Thanks for sharing this and your experience.
Having spoken to you many times I know you have worked hard on diet and exercise and all your supplements are safe ones - nothing too drastic.
Funnily enough I have been watching many of Dr Mark Gordon youtube discussions, a world leader in TBI and PTSD.
I am not pushing clomid but I know it is one of his protocols and I am sure I posted this recently.
He says that some people with TBI have practically no T and also states that PTSD sufferers have altered hormones.
You have obviously been doing some great research and i really appreciate that you have shared this with us.

You should add this to your sources:

"In the case of patients reported to the Norwegian Medicines Agency, single photon emission computed tomography (SPECT) of the brain was performed in 15 cases who reported lasting neurological symptoms. Altered brain function was seen in all cases involving altered or reduced frontal lobe blood flow. Ten of these patients were evaluated to have organic brain damage." - Source

Notice the distinction made there. it's not just brain alterations we see with Accutane. There are actual documented instances of brain damage.

I've said this before and I'll say it again: Accutane's effects are vast: It has been documented to mess with everything from testosterone, DHT, thyroid, hippocampus, orbitofrontal cortex, microbiome, etc.  Some of us are probably affected by different facets of the drug. But your angle is certainly worth exploring, given the available literature.

Interestingly, it appears alcoholism damages a similar part of the brain that Accutane can. And it does appear the brain will naturally improve with time, so for those of us with predominately psychiatric problems, there is hope.

"Results showed a positive relationship between perfusion levels in the left inferior frontal brain region and years of sobriety. Alcoholics with less than 4 years of sobriety had significantly reduced left inferior frontal perfusion, compared with both non-alcoholic controls and alcoholics having longer periods of sobriety. The findings support the hypothesis that frontal brain abnormalities in alcoholics may subside with extended abstinence." -Source

Like Accutane, alcoholism can cause reduced bloodflow in a frontal region of the brain. Recovery is slow, but it happens. With the proper nutritional and supplemental assistance, perhaps we can speed this up.

As @hatetane alluded to, I think the documented hormonal disturbances and the documented and brain damage/alterations from Accutane potentially go hand-in-hand. Speaking of hormones, Progesterone has recently gained traction as a hormone that can assist in treating traumatic brain injury:

"A large and rapidly growing body of preclinical studies suggested that PROG has neuroprotective properties in many brain injury models. The mechanism for PROG's neuroprotection clearly does not target a single aspect of the TBI cascade, instead it works through multiple mechanisms to enhance the repair of damage to nerve cells caused by CNS injury; for example, neurotrophic, anti-inflammatory, anti-excitotoxicity, anti-lipid peroxidation and anti-apoptotic properties and so on." - Source

Excellent post, by the way. It serves as a reminder that there is so much more to explore before committing to something drastic and costly like testosterone replacement therapy.

3 hours ago, Fchawk said:

The way Im treating myself is through the nutrition approach. It has been shown that creatine, fish oil, (unheated) extra virgin olive oil, vitamin d, zinc, magnesium, glutamine, taurine all also promote neuroplasticity.

Nice post. Thx for putting in the effort to post all this. Could you elaborate on the supplements and dosages you felt helped in your recovery?

5-reductase reduces progesterone
Some PFS guys suggest progesterone helps with there sides.

Google progesterone PFS example:
http://www.peaktestosterone.com/forum/index.php?topic=8051.0

23 hours ago, hatetane said:

 5±-reductase reduces progesterone
Some PFS guys suggest progesterone helps with there sides.

Google progesterone PFS example:
http://www.peaktestosterone.com/forum/index.php?topic=8051.0
 

 

 

this is another example in my opinion of Accutane giving us a problem(giving us brain trauma) while hurting our ability to deal with it (lowering the amounts of neuroprotective agents in our bodies)
 

Are y'all really going along withrandom band aid bullshit. Why don't we actually make people aware of this by all killing ourselves together in the same place at once, Jim Jones style. Since we're permaneantly fucked and the surrounding planet is fucked it would be the best way out. If we made media attention, think of all the lives we would spare from the soul consumers. Hopefully somehow we could get the stuff banned (though is might be kinda hard for a few years in the US with brain dead Nazis running the country). This would truly be a noble thing to do, especially if we all did it in the middle of an iconic location like Times Square, or the DC lawn, and the Brits could kill themselves in maybe Trafalgar Square, or in front of Buckingham Palace.

All we need is to figure out a quick way, yet a way that will freak people out.

Thanks for derailing the topic and making it your own. Hey, I like your idea, why don't you start the process for us there, and we'll be sure to follow.

Is it noble for the group of people likely working harder than anyone else to alleviate the problems caused by accutane to band together, abandon their research and kill themselves in what would likely be a futile effort to get the drug removed from the market? Many people have already killed themselves after taking the drug, yet the drug remains. All that would likely do is cause immense suffering for those that love or care for us. It would be far nobler to spare those people from feeling the pain you're in now and to dedicate your LIFE.. not death, to campaigning to get the drug removed from the market, spreading information and working on helping yourself, so that you can in turn help others.

