increase in free T in men does not detract from the possibility of isotretinoin competitively binding to binding proteins.
Unlike women, men have a homeostatic mechanism (via LH regulation) to maintain stable serum levels of free T.
So our findings are consistent with the possibility that isotretinoin competes with testosterone for protein binding, but confirmatory work is needed. Even if confirmed, the increased free T that we observed appears not to exert a clinical effect, particularly in regards to sebaceous glands, which would be expected to be stimulated.
Instead, isotretinoin produces, probably via a nonhormonal mechanism, a marked reduction in sebaceous gland size and function. This, in turn, appears to secondarily result in decreased production of tissue-derived androgens. The foregoing sequence of events is the most likely explanation for the decreases we observed in serum levels of DHT and 3a-diol G in patients receiving isotretinoin therapy.
*********************
It has been hypothesized some side effects are permanent because the changes are so profound that no matter what is done, it can't be reversed.
This is a message I read in a Youtube video:
**
The permanent damage from this medication can happen after it is discontinued even without side effects or any warnings/abnormal blood results when you are taking it. Just be warned, this drug could seriously ruin your body (eyes, bones, joints, hair, teeth, spine, skin, brain, nerves, tendons, ligaments) for the rest of your life. This happened to me despite normal/mild side effects while taking the drug. The damage suddenly set in about 5 months after I stopped taking it. This happens due to permanent gene expression changes, DNA damage, stem cell death, and bodywide apoptosis (cell death) that the drug causes. I took only 20mg (a 'low' dose) for 5 months and still got destroyed months after I stopped taking it. This is just a warning to anyone who is watching these videos and thinking about taking the drug. Your doctor may not necessarily be aware of these risks!
*****
No one can tell if that's really the case for ALL side effects. Why? Because we lack studies detailing if these people changed anything I suggested before. And there are not enough tests available.
Without enough data it's impossible to tell if there's a way to improve things or not.
Again, this is what having low DHT implies:
Symptoms:
Since DHT plays an integral role in the brain functioning at its best, other symptoms of low DHT have been found to affect mental health.
Low DHT can lead to low mood symptoms like depression and mood swings have become associated with low DHT. Feeling more grumpy, irritable, more easily annoyed, unmotivated, lethargic these are all possible symptoms of low DHT.
With DHT being one of the main sex hormones, along with testosterone and estrogen, low DHT can drastically lower a persons sex drive.
DHT also plays a role in muscle building and the bodys ability to maintain lean mass. Other low DHT symptoms could include a loss of lean muscle and an increase in body fat.
Remember that next time you find Accutane's actions to fix acne justifiable. The only reason this is still being considered is because the criminals that sell this poison have deep pocket$$$$$$. Low DHT, B12 deficiency... no wonder why people take this and commit suicide.
All the quacks that pretend to be doctors will never recognize the extension of these damages. These people will never ask for blood tests that are relevant. They don't want the victims to know the truth.
Whatever Accutane does to fix a problem causeothers. Undeniable.That's why resorting to drugs to fix a health conditionshould be the last resort after all (natural) ways of fixing have failed or can't produce the same effect by a long shot. If acne can be fixed by changing all I said previouslyin terms of vitamin deficiencies, diet, sleep, etc. then waiting a few years would suffice for us tosee tangible results.
When we are young we don't want to wait andfix things with more work. We want our skin cleared for good, and fast.Accutane IS thatmagic drug. However that comes with a cost... Like the devil collecting our soul later, after grating our wishes.
It's so fucked up that they sell drug which messes up with your hormones to kids who are going through puberty. I was promised a magic pill that clears up my skin for good and maybe dries my face which would return to normal when the drug use is discontinued and that's it. I have spoken with a few dermatologists afterwards and they seem pretty clueless about how isotretinoin works. They're probably confident about it, because they've just seen how it can clear acne, but haven't really got any bad reports back from patients. Many isotretinoin users are teenagers, you really can't expect them do that. Most lack life experience, they're awkward and already confused by all the changes their bodies are going through anyway.
My son's body issues break me all the time. He is OBSESSED with his hair. It does seem to be coming out. He pulls on it and has strands all the time. It does not look thinner, but I dunno, that is a process. I can tell that is it certainly thinner. He has so many other issues, he should not have to suffer baldness as well. It is also stressful/annoying/heartbreaking to have him OBSESS over it. Please stop, just stop, son. 
On 2/17/2021 at 11:37 AM, DeepAcceptance said:Hey everyone, I have scheduled my 10 day water fast at the Siddhayatan spiritual retreat. I am skeptical that it will change that much but I have it scheduled right now. The 6 day water fast that I did was unsupervised and I broke the fast half way through with one bowl of ramen noodles. I will be flying out to Texas on Monday.
I am suspicious that the mechanism of action with accutane is to lower testosterone because high testosterone levels cause large, oily pores. Scientists currently don't know why accutane works at clearing skin. I feel like I am not even a man after accutane use. I am hoping that this clears things up.
I am going to have to use Togkat Ali! Currently I am using HCG to boost testosterone.
If you are interested in fasting, check out Dr. Fung's fasting protocal, he has books, videos and a VERY Facebook site. He does NOT advocate over 7 days at a time, although people do it. They tend to work up to it, cut carbs ahead of time, get in the habit and then roll on and off with fasts. He does not, nor would I ever recommend a Dry Fast, esp as dried out as victims bodies are. Good luck.
My current theory is that accutane causes permanent damage to the body's autonomic nervous system, and if you can restore autonomic balance, you resolve all issues post accutane.
The prostate has an intimate relationship with the ans. If the ans is dysfunctional, the prostate will be dysfunctional. And if the prostate is dysfunctional, so will the penis be dysfunctional.
Now, we already know that finasteride and saw palmetto are no good for us. I know that flomax does a decent job of relaxing shit down there, but who wants to live with retrograde ejaculation for the rest of their life? Not me.
That's where swedish flower pollen comes into play. I've got a bottle of it from source naturals coming in from Amazon Tuesday. First dose will be Tuesday night. Now, if this product can resolve my prostate issues, I believe it will resolve post accutane sexual issues, and many other issues throughout the body. Tons of positive reviews from men and women alike who swear by it. Will keep the board posted on it, good or bad, soon.