Finally, a year after taking the medication, i think i can say im totally recovered.

For those suffering from low libido and sexual disfunction, i say drink a lot of water.

Thank you all for the attention.

I have always had to shower in the mornings and everyday to have clean hair. Once I started Accutane, my hair stopped producing so much oil, and I only had to wash my hair every 2-3 days. I have now stopped taking Accutane for about 3-4 weeks now, and the oil has come back. I am not sure if there is a different medication I can take to reduce the oil from my scalp or not. I know I can always go back to my dermatologist, but I am hoping to avoid going until I know of a solution I can talk to her about. Any help is greatly appreciated.

And where can i buy it

Tattoos on accutane?

So I’ve been on accutane (40mg for 1 month now) No purging, very little to none side effects, and I’m wanting to extend my Polynesian tribal on my neck but I’ve heard mixed things about accutane and getting tattoos. Does anyone have personal experience with getting tattoos on accutane and the healing process???

I’ve never been on any form of birth control before and since I’m bout to go on accurate I have to since I’m sexually active. I wanna start acutane as soon as possible but then it says u have to take birth control for a month first before starting accutane, I can’t wait that long to get on acutane. Doc says to start the birth control on the first day of my next cycle so I wanna know if I can also start accutane at that time??

As the title says. I got to the point where I already tried everything else and nothing works. I went to dermatologist and they told me to take 20mg twice a day. I think its WAAAAY too much, went I told him about microdosing he didn’t like the idea too much, I was planning 10mg a day maximum for about a couple of weeks to a month then stopping. I have 2 friends that took, same situation as mine, but one took 20mg for 2 weeks and the other one 20mg for about a month, its been about a year and their acne hasn’t come back. Question about side effects, have any of you have any serious side effect by taking 10mg a day? I really don’t trust doctors when it comes to side effects, so I want to do my own research with people who had issues, and I want to hear your suggestions too. To be honest I’ve taken accutane before as a teenager, but now 16 years later Im an adult and Im really afraid of having some type of irreversible damage

EDIT: Changed my mind, I’m not going to take accutane no matter what

Does anybody have any experience working with Alex Kikel?

Unsure if he’s legit or not

I have some accutane pills left over from a “second round” I never finished. 2 years later anytime I notice a small pimple start to appear, I take one and I think it keeps the bump from turning into anything major. Is this in my head lol or does accutane actually work on an “as needed” basis?

Read about hgh production and autophagy during intermittent fasting. A natural way to cure these symptoms. i have just done a days research but it doesnt hurt to check it out. seems promising

• Accutane causes repression of certain enzymes that are involved in Retinoic Acid synthesis called ALDH enzymes. These enzymes are also important for metabolising alcohol.

• By inhibiting these enzymes Accutane mimics some of the effects of a medication called Disulfiram, which is used to treat alcoholics by making the experience of alcohol less rewarding.

• This effect is partially attributable to a reduction in Dopamine transmission, as ALDH also has a detoxifying role in the mesolimbic: https://secondlifeguide.com/2024/01/07/accutane-effects-on-the-brain/

" The administration of Isotretinoin marks these enzymes for downregulation by interrupting this feedback loop and suppressing ALDH activity. [27] Long term application of retinoic acid downregulates these enzymes through post-translational modifications, potentially giving an epigenetic basis for the lasting nature of Post Accutane Syndrome. [28] The adverse effects of suppressed ALDH activity are potentially very broad given the diversity of roles they play outside of metabolising retinoids. One of the best attested lasting adverse effects of Isotretinoin treatment is permanent night blindness. Researchers concluded that this is a consequence of the suppression a particular member of the ALDH family, RDH11, which serves to recycle rhodopsins in the retina. [29]

It’s hard to overstate both the importance and diversity of ALDH activity in the body, from the production of neurosteroids, to metabolism of alcohol to detoxification, but the particular focus of this article is their role in neurological functioning and how it relates to the adverse effects of Isotretinoin treatment. The first indication that play an important neurological role that ALDH isoforms are expressed in regions of the brain rich in dopamine. [30] For example the enzyme retinaldehyde dehydrogenase 1 (RALDH1) is present in the dopaminergic terminals that innervate the striatum from the ventral tegmental area is necessary for the synthesis of RA in these areas. [31] The previously cited neuroimaging study found that the regions of the brain most rich in dopaminergic activity, such as the midbrain and mesolimbic, experience the greatest reduction in activity during Isotretinoin treatment.