I'm truly sorry you're in so much pain, if a bandaid might end that pain (without hurting those who care for you), is it not worth trying? I understand it seems hopeless but posts such as Fchawks' detailing how he has made great headway overcoming his problems are proof that it is not. Please keep fighting for the happiness and life that you deserve, things can only get better.

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Thank you so much Fchawks for all the hard work and the great information that you have shared. I have suspected similar but have been unsure how to proceed, the direction provided is fantastic.

One supplement that I looked at which may promote neurogenesis is Lithium orotate. Although with all the options you've already provided an additional one is likely unnecessary, and also lithium is quite controversial. I'm not sure about linking other forums here but if anyone is interested there is good discussion on the supplement on the longecity forums.

Hatetane those videos were spot on, wow.

http://www.ehealthme.com/ds/accutane/post concussion syndrome/

Long Post, but highly recommend you read it all

What do we know about accutane? Well certainly the people that make it claim to know nothing. All they claim to know is that it causes birth defects, and it causes acne to go away. They also claim it causes no lasting side effects, which is obviously incorrect. However, that is because not everyone suffers the same side effects. The reason for this, is because it inhibits neurogenesis and causes hippocampal atrophy, which causes varying degrees of brain damage

http://www.ncbi.nlm.nih.gov/pubmed/25689814

"A 25-question survey was emailed to 7,013 dermatologists included in a proprietary database (MBD, Inc.) and anonymous responses were collected. 591 board-certified dermatologists participated. Thirty-seven percent of the responding dermatologists believe that isotretinoin may cause psychiatric disturbances. Dermatologists' opinions on this relationship did not significantly impact prescription practices in patients with history of depression (P=0.056) or in patients being treated with an antidepressant (P=0.118)."

http://www.ncbi.nlm.nih.gov/pubmed/15863802
 

sotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression. 
Conclusion: This study suggests that isotretinoin treatment is associated with changes in brain functioning."

œA 4-month treatment trial with isotretinoin was associated with a decrease in brain functioning in the orbito-frontal cortex, a brain region implicated in depression.

http://www.ncbi.nlm.nih.gov/pubmed/15251924

œWe now show, in a mouse model, that endogenous RA generated by synthetic enzymes in the meninges acts on hippocampal granule neurons, and chronic (3-week) exposure to a clinical dose of 13-cis RA may result in hippocampal cell loss.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC387382/

"This report demonstrates that a clinical dose (1 mg/kg/day) of 13-cis-RA in mice significantly reduces cell proliferation in the hippocampus and the subventricular zone, suppresses hippocampal neurogenesis, and severely disrupts capacity to learn a spatial radial maze task. The results demonstrate that the regions of the adult brain where cell proliferation is ongoing are highly sensitive to disruption by a clinical dose of 13-cis-RA."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276716/#R173

"Increased concentrations of homocysteine have also been associated with attacks of violent anger. Isotretinoin administration to human subjects was shown to be associated with increased concentrations of homocysteine, as well as decreases in 5-methyl-tetrahydrofolate, providing a potential metabolic mechanism by which isotretinoin may promote depression."

"In the case of patients reported to the Norwegian Medicines Agency, single photon emission computed tomography (SPECT) of the brain was performed in 15 cases who reported lasting neurological symptoms. Altered brain function was seen in all cases involving altered or reduced frontal lobe blood flow. Ten of these patients were evaluated to have organic brain damage."

https://www.ncbi.nlm.nih.gov/pubmed/20708044

"13-Cis-retinoic acid (13-cis-RA) causes depression-related behavior in mice. Hypothalamic dysregulation has been implicated in clinical depression. In fact, apoptosis of hypothalamic neurons may lead to depression after myocardial infarction. . . .We hypothesize that the ability of 13-cis-RA to decrease hypothalamic cell number may contribute to the increased depression-related behaviors observed in mice."

Now that we have established that Accutane causes hippocampal atrophy and varying degrees of brain damahe, what are the consequences?

Traumatic brain injury: a disease process, not an event.

https://www.ncbi.nlm.nih.gov/m/pubmed/20504161/

œTraumatic brain injury (TBI) is seen by the insurance industry and many health care providers as an "event." Once treated and provided with a brief period of rehabilitation, the perception exists that patients with a TBI require little further treatment and face no lasting effects on the central nervous system or other organ systems. In fact, TBI is a chronic disease process, one that fits the World Health Organization definition as having one or more of the following characteristics The purpose of this article is to encourage the classification of TBI as the beginning of an ongoing, perhaps lifelong process, that impacts multiple organ systems and may be disease causative and accelerative. Our intent is not to discourage patients with TBI or their families and caregivers, but rather to emphasize that TBI should be managed as a chronic disease and defined as such by health care and insurance providers. Furthermore, if the chronic nature of TBI is recognized by government and private funding agencies, research can be directed at discovering therapies that may interrupt the disease processes months or even years after the initiating event.

