EDIT:*I've recently talked to others who's post accutane syndrome makes mine pale in comparison. For me, it was completely life changing, I thought about ending it, but I could still live. Before recovery, I could still live a life, if I lowered my expectations low enough, dropping out of Uni and accepting I would never have a sexual relationship, and that I would never be particularly happy or successful, while post recovery, I I think I can now achieve a good life, going to Uni and dating, etc. However, for others, it affects them a lot harsher than it did me, and so for promising a cure, I feel like a fraud. I'm going to leave it up, because I know it can still help SOME people regain control of their life, but for plenty of people, who accutane his much harder than myself, it may not bring much respite, and so I apologise for any whom I gave false hope
Everythingis in the google document, I've expanded it below. I think I am 90% cured, no longer get anxious or brainfog, sexually I'm about 50%, but an optimistic for continued improvement, and though things like joint health and injuries obviously didn't heal, but I have done a lot of PT and my body responds positively to it, though they aren't as good as pre-accutane.
Anyway, I'm gonna leave this here and get on with my life. For brain fog, I strongly recommend meditation, I feel my focus is stronger then its ever been, though the supplements will help with that as well. I didn'trecommend meditation that strongly below, because I hadn't started it yet and didn't realise how beneficial it was. And with that said,hopewhatI'vewrittenbelowhelpsyouand au revoir!
https://docs.google.com/document/d/1gGkP_NQ8tmYkOADlG2VuEX17YvQJKgnfcEtgy5_6y7c/edit#
Curing PRSD
Hey, I am a 22 year old who suffered from Accutanes side effects since I was 16, andthough for me while sexual dysfunction was the side effect that made me notice accutane had affected me, it was not the only side effect. The route to curing my own side effects was by using nutrition and supplements, to undo the damage accutane did to my brain. Personally I believe Accutane causes its negative side effects by changing brain metabolism and causing a degree of brain damage. The brain damage is not caused by outright irreparable cell death, because the main place where cell death occurs is in the hippocampus, where neurogenesis can occur anyway and most of the damage can be reversed. The problem is that accutane also inhibits neurogenesis, so for some people, they suffer this brain damage quite severely, while others get back on their feet pretty quickly and dont even regret taking it.
Now as a disclaimer, I only took accutane for 9 weeks at 2x40mg per day, which was enough to give me no feeling in my penis for 2 months, and several years of not being aroused and not being attracted to any person irl at all, though with porn I could masterbate, though I was very insecure if I would actually be able to perform under pressure, and avoided any situation where anything might happen. I developed social anxiety, I lost my passion for all my subjects, competitiveness for sport and academics, couldnt concentrate or focus, and lost most hope and ambition for my future. I wasnt completely antisocial, and still had a few friends, male and female, but only because my brain wouldnt really care if it was female and if there was zero chance of being aroused, there was zero chance of being anxious as well
Accutane
What do we know about accutane? Well certainly the people that make it claim to know so little it is scary. All they claim to know is that it causes birth defects, and it somehow causes acne to go away. They also claim it causes no lasting side effects, except the magical disappearance of acne. However, that is because not everyone suffers the same side effects, though the loss of acne is the most common one. The reason for this, is because it inhibits neurogenesis and causes hippocampal atrophy(brain cell death), which results in varying degrees of brain damage. Below or the studies that prove this, further down is how to fix it, which is very possible with the right knowledge
Dermatologists' attitudes, prescription, and counseling patterns for isotretinoin: a questionnaire-based study.
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)."
Functional brain imaging alterations in acne patients treated with isotretinoin.
http://www.ncbi.nlm.nih.gov/pubmed/15863802
-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression.
This study suggests that isotretinoin treatment is associated with changes in brain functioning."
A 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.
13-cis Retinoic acid (accutane) suppresses hippocampal cell survival in mice.
http://www.ncbi.nlm.nih.gov/pubmed/15251924
We 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."
Retinoic Acid and Affective Disorders: The Evidence for an Association
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276716/
"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."
13-Cis-retinoic acid decreases hypothalamic cell number in vitro.
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."