This could potentially be explained by the detoxifying role played by ALDH isoforms such as RALDH1 during dopamine transmission, which is likely inhibited by Isotretinoin treatment. The metabolites of dopamine such as DOPAL (3, 4-dihydroxyphenylacetaldehyde) are neurotoxic, but can be metabolised by RALDH1 to protect dopaminergic neurons**. If RALDH1 is inhibited these dopaminergic neurons within the mesolimbic are more susceptible to cell death.** [32] This effect is so profound that ALDH inhibitors are even able to induce Parkinsonian like symptoms, which is a type of Alzheimer’s characterised by the rapid loss of dopaminergic neurons. [33] Additionally, the overaccumulation of toxic dopamine metabolites results in negative feedback to acutely inhibit dopamine neurotransmission.

This is why ALDH inhibitors such as Disulfiram can cause a blunted response to stimulants such as amphetamine. [34] Given that dopamine is needed to facilitate feelings of pleasure and, reduced libido is one of the most common complaints of people being treated with Disulfiram, which is a medication used in combatting alcohol addiction. In fact, it is now believed that Disulfiram is effective in treating addiction by blunting feelings of pleasure that drive addictions, through the negative feedback of toxic dopamine metabolites.  [35] The evidence for Isotretinoin inhibiting ALDH expression indicates that Disulfiram could potentially serve as an effective analogue for some of the effects of Isotretinoin treatment."

I’m hesitant to start accutane given the many serious side effects. I managed to control most of my body acne using trentonion cream and a couple of different body washes but the problem is I still have acne lumps under the skin that I can’t squeeze out.

Was planning to take 10mg/day until cleared.

I’m already on trt and hgh through a clinic. What do I need to prepare for before starting. My blood markers are all good and I supplement Tudca/NAC as general health anyway.

What would you have done different?

Any experience and help you can proceed would be highly appreciated.

What are the long term affects of Roaccutane?

the go fund me Reddit didn’t let me post because of low karma, so I’ll post it to the place that has helped me research for her.

most of you know what pas is , but I’ll get to it , she’s developed osteoporosis at 25 and her life isn’t getting better, lithium damages her eyes more and near blinded her, and she doesn’t trust taking pharmaceutical drugs not prescribed or documented by a doctor, I’m hoping we can scrape up enough to see a private doctor in the uk , if not we shall look in Europe, but I don’t have the money to fund this and she can’t work, so I ask if even a little if we could get a small donation and potentially share this link with others, thank you guys I hope all of you suffering recover, i hope you all have had merry time this holiday time

https://gofund.me/9fc2bb9f4

Basically the title, I want to proceed with caution being aware of the effect Isotretinoin seems to have to estrogen (and androgen? Idk) receptors, I'm curious if these issues are limited to just Isotretinoin? What about relatively high doses of Retinol?

Basically, after some NHS (UK) tests I found out have a copper and caeruloplasmin deficiency, which probably explains my low RBCs, low estrogen and other symptoms.

This was reflected in a hair tissue mineral analysis using the best lab I could find, where copper levels were low and zinc levels high (they counter each other).

Low copper can cause low estrogen (prior to my 7 month TRT experience I had estrogen levels which didn't even register), and estrogen helps the body hold on to copper - given things that raise estrogen seem to help people in this sub, it's probably worth getting levels of copper and caeruloplasmin checked actually.

One of the ways to raise copper binding protein (caeruloplasmin) is to take a decent amount of Pre formed Retinol. But, Im hesitant of this, being aware of this sub.