Currently there is no acknowledgement of this from anywhere, which is why mental illness is becoming an epidemic. In a few decades though I think this will become mainstream knowledge

https://www.ncbi.nlm.nih.gov/pubmed/16425236

œThe hippocampus is one of several limbic brain structures implicated in the pathophysiology and treatment of mood disorders. Preclinical and clinical studies demonstrate that stress and depression lead to reductions of the total volume of this structure and atrophy and loss of neurons in the adult hippocampus. One of the cellular mechanisms that could account for alterations of hippocampal structure as well as function is the regulation of adult neurogenesis. Stress exerts a profound effect on neurogenesis, leading to a rapid and prolonged decrease in the rate of cell proliferation in the adult hippocampus. In contrast, chronic antidepressant treatment up-regulates hippocampal neurogenesis, and could thereby block or reverse the atrophy and damage caused by stress. Recent studies also demonstrate that neurogenesis is required for the actions of antidepressants in behavioral models of depression. This review discusses the literature that has lead to a neurogenic hypothesis of depression and antidepressant action, as well as the molecular and cellular mechanisms that underlie the regulation of adult neurogenesis by stress and antidepressant treatment.

In this we see that accutane, in many ways, affects us like a chronic bout of stress. It is also why people who use antidepressants feel better, and why you often find people recommending SSRIs to treat accutane™s sides. That is because they DO help.

Now we established that hippocampal atrophy may be the cause of many of our symptoms, and that the way antidepressants work is by stimulating neurogenesis, here is how you can improve your recovery naturally, though if you wish to use antidepressants as well that fine as well

Nutritional treatment for acute and chronic traumatic brain injury patients.

https://www.ncbi.nlm.nih.gov/m/pubmed/24844176/?i=6&from=/24605947/related

"omega 3 fats, vitamin D, N-Acetylcysteine, branched chain amino acids, zinc, alpha-lipoic acid, magnesium, taurine, coenzyme Q10, and many phytonutrients may be helpful in the recovery from a a TBI"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705194/

Mindfulness Meditation can stimulate hippocampal brain cell growth. A smaller hippocampus is correlated with a poorer recovery from TBIs, in the case of war veterans suffering PTSD at least.

http://www.ncbi.nlm.nih.gov/m/pubmed/11079535/

Study supporting Creatine consumption as one of the top supplements for recovering from a TBI, and the one below supports Taurine use as well.

http://www.ncbi.nlm.nih.gov/m/pubmed/27156064/

Long-term effects of a ketogenic diet in obese patients

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716748/

"Beneficial changes in the brain energy profile have been observed in subjects who are on a ketogenic diet (28). This is a significant observation because cerebral hypometabolism is a characteristic feature of those who suffer from depression or mania"

Currently I  doing:

Creatine - increases Dihydrotestosterone (DHT) and testosterone. Increases muscle power and ALSO improves neuroplasticity

Fish Oil - improves joint pain, helps heart disease, and ALSO improves neuroplasticity

Zinc - increases levels of male hormones and ALSO improves neuroplasticity

Magnesium - helps with chronic pain, fatigue and insomnia and ALSO neuroplasticity

Vitamin D: Improves bone health, physical fitness, and ALSO improves neuroplasticity
CoQ10: Improves cardiovascular fitness and heart health, and ALSO improves neuroplasticity

Multivitamin - makes me less likely to be malnourished.

I try to do meditation regularly, but I don't prioritise it enough... Though it helps with anxiety and stress, as well as neuroplasticity, and i plan to add it into my daily routine.  

I feel much better than I have in years. I think for the last two months I have woken with morning wood 95% of the time, social anxiety is limited, confidence in my abilities in much higher, and motivation to reach my goals, and also willingness to do the work to reach them, is also one of the main things I have noticed. Before I did the work still expecting to fail, while now I do the work and I expect success, which makes me actually enjoy the work, and that™s just one example. My life and my future doesn™t seem so hopeless, there is plenty to celebrate and I™m sure plenty I will celebrate in the future

Things I plan to do:

Ketogenic Diet: Improves body composition, can help ED, and ALSO improves neuroplasticity

I try to do meditation regularly, but I don't prioritise it enough... Though it helps with anxiety and stress, as well as neuroplasticity, and i plan to add it into my daily routine.  

Things that might help, but are on the riskier side and I am unlikely to attempt myself, but possibly would help

Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121947/

The regulation of adult rodent hippocampal neurogenesis by deep brain stimulation.

https://www.ncbi.nlm.nih.gov/pubmed/18173322

œHigh-frequency stimulation of the AN increases the hippocampal neurogenesis and restores experimentally suppressed neurogenesis. Interventions that increase hippocampal neurogenesis have been associated with enhanced behavioral performance. In this context, it may be possible to use electrical stimulation to treat conditions associated with impairment of hippocampal function.