Anxiety, Depression and the Hippocampus
After taking Accutane, I suffered depression and anxiety, and so far from normal that I went to a psychologist and explained my symptoms, and went there several times, and while I considered antidepressants, I never took them. On Accutane forums, many people are depressed, and so many have taken SSRIs, and many people feel much better having taken them. They still do not feel 100%, but while on them they regain a lot of feeling and emotion that they have missed, antidepressants obviously have their own side effects so it is not always worthwhile. There is much research showing there are natural ways to stimulate neurogenesis in the hippocampus, that does not risk the side effects of antidepressants
Hippocampal neurogenesis: opposing effects of stress and antidepressant treatment.
https://www.ncbi.nlm.nih.gov/pubmed/16425236
The 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.
This study basically states the reason SSRIs work again depression is because they upregulate hippocampal neurogenesis
Ventral hippocampal lesions affect anxiety but not spatial learning.
https://www.ncbi.nlm.nih.gov/pubmed/12642189
Rats with cytotoxic ventral hippocampal lesions which removed approximately 50% of the hippocampus (including dentate gyrus) starting from the temporal pole, displayed a reduction in freezing behaviour following the delivery of an unsignalled footshock in an operant chamber. This was more plausibly a result of reduced susceptibility to fear than a result of a lesion-induced increase in general motor activity. There was no consistent difference between sham and lesioned animals in spontaneous locomotor activity, or locomotion following acute or chronic treatment with amphetamine. In contrast, ventral hippocampal lesioned animals were quicker to pass from the black to the white box during a modified version of the light/dark exploration test, and were quicker to begin eating during tests of hyponeophagia. Furthermore, rats with ventral hippocampal lesions defecated less than their sham counterparts both during open field testing and in extinction sessions following contextual conditioning. In contrast to these clear lesion effects, there were no signs of any spatial learning impairment either in the watermaze or on the elevated T-maze. Taken together these results suggest that the ventral hippocampus may play a role in a brain system (or systems) associated with fear and/or anxiety, and provide further evidence for a distinct specialisation of function along the septotemporal axis of the hippocampus.
Anxiety and hippocampus volume in the rat.
https://www.ncbi.nlm.nih.gov/pubmed/16192979
In depressed patients as well as healthy controls, a positive relationship between hippocampal volume and trait anxiety has been reported. This study sought to explore the possible inter-relation between hippocampal volume and trait anxiety further. Magnetic resonance imaging at 7 T was used to measure hippocampal volumes in a rat model of extremes in trait anxiety (experiment 1) and in a Wistar population with normal anxiety-related behavior (experiment 2). In addition to anxiety-related behavior, potentially confounding factors (depression-like, exploratory, and locomotor behavior) were assessed. Experiment 1 globally supported the hypothesis of a positive relationship between hippocampus volume and trait anxiety but did not allow for ruling out possible confounds arising from cosegregation of other behavioral traits. Experiment 2 yielded strong evidence for a negative relationship which was specific for trait anxiety. Thus, the relationship between hippocampal volume and anxiety may be more complex than expected. Interestingly, anxiety-related behavior in experiment 2 had a stronger influence on hippocampal volume than depression-like behavior. In the light of hippocampal volume loss in anxiety disorder and frequent comorbidity of anxiety and depression, this finding suggests that further research into the relationship between anxiety and hippocampal volume may be critical for understanding hippocampal contributions to normal and pathological behavior.
The studies above show that hippocampal volume, which is the most common measure of neurogenesis and neuroplasticity, are very accurate in determining whether someone suffers from depression and generalised anxiety disorder, and also the severity of the mental illness.
Hippocampal volume is also an accurate predictor of how well someone will recover from a brain injury, or how well they will cope when faced with a stressful situation.
The cure is focussed in restoring neuroplasticity and hippocampal growth (aka promoting neurogenesis, they are all basically the same thing), and while following the routine your brain should regain this ability to heal itself and over several months a close to full recovery should be within reach. As a bonus, the depression and anxiety also being suffered should be much reduced after following the protocol
Effects of Hippocampal atrophy/ negative changes in brain metabolism
Traumatic brain injury: a disease process, not an event.
https://www.ncbi.nlm.nih.gov/m/pubmed/20504161/
Traumatic 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: it is permanent, caused by non-reversible pathological alterations, requires special training of the patient for rehabilitation, and/or may require a long period of observation, supervision, or care. TBI 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. 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
Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819093/
In 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 pairsboth the trauma-exposed and unexposed membershad 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 maybe the worse his mental state before the injury happened, the worse his recovery will be, rather than simply being optimistic improves outcomes.