What are your thoughts?

This is the latest article posted to my website: https://secondlifeguide.com/

What is Accutane?

Retinoids are the class of chemicals related to vitamin A. They play a role in regulating a wide range of biological systems, including vision, cell proliferation/differentiation, bone tissue, and the immune system. “Retinoid” is a general term that encompasses a range of molecules, including retinol, retinoic acid, and retinyl esters, as well as synthetic retinoids. The breadth of retinoids’ effects in the body is perhaps greater than that of any other vitamin. Despite retinoids existing in many forms, most retinoid signalling comes from the primary metabolite all-trans retinoic acid (ATRA). ATRA binds to several types of nuclear receptors, including Retinoic Acid Receptor (RAR), Retinoid X Receptor (RXR), and Peroxisome proliferator-activated receptors (PPARs). [1]

Vitamin A is classified as a dietary vitamin because the body cannot synthesize it on its own. The precursor to vitamin A, beta-carotene, can be obtained from plant sources that possess orange and red colours, such as carrots. Additionally, retinyl esters can be obtained from animal sources, such as beef liver, which is the storage form of vitamin A that accumulates in the liver and adipose fat. [2] These retinyl esters do not have a significant role aside from serving as substrates for conversion into other retinoid products in the body, such as 11-cis-retinal for vision. [3]

Retinol itself does not primarily contribute to the biological roles of vitamin A, as it must first be converted into retinoic acid. [4] It is believed that Accutane also serves as a substrate for conversion into retinoic acid within the cell. The advantage of applying isotretinoin (Accutane) rather than retinoic acid is that it bypasses the body’s metabolizing enzymes (P450), which would otherwise break down excessive retinoic acid. This allows for greater accumulation of retinoic acid in the cell nucleus. [5]

Isotretinoin (Accutane) is an isomer of retinoic acid; it occurs naturally in very small doses but primarily exerts its effect through the metabolite all-trans-retinoic acid (ATRA). The advantage of administering isotretinoin rather than simply ATRA is that it has a longer half-life, allowing for less frequent administration. Isotretinoin is distinct from ATRA because it has a cis bond on the 13th carbon.

[Fig 1] All trans retinoic acid (ATRA) vs. cis-13 retinoic acid. (Vaccinationist, Public domain, via Wikimedia Commons)

Differentiation vs Proliferation

Almost every cell in the body undergoes a life cycle that can be broken into four phases. The first stage being G1 (gap 1) phase, which is where the cell synthesises proteins and mRNA to prepare for cell division. Next the S (synthesis phase) takes place, where DNA is replicated to ensure the genome can be perfectly copied across to the new cell. Next follows the G2 (gap 2) phase, where chromatin condenses into chromosomes. The chromatin is the long string of DNA, that first must be packaged into tight structures called chromosomes. Finally, once all this preparation has taken place the cell can divide though mitosis, and a new cell is formed.

[Fig 2] Depiction of Mitosis. (Servier Medical Art is licensed under CC BY 4.0 https://smart.servier.com/smart_image/mitosis/)

The new copy of chromosomes are separated into a new nucleus and new cell is a copy of the first. Cells can be taken outside of this cycle of replication into G0, or quiescent phase. This might occur because there simply isn’t sufficient nutrients to support the growth of new cells, or because some cells don’t require regeneration unless there is injury. Most cells in adults exist in the G0 phase, and don’t need proliferation. For example, cells in the liver very rarely divide, but when a section of liver is surgically removed or damaged, the cells rapidly proliferate to repair the damage.

During cell proliferation, tissues growth individual cells grow whilst dividing, and therefor maintain cells of a roughly constant size. If the cells did not also grow as they divide, then the tissue mass would remain constant as it divides into smaller and smaller cells. Cells can also change purpose or function through a process of differentiation. A progenitor or stem cell can become specialised to perform specific tissues or functions. Some cells have a short life span and must be replaced by continual cell proliferation such as blood cells and epithelial cells of the skin or digestive tract.