Stimulation of entorhinal cortex promotes adult neurogenesis and facilitates spatial memory.

https://www.ncbi.nlm.nih.gov/pubmed/21940440

œDeep brain stimulation (DBS) is an established therapeutic modality for the treatment of movement disorders and an emerging therapeutic approach for the treatment of disorders of mood and thought. For example, recently we have shown that DBS of the fornix may ameliorate cognitive decline associated with dementia. However, like other applications of DBS, the mechanisms mediating these clinical effects are unknown. As DBS modulates neurophysiological activity in targeted brain regions, DBS might influence cognitive function via activity-dependent regulation of hippocampal neurogenesis. Using stimulation parameters analogous to clinical high-frequency DBS, here we addressed this question in mice. We found that acute stimulation of the entorhinal cortex (EC) transiently promoted proliferation in the dentate gyrus (DG). Cells generated as a consequence of stimulation differentiated into neurons, survived for at least several weeks, and acquired normal dentate granule cell (DGC) morphology. Importantly, stimulation-induced promotion of neurogenesis was limited to the DG and not associated with changes in apoptotic cell death. Using immunohistochemical approaches, we found that, once sufficiently mature, these stimulation-induced neurons integrated into hippocampal circuits supporting water-maze memory. Finally, formation of water-maze memory was facilitated 6 weeks (but not 1 week) after bilateral stimulation of the EC. The delay-dependent nature of these effects matches the maturation-dependent integration of adult-generated DGCs into dentate circuits supporting water-maze memory. Furthermore, because the beneficial effects of EC stimulation were prevented by blocking neurogenesis, this suggests a causal relationship between stimulation-induced promotion of adult neurogenesis and enhanced spatial memory.

Nootropic agents stimulate neurogenesis.

https://www.ncbi.nlm.nih.gov/pubmed/19441945

Electrical Stimulation Elicits Neural Stem Cells Activation: New Perspectives in CNS Repair

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4610200/

Acupuncture stimulation induces neurogenesis in adult brain.

https://www.ncbi.nlm.nih.gov/pubmed/24215918

Hippocampal Neurogenesis and Antidepressive Therapy: Shocking Relations

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4055571/
"A strong enhancement of neurogenesis has been observed in various species following experimental ECS treatments [20, 21]. Several studies indicated a close relation between hippocampal function and mood regulation. The observation of an antidepressive-like effect and an upregulation of hippocampal cell proliferation upon experimental ECS raised speculations on the participation of neurogenesis in the antidepressive mode of action. However, evidence for a direct participation of neurogenesis in antidepressive mechanisms still remains to be convincingly demonstrated [17].

Systematic review of effect of coenzyme Q10 in physical exercise, hypertension and heart failure.

https://www.ncbi.nlm.nih.gov/pubmed/14695924

COENZYME Q10 IN PHYSICAL EXERCISE. We identified eleven studies in which CoQ10 was tested for an effect on exercise capacity, six showed a modest improvement in exercise capacity with CoQ10 supplementation but five showed no effect. CoQ10 IN HYPERTENSION. We identified eight published trials of CoQ10 in hypertension. Altogether in the eight studies the mean decrease in systolic blood pressure was 16 mm Hg and in diastolic blood pressure, 10 mm Hg. Being devoid of significant side effects CoQ10 may have a role as an adjunct or alternative to conventional agents in the treatment of hypertension. CoQ10 IN HEART FAILURE. We performed a randomised double blind placebo-controlled pilot trial of CoQ10 therapy in 35 patients with heart failure. Over 3 months, in the CoQ10 patients but not in the placebo patients there were significant improvements in symptom class and a trend towards improvements in exercise time.

Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819093/

œIn animals, exposure to severe stress can damage the hippocampus. Recent human studies show smaller hippocampal volume in individuals with the stress-related psychiatric condition posttraumatic stress disorder (PTSD). Does this represent the neurotoxic effect of trauma, or is smaller hippocampal volume a pre-existing condition that renders the brain more vulnerable to the development of pathological stress responses? In monozygotic twins discordant for trauma exposure, we found evidence that smaller hippocampi indeed constitute a risk factor for the development of stress-related psychopathology. Disorder severity in PTSD patients who were exposed to trauma was negatively correlated with the hippocampal volume of both the patients and the patients™ trauma-unexposed identical co-twin. Furthermore, severe PTSD twin pairs”both the trauma-exposed and unexposed members”had significantly smaller hippocampi than non-PTSD pairs.

here is another interesting study about recovering from a TBI, it's basically like the worse the patient thinks his recovery will be, the worse it will be

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077969/

The reason for this may be the worse the TBI is, the less likely the patient is optimistic about his recovery, or the worse his mental state before the injury happened the worse his recovery will be, rather than being optimistic improves outcomes

This is pretty much all the information needed for taking this approach to curing Post-Accutane Syndrome in one place. Obviously I would have missed things, and thats why I want everyone to discuss and suggest things that I have missed, and while I am certain that this will wipe away many of the sides, there are other mechanisms in which accutane acted, and while this counters one way it wrecked havoc in our lives, any ideas of the things we may do to address its other issues will always be appreciated

Love you all, don™t give up, we will continue getting better together!