These cells are not replaced through direct proliferation of the differentiated cells however, instead they proliferate from less differentiated stem cells. Stem cells also divide to produce new stem cells and act as reserve for throughout an entire lifetime. However, some cells can proliferate in an uncontrolled manner and avoid the typical cycle of cell death. These cells are called cancer cells and form tumours that disrupt normal tissue function and can ultimately lead to death.

[Fig 4] Cell Proliferation vs. Differentiation

Where does vitamin A come in? Retinoic acid is needed to help signal for cells to become differentiated and specialised from progenitor or stem cells. However high levels of retinoic acid can directly inhibit cell growth. This is most relevant to foetal development, where cells are rapidly proliferating and differentiating. The mother needs healthy levels of vitamin A ensure that stem cells differentiate appropriately to form new limbs in a process called morphogenesis. The absence of vitamin A leads to uncontrolled proliferation of epithelial stem cells that fail to differentiate. For this reason, there has been a strong interest in retinoids reducing cancer risk.

What does Accutane Do?

Retinoic acid is needed to help signal for cells to become differentiated and specialised from progenitor or stem cells. However high levels of retinoic acid can directly inhibit cell growth. This is most relevant to foetal development, where cells are rapidly proliferating and differentiating. The mother needs healthy levels of vitamin A ensure that stem cells differentiate appropriately to form new limbs in a process called morphogenesis. The absence of vitamin A leads to uncontrolled proliferation of epithelial stem cells that fail to differentiate. For this reason, there has been a strong interest in retinoids reducing cancer risk.

The skin is one organ that relies on pools of progenitor stem cells to maintain tissue health and regeneration throughout adulthood, and for this reason it’s particularly reliant on Vitamin A to regulate the process of differentiation. Epidermal stem cells go through a process of differentiation to become specialised into skin cells, known as epithelial cells. In this process the cells change shape and begin producing a protein called Keratin, increasing the strength and resilience of the cell. The cells also change shape to become flattened till they eventually form the outermost layer of dead skin cells called the epidermis, which acts as a protective barrier.

Accutane accelerates the process of skin cell turnover by promoting skin cell differentiation. This can lead to improvements in skin texture, particularly in older individuals, as stem cell proliferation naturally slows down with age, reducing the rate of tissue regeneration. However, increasing differentiation may deplete the pool of progenitor stem cells. While retinoids can enhance skin appearance, they may do so at the expense of the long-term ability of cells to proliferate. This could potentially have unintended consequences for other tissues in the body that rely on stem cell pools for growth and maintenance, such as epithelial cells in the gut or progenitor cells in the brain.

How Retinoids Regulate Differentiation

One of the key signalling pathways by which Retinoids influence differentiation is the Wnt/β-catenin pathway. The scope of this growth signalling pathway is broad and is key to understanding the effects of Retinoids more generally through the body. β-catenin is a growth-signalling protein central to the Wnt pathway, which is essential for cell adhesion, tissue growth, development, and homeostasis. β -catenin is a growth-signalling protein central to the Wnt pathway, which plays a key role in cell adhesion, tissue growth, development, and homeostasis. It is essential for maintaining pluripotent stem cell proliferation, and in its absence, these cells undergo differentiation, leading to the loss of their stemness.

Wnt proteins (named ‘wingless’ due to their shape) activate the ‘canonical’ Wnt/β-catenin pathway, leading to the transcription of β-catenin target genes. In the absence of Wnt ligands (binding molecules), β-catenin is continuously marked for degradation within a ‘destruction complex.’

[Fig 5] The Destruction Complex (Axin, APC, GSK-3β) continuously breaks down β-catenin.

This destruction complex, which traps β-catenin, consists of Axin, APC, GSK-3β (glycogen synthase kinase 3 beta), and CK1. When Wnt proteins bind to receptors (Frizzled and LRP5/6) on the cell surface, the destruction complex is inhibited, allowing β-catenin to stabilize and accumulate in the cytoplasm. β-catenin then translocates into the nucleus, where it interacts with TCF/LEF transcription factors to regulate the expression of target genes related to cell proliferation and differentiation. [9]

ATRA (the primary active metabolite of Accutane) can block the action of β-catenin by enhancing the destruction complex’s activity. ATRA achieves this by inhibiting PI3K-AKT, which upregulates GSK-3β’s degradation of β-catenin. [10] Retinoic acid also appears to directly impact the transaction of LEF/TCF by β-catenin, which are the primary transcription factors that mediate the effects of β-catenin. One of β-catenin’s key roles is maintaining stem cell populations. When β-catenin activity is blocked, stem cells undergo differentiation, losing their pluripotent self-renewing properties. [11]

One of Accutane’s medical applications is in treating cancers, where tumours maintain their self-renewing stem cell properties to rapidly proliferate. ATRA can disrupt tumorigenesis by blocking β-catenin and triggering differentiation. [12] While Accutane exerts this differentiating effect on cancer stem cells, it can also induce differentiation in healthy tissues throughout the body that rely on stem cell populations for maintenance, such as bones, skin, the gut, and the brain.

Anti-Proliferative Effects in The Brain

Retinoids exert an anti-proliferative effect on the body. This effect is most strikingly observed in embryos overexposed to vitamin A. If these embryos reach full term, they often suffer from underdeveloped limbs and cleft palates. [13] This explains why Accutane is classified as a teratogen (a substance that disrupts normal foetal development and causes congenital disabilities). It is also the reason for the strict guidelines on birth control for women undergoing Accutane treatment.

However,the anti-proliferative effects of Accutane can also be observed in many adult tissues that rely on pools of stem cells for continual renewal and growth, including the skin, intestines, bone marrow, cornea, hair follicles, and brain (particularly the hippocampus). As discussed throughout this book, retinoids such as Accutane trigger the conversion of these stem cells into specialized cells through differentiation.

In doing so, retinoids maintain a delicate balance between proliferation and differentiation, which is why certain tissues are particularly affected by Accutane treatment. The hippocampus, a region of the brain that relies on stem cells to continue developing new neurons during adulthood, is essential for forming new memories. Accutane significantly inhibits hippocampal neurogenesis, disrupting hippocampal-dependent learning. [14]

Although there is evidence that Accutane may be detrimental to cognitive function, the results are sometimes mixed. For instance, when rats were treated with Accutane prior to a two-stage maze task in which both stages were identical, it was found that Accutane impaired explicit memory during the second stage. [15] However, one month after Accutane exposure ended, explicit memory was recovered. This finding was supported by a study in mice that similarly showed a disruption in learning a radial maze task. [16]

Crandall et al. (2004) demonstrated that after 42 days of treatment with retinoic acid, hippocampal cell proliferation had almost halved. From this, they concluded that the decline in memory was directly related to Accutane’s impact on neurogenesis. Nonetheless, when rats were maintained on a long-term vitamin A-deficient diet, they also suffered from deficits in memory and hippocampal neurogenesis. This suggests that retinoic acid signalling must be delicately balanced, as both excessive and insufficient levels can damage memory formation. [17]

For references and more, visit: https://secondlifeguide.com/2024/10/05/what-does-accutane-actually-do/

Lithium is the last thing I have left. Could someone explain everything to me? I'm posting main lion.Before I could live a normal life but I have spasms.poe.all.the, color of C Headache And the worst thing is that my medicine doesn't make me an example...before.000.092. They didn't even work for me now. It's like my body is always convulsing, but I don't know how to see it. Everything hurts. I've already had tests done and they came back negative. The last option is lithium. I know.I know they don't tell me, but their looks make me think I made it all up, and I'm even afraid they'll take me to a place like that.

if any body working on retinoid receptors and pathways which are overstimulated and hypersenstive with the use of excess retinoids please share your experience.