Great post Fchawk - its comprehensive and rings very true to someone like me who's 20 years post tane.

Following this forum can be both encouraging and very frustrating. You discuss TBI and follow up with both diet and supplements, how do we stay on track though before someone says you've just got a Thyroid problem or Testosterone issue - both of these get raised very often on forum, these could be just symptomatic though of the bigger issue of TBI correct??
Even gut health could be altered by TBI correct?

In terms of antidepressants have you tried:

Tianeptine
5-HTP

I'm looking at the more natural ones, I've tried Sam e, St johns wort both of which work quiet well but I'm wondering if there's something more beneficial for us tane victims?? ( natural )

Also have you tried Hyperbaric Oxygen Therapy? - this field sounds very promising!!

Yeah, often TBIs can have a range of different effects, and thats why while I don't get half the symptoms that are displayed on this forum, I still did get more than I cared for.
https://www.ncbi.nlm.nih.gov/pubmed/20504161
"TBIs increases long-term mortality and reduces life expectancy. It is associated with increased incidences of seizures, sleep disorders, neurodegenerative diseases, neuroendocrine dysregulation, and psychiatric diseases, as well as non-neurological disorders such as sexual dysfunction, bladder and bowel incontinence, and systemic metabolic dysregulation that may arise and/or persist for months to years post-injury."
So yeah, symptoms of a TBIs can encompass pretty much anything, but while I cant promise it will fix everything, but it should still fix a lot and improve Quality of Life, with no potential of downside. Also many of the things which people have improved by having can be traced to them promoting neurogenesis, even if they didnt know it at the time

No, I have not tried Hyperbaric Oxygen Therapy, but I agree it seems very promising

"Hyperbaric oxygen induces late neuroplasticity in post stroke patients--randomized, prospective trial."
https://www.ncbi.nlm.nih.gov/pubmed/23335971

"The results indicate that HBOT can lead to significant neurological improvements in post stroke patients even at chronic late stages. The observed clinical improvements imply that neuroplasticity can still be activated long after damage onset in regions where there is a brain SPECT/CT (anatomy/physiology) mismatch."
Hyperbaric oxygen Therapy seems to be very good forpromoting neuroplasticity/neurogenesis

I also haven't tried antidepressants, andIdon'tthink I will everneed to,butthatdoesn't. The way they work against depression is that they seem to promote neurogenesis, in the increase in hippocampal volume directly relates to the improvement in symptoms
https://www.ncbi.nlm.nih.gov/pubmed/16425236

Neurobiological and clinical effects of the antidepressant tianeptine.
https://www.ncbi.nlm.nih.gov/pubmed/18072812
"The precise neurobiological processes involved in depression are not clear, but it is recognized that numerous factors are involved, including changes in neurotransmitter systems and brain plasticity. Neuroplasticity refers to the ability of the brain to adapt functionally and structurally to stimuli. Impairment of neuroplasticity in the hippocampus, amygdala and cortex is hypothesized to be the mechanism by which cognitive function, learning, memory and emotions are altered in depression. The mechanisms underlying alterations in neuroplasticity are believed to relate to changes in neurotransmitters, hormones and growth factors. Structural changes in the hippocampus that have been proposed to be associated with depression include dendritic atrophy, reduced levels of cerebral metabolites, decreased adult neurogenesis (generation of new nerve cells) and reduced volume. Increased dendritic branching occurs in the basolateral nucleus of the amygdala. Reduced neuronal size and glial cell density occur in the prefrontal cortex. Clinically, tianeptine is an antidepressant effective in reducing symptoms of depression in mild to moderate-to-severe major depression, including over the long term. Tianeptine is also effective in alleviating the symptoms of depression-associated anxiety. It is generally well tolerated, with little sedation or cognitive impairment. The efficacy profile of tianeptine could be explained by its neurobiological properties observed in animal models. Tianeptine prevents or reverses stress-associated structural and cellular changes in the brain and normalizes disrupted glutamatergic neurotransmission. In particular, in the hippocampus, it prevents stress-induced dendritic atrophy, improves neurogenesis, reduces apoptosis and normalizes metabolite levels and hippocampal volume. Tianeptine also has beneficial effects in the amygdala and cortex and can reverse the effects of stress on neuronal and synaptic functioning. The neurobiological properties of tianeptine may provide an explanation not only for its antidepressant activity, but also for its anxiolytic effects in depressed patients and its lack of adverse effects on cognitive function and memory."

Neuropharmacologic treatment of bronchial asthma with the antidepressant tianeptine: a double-blind, crossover placebo-controlled study.
https://www.ncbi.nlm.nih.gov/pubmed/9728903
Treatment of bronchial asthma with tianeptine.
https://www.ncbi.nlm.nih.gov/pubmed/15632955

I hadnt heard of Tianeptine before, but seems very interesting Not only does it promote neurogenesis, but it can also aid in asthma, which is something that Ive had to deal with since I had accutane and notice a lot because it flares up so often whenever I try to play sport(and I try to play a lot of sport), and it also helps with IBS I know I said I wasnt really interested in antidepressants, but that in particular shows a lot of potential

Also I would say that everything that I listed before in my post to promote neuroplasticity, is a natural antidepressant.

http://www.medicationsense.com/articles/jan_dec_08/toxicity070508.php

NAC precursor to glutathione - lends weight to your theory Fchawk

http://vitalitymagazine.com/article/healing-brain-injuries-naturally/

Look Fchawk, you are not the only one who suspects TBI. PFS guys considering it too.
[removed]

We need someadvice on a good but basic start off protocol.

If a guy on the propecia forum mentions a cure the rest of the guys are all over it wanting every single detail and embarking on the protocol himself.
Accutane - not so much!

https://www.sciencedaily.com/releases/2007/11/071129121127.htm

As suspected - drug induced TBI

If anyone has time can they research drug induced TBI and see what you can come up with.

https://raypeatforum.com/community/threads/thoughts-on-5ar-and-post-finasteride-syndrome.16194/

Fchawk - more and more people talking about the brain connection.

Hello ladies and gentlemen,

It was only yesterday that I made the connection between ten years of sexual dysfunction and taking accutane. I was prescribed accutane at 14 years old for my moderate acne. It cleared up my skin but stole my sex drive. I can honestly say, I no longer have a libido or sexual desire, and I can only link this to accutane use as I have never been on other prescription meds and had normal sex drive prior to usage. Otherwise I am a healthy, athletic male, who has experimented with high levels of testosterone as well as other drugs but to no avail. My sex drive remains at zero. Words cannot express the regret and deep sadness I feel, when I reflect on the fact that I may have potentially lost one of the most important things in life which will and probably has affected countless relationships, my personality, my susceptibility to depression and the fun/excitement I have missed out on, in exchange for an acne-free face. This is beyond words. There is no justice here, and I doubt there is going to be a happy end to this story.

I have seen many people proposing reasons as to why accutane affects libido. I have a theory which I have not seen anyone put forward yet. However it seems to account for a lot of the reasons changing hormonal levels etc. has had little effect on libido. To look at the effect of a drug on sex drive we must ultimately look at the brain, as this is the place all libido and sexual desire is derived from. Hormones alone dont give you, your libido, hormones stimulate neuronal activity in specific areas of the brain, it is this activity which gives you a libido.

Bremner et al, is one of the only studies which looked into functional brain imaging of patients treated with accutane (Isotretinoin) (1).This study revealed that Isotretinoin specifically altered the activity and metabolism of a brain region called the orbitofrontal cortex in those who took Isotretinoin versus controls. Unfortunately, brain images were not taken after treatment was discontinued, so we cannot say whether these effects were reversed once treatment was removed or whether they persisted. I have contacted an author of the study for more information. Given the possibility that Isotretinoin can cause epigenetic changes, it is possible that these changes are maintained after treatment.

Now, interestingly one of the only studies which has been conducted on brain activity in hypoactive sexual desire disorder in males, which is essentially sexual dysfunction. Showed that, the major difference in response to sexual stimuli, in males with sexual dysfunction and normal males was a difference in the activity of the orbitofrontal cortex (2). As such, it appears the orbitofrontal cortex plays a key role in sexual desire, and it appears that Isotretinoin specifically alters activity of this brain region.

Given this, it seems highly plausible to me that this could be the culprit we have been looking for. However what is really needed now, is to see whether those changes in the orbitofrontal cortex remained after treatment had been stopped. As it is also quite possible that these changes were only temporary. If these changes in orbitofrontal activity/metabolism were reversed after a period of stopping treatment, then my theory is incorrect.

Unfortunately, this puts us fellow sufferers in a slight predicament. The orbitofrontal cortex is not a very well studied part of the brain. If it has been changed in a fundamental way, possible treatments will be difficult to come by. This will sound extreme, but I can only propose deep brain stimulation as a viable and potential treatment. This is a medical technology which is progressing at a rapid rate. It has recently been used for Anorexia, and so I can see someone easily making the case to use this for a debilitating issue such as sexual dysfunction. Interestingly, a deep brain stimulation protocol for the orbitofrontal cortex has already been developed by Scientists out of Oxford University. One was implanted into a woman with low sex drive, which markedly improved her sex drive. According to this article (3). However I cannot actually find the original paper, in which the woman had the device implanted. If someone could post it, that would be great.

I am sorry this is such a long post, but I wanted it to be conclusive and offer some hope, in a seemingly hopeless situation. I can only ask that we all investigate this further, but what is more important, is that we email and message researchers and neurosurgeons raising the topic of brain imaging studies and deep brain stimulation for sexual dysfunction. If we remain on forums and message boards, nothing will be done. Nobody will bother researching conditions which they dont know exist or see no clinical benefit in treating.