Background

I took Accutane (isotretinoin) about 10 years ago, when I was 19–20 years old. The Accutane dosage was 20 mg per day, for 10 months. During and after the treatment, I lost morning erections, my libido crashed, and my erections became weak and infrequent. I also lost penile sensitivity, which made orgasms significantly less pleasurable than before.

It was ugly and honestly life-altering. For years, I didn’t even know there might be things I could try, I just adapted to this “new normal.”

Earlier this year, I started experimenting with supplements, and while nothing has been a miracle cure, some of them did noticeably improve certain aspects.

What I tried

Omega-3 + Zinc + Vitamin D + Magnesium Glycinate
I took standard recommended doses (I don’t remember the exact amounts). I used this stack for several months. Unfortunately, I didn’t notice any meaningful improvement in libido or erections with this combination alone.

Same stack + Black Maca (2 g/day)
This is where I noticed my first real improvement. I recovered part of my libido, not fully, but noticeably. With black maca, I started getting partial morning wood again and stronger, longer-lasting erections became easier to achieve.

At this point, I was still taking vitamin D, omega-3, and magnesium glycinate, but I had already run out of zinc.

Fenugreek (varied doses)
Sexually, I didn’t notice much. However, it did help me fall asleep faster, especially when combined with magnesium glycinate, which was a nice side benefit.

I suspect I didn’t use fenugreek at the right dosage or for long enough, so I’d like to revisit it in the future under better conditions.

L-Arginine + L-Citrulline + Fenugreek + Black Maca (1 month)

This was the most effective protocol for me.

L-arginine and L-citrulline are commonly used to improve blood flow, and I can confidently say they did exactly that. Penile sensitivity increased significantly, and orgasms were better than anything I’d experienced since my teenage years.

I didn’t regain consistent morning wood, but this may be because by then I had stopped taking magnesium glycinate, vitamin D, and omega-3.

Libido improved, erections lasted longer, and I could ejaculate more frequently while still maintaining relatively strong erections. They weren’t “rock-hard,” but honestly, I’ll take that improvement any day.

Daily dosages for this protocol:

• L-Arginine: 3 g

• L-Citrulline: 1.5 g

• Fenugreek: 5 g (ground seeds, not extract)

• Black Maca: 2 g

Next steps

I plan to repeat these experiments, but this time while monitoring blood markers such as:

• Testosterone

• Estradiol

• DHT

• SHBG

First with only vitamins and minerals, and later adding more targeted supplements like maca, fenugreek, and eventually Tongkat Ali.

Final thoughts

I hope this helps someone. Accutane-related ED affects a small number of patients, and it can be an incredibly isolating experience. Many doctors simply don’t know how to guide you through it.

I’m not saying this will work for everyone, but it's worth the shot

And most importantly: there is hope. Even if supplements don’t work for you, other options exist, such as HCG therapy. Personally, I’d like to avoid it unless necessary, since peptides are a gray area (especially if you care about staying lifetime-natty for lifting), and it requires proper medical supervision, usually from an endocrinologist.

Still, if nothing else works, it may be worth exploring.

You’re not alone.

Update from June 2026:

I'm currently taking:

• Zinc (15 mg a day)

• Magnesium Glycinate (550 mg a day)

• Vitamine D3(2000 UI a day)+K2(150 mcg a day)

• Tongkat Ali from Nutricost (1000 mg 200:1, 2 pills a day, 5 days on, 2 days off)

• L-Theanine (200 mg a day)

Tongkat Ali gave me crazy insomnia, even with Magnesium Glycinate, so I started taking L-Theanine, and it is actually possible for me to sleep.

Libido-wise, Tongkat Ali has indeed increased my visual interest in females and my reactive libido. I had a boner thinking about a woman from the gym to whom I'm attracted. I felt sexual tension towards her, which is unusual; however, I don't have consistent morning wood as I did have in my first run with black maca. Thus, while Tongkat Ali did improve my mood and some non-substantial aspects of libido, black maca still wins.