Sexual dysfunction in many ways is a far greater and more debilitating ailment than anorexia or many illnesses. It strikes us in a very personal way, and in a way that most people would never be able to appreciate or understand. Additionally, this may also be the mechanism by which other drugs such as Finasteride work.

Feel free to message me, also send over email address with your symptoms /info. We need to start to amass patient with these problems if we are to have any kind of case or chance of making this a legitimate topic of research/concern.

Also if anyone has had any success with Bremelanotide / PT-141, please let me know.

My email is [removed]

I tried to make a group, as I feel we need something more concrete than forums. Please make better suggestions. - [removed]

Much Love,

Nine livez

(1) - http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.162.5.983

(2) - https://www.ncbi.nlm.nih.gov/labs/articles/14561426/

(3) - [removed]

On 5/18/2017 at 8:25 AM, baptistegia said:

@Fchawk @ACCUiTy_drANE I've read through half of the accutane repair thread but wanted to ask you guys 2 questions since you guys seem the most knowledgable.

1. should accutane victims supplement with additional vitamin A (retinyl palmitate) when recovering? I've read mixed reviews on the accutane repair thread and can't seem to find an answer. I personally feel really good for about a week when supplementing vitamin a then crash....
2. in your opinion what supplements/drug/etc have made a difference to recovery?

Thank you guys so very much!

I tried megadosing vitamin A, I wouldn't recommend anyone else trying it. That said 5000IU can't hurt, I was taking much more than that, I think it was around 100,000IU/day for a few weeks. It was because I thought it would "reboot" vitamin A regulation, because I thought any problems I might be having may be due to poor vitamin a regulation. But I actually think the negative sides are due to changes in brain metabolism brought on by accutane, and megadosing vitamin A didnt help that. Maybe a little would have been good, but having years worth in a month was excessive.

Today I'm healthy and hearty, but not thanks to vitamin A

Creatine - increases Dihydrotestosterone (DHT) and testosterone. Increases muscle power and improves neuroplasticty
Fish Oil - improves joint pain, helps heart disease, and improves neuroplasticity 
Zinc - increases levels of male hormones and improves neuroplasticity
Magnesium - helps with chronic pain, fatigue and insomnia and improves neuroplasticty 
Multivitamin - makes me less likely to be malnourished  
Vitamin D & K

On 4/27/2017 at 12:43 AM, nine_lives said:

Hello ladies and gentlemen,

It was only yesterday that I made the connection between ten years of sexual dysfunction and taking accutane. I was prescribed accutane at 14 years old for my moderate acne. It cleared up my skin but stole my sex drive. I can honestly say, I no longer have a libido or sexual desire, and I can only link this to accutane use as I have never been on other prescription meds and had normal sex drive prior to usage. Otherwise I am a healthy, athletic male, who has experimented with high levels of testosterone as well as other drugs but to no avail. My sex drive remains at zero. Words cannot express the regret and deep sadness I feel, when I reflect on the fact that I may have potentially lost one of the most important things in life which will and probably has affected countless relationships, my personality, my susceptibility to depression and the fun/excitement I have missed out on, in exchange for an acne-free face. This is beyond words. There is no justice here, and I doubt there is going to be a happy end to this story.

I have seen many people proposing reasons as to why accutane affects libido. I have a theory which I have not seen anyone put forward yet. However it seems to account for a lot of the reasons changing hormonal levels etc. has had little effect on libido. To look at the effect of a drug on sex drive we must ultimately look at the brain, as this is the place all libido and sexual desire is derived from. Hormones alone don™t give you, your libido, hormones stimulate neuronal activity in specific areas of the brain, it is this activity which gives you a libido.

Bremner et al, is one of the only studies which looked into functional brain imaging of patients treated with accutane (Isotretinoin) (1).This study revealed that Isotretinoin specifically altered the activity and metabolism of a brain region called the orbitofrontal cortex in those who took Isotretinoin versus controls. Unfortunately, brain images were not taken after treatment was discontinued, so we cannot say whether these effects were reversed once treatment was removed or whether they persisted. I have contacted an author of the study for more information. Given the possibility that Isotretinoin can cause epigenetic changes, it is possible that these changes are maintained after treatment.

Now, interestingly one of the only studies which has been conducted on brain activity in hypoactive sexual desire disorder in males, which is essentially sexual dysfunction. Showed that, the major difference in response to sexual stimuli, in males with sexual dysfunction and normal males was a difference in the activity of the orbitofrontal cortex (2). As such, it appears the orbitofrontal cortex plays a key role in sexual desire, and it appears that Isotretinoin specifically alters activity of this brain region.

Given this, it seems highly plausible to me that this could be the culprit we have been looking for. However what is really needed now, is to see whether those changes in the orbitofrontal cortex remained after treatment had been stopped. As it is also quite possible that these changes were only temporary. If these changes in orbitofrontal activity/metabolism were reversed after a period of stopping treatment, then my theory is incorrect.

Unfortunately, this puts us fellow sufferers in a slight predicament. The orbitofrontal cortex is not a very well studied part of the brain. If it has been changed in a fundamental way, possible treatments will be difficult to come by. This will sound extreme, but I can only propose deep brain stimulation as a viable and potential treatment. This is a medical technology which is progressing at a rapid rate. It has recently been used for Anorexia, and so I can see someone easily making the case to use this for a debilitating issue such as sexual dysfunction. Interestingly, a deep brain stimulation protocol for the orbitofrontal cortex has already been developed by Scientists out of Oxford University. One was implanted into a woman with low sex drive, which markedly improved her sex drive. According to this article (3). However I cannot actually find the original paper, in which the woman had the device implanted. If someone could post it, that would be great.

I am sorry this is such a long post, but I wanted it to be conclusive and offer some hope, in a seemingly hopeless situation. I can only ask that we all investigate this further, but what is more important, is that we email and message researchers and neurosurgeons raising the topic of brain imaging studies and deep brain stimulation for sexual dysfunction. If we remain on forums and message boards, nothing will be done. Nobody will bother researching conditions which they don™t know exist or see no clinical benefit in treating.

Sexual dysfunction in many ways is a far greater and more debilitating ailment than anorexia or many illnesses. It strikes us in a very personal way, and in a way that most people would never be able to appreciate or understand. Additionally, this may also be the mechanism by which other drugs such as Finasteride work.

Feel free to message me, also send over email address with your symptoms /info. We need to start to amass patient with these problems if we are to have any kind of case or chance of making this a legitimate topic of research/concern.

Also if anyone has had any success with Bremelanotide /  PT-141, please let me know.

My email is [removed]

I tried to make a group, as I feel we need something more concrete than forums. Please make better suggestions. - [removed]

Much Love,

Nine livez

 

(1) - http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.162.5.983

(2) - https://www.ncbi.nlm.nih.gov/labs/articles/14561426/

(3) - [removed]

Sorry for the late reply, I totally agree with the diagnosis, but not the treatment. Not saying the treatment wouldn't work, but for many people its not feasible, especially seeing we can not get an offical "diagnosis" anyway, much less validate the fact that accutane causes changes in the brains metabolism(even though its a scientifically proven fact) 

Personally I think the natural ways of promoting neurogensis through diet/supplements and meditation can do just as much as much as stimulation can. These are also scientifically proven, but yet much more accessible. If it is within you means to do the brain stmulation, then by all means go ahead, but if you are going to such great lengths you may as well do the other things as well  

@FchawkHow r u now? Almost completely cured?

I'm having a nightmare with my mild acne at the moment. I'm 30 years old and suffer from mild/persistent acne. I've had quite a ride with this drug, and to be honest I'm having my doubts with it. I first started on 20mg ( 1 tablet ) then 40mg, but wasn't effective. So to get results I had to go to 60mg for 3 months and got great results. After my dermatologist and myself were happy with the results, he decided to bring me down to 2 tablets a day. My acne broke out badly roughly in about a month. So I had to go back and go on 60mg a day again. It's been nearly 5 months now and still, it persists in taunting me. But what I can't work out is why it's being harder to get rid of compared to the last lot of 60mg of 3 months from last time. I don't know what to do anymore. Am I wasting my time or should I stick it out for a bit longer with this medication? I have the usual side effect that everyone knows and loves, but nothing I can't handle. At this stage, i can't even get the acne to leave, let alone moving onto the next stage of what if scenariosof having lingering effects of the drug.

Hi Everyone,

Excellent knowledge in this thread. Great to see such collaborative effort. I'm also doing some work with a survey at the moment in case you haven't seen. I would appreciate it if you checked it out.

Thanks,

MT

On 7/21/2017 at 1:41 AM, Sprinterguy98 said:

@FchawkHow r u now? Almost completely cured?

Yeah, I would say so. Feel pretty much 100%, but I think the routine* I am following is very healthy in general, and I make sure not do overdo it, because more isn't always better.

*routine
Creatine - increases Dihydrotestosterone (DHT) and testosterone. Increases muscle power and improves neuroplasticity
Fish Oil - improves joint pain, helps heart disease, and improves neuroplasticity
Zinc - increases levels of male hormones and improves neuroplasticity
Magnesium - helps with chronic pain, fatigue and insomnia and neuroplasticity
Vitamin D: Improves bone health, physical fitness, and improves neuroplasticity
CoQ10: Improves cardiovascular fitness and heart health, and improves neuroplasticity
Multivitamin - makes me less likely to be malnourished.
I try to do meditation regularly, it helps with anxiety and stress, as well as neuroplasticity, and i do it a few times a week

Been doing it for several months now, and I am certain I have improved from the start to now!

EDIT: I was probably the best I'd been since I was 16, probably more like 95%. Since last year some shit happened (unrelated to accutane) and I defs lost some momentum, but that was more mental than physical. Physically I've probably improved, while mentally I got depression/anxiety, but that was probably due to the situation and now I am in a better place