In this we see that accutane, in mant 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 accutanes sides. That is because they can help treat some of accutanes sides in specific instances, because SSRIs can promote neuroplasticity, though it doesnt cut through to the heart of the issue, and it means you cant stop taking SSRIs.
Now we established that hippocampal atrophy is 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 and safely, without the need to put your health under any further risks
Stimulating hippocampal growth/neurogenesis/neuroplasticity
First line of treatment is just some nutritional supplements
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 TBI"
Dietary supplement creatine protects against traumatic brain injury.
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.
Protective effects of taurine in traumatic brain injury via mitochondria and cerebral blood flow.
http://www.ncbi.nlm.nih.gov/m/pubmed/27156064/
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.
Fish Oil Intake and Seizure Control in Children with Medically Resistant Epilepsy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4525390/
Table 1 and Figure 2 compare the distribution of children according to the number of seizure attacks per month, before the intervention, after one month, after two months, and after three months of the study. In the intervention group, it is quite obvious that the cases are significantly improving and the number of epileptic attacks per month is decreasing after starting the fish oil supplementation. The percentage of children having zero attacks per month increased from 0% to 57.1% at the end of the third month in the intervention group, while it only reached 2.9% in the control group.
Changing diet
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"
Lifestyle choices and activities
Meditation effects within the hippocampal complex revealed by voxel-based morphometry and cytoarchitectonic probabilistic mapping
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.
Mindfulness-based stress reduction (MBSR) improves long-term mental fatigue after stroke or traumatic brain injury.
https://www.ncbi.nlm.nih.gov/pubmed/22794665
The Effect of Mindfulness-Based Therapy on Anxiety and Depression: A Meta-Analytic Review
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848393/
Effect size estimates suggest that mindfulness-based therapy was moderately effective for improving anxiety (Hedges g = 0.63) and mood symptoms (Hedges g = 0.59) from pre to post-treatment in the overall sample. In patients with anxiety and mood disorders, this intervention was associated with effect sizes (Hedges g) of 0.97 and 0.95 for improving anxiety and mood symptoms, respectively. These effect sizes were robust, unrelated to publication year or number of treatment sessions, and were maintained over follow-up.
Larger hippocampal dimensions in meditation practitioners: differential effects in women and men
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351565/
Descriptively, left and right hippocampal volumes were larger, on average, in male meditators compared to male controls; they were also larger in female meditators compared to female controls (see Table Table1).1). The group-by-sex interaction was significant for the left hippocampus (p = 0.002) but not for the right hippocampus (p = 0.46). Conducting post hoc comparisons separately within males and females, left hippocampal volumes were significantly larger in male meditators than male controls (p = 0.02) as well as in female meditators than female controls (p = 0.046). Significant meditation effects with respect to right hippocampal volumes were not detectable in males (p = 0.722) or in females (p = 0.291).
Mindfulness meditation improves cognition: evidence of brief mental training.
https://www.ncbi.nlm.nih.gov/pubmed/20363650
After four sessions of either meditation training or listening to a recorded book, participants with no prior meditation experience were assessed with measures of mood, verbal fluency, visual coding, and working memory. Both interventions were effective at improving mood but only brief meditation training reduced fatigue, anxiety, and increased mindfulness. Moreover, brief mindfulness training significantly improved visuo-spatial processing, working memory, and executive functioning. Our findings suggest that 4days of meditation training can enhance the ability to sustain attention; benefits that have previously been reported with long-term meditators.
Hyperbaric oxygen therapy promotes neurogenesis: where do we stand?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3231808/
Abounding evidence has shown that HBOT promotes neurogenesis. Future investigations need to be extended to models of neurological diseases, including subarachnoid hemorrhage (SAH), cerebral hemorrhage, AD, PD, surgical brain injury (SBI) and autism for cell proliferation, survival and differentiation. Furthermore, studies need to be conducted to explore whether HBOT induced neurogenesis leads to a functional improvement followed by large scale, strictly controlled clinical trials to establish HBOT as a prevention and/or treatment modality for neurological diseases.
The influence of creatine supplementation on the cognitive functioning of vegetarians and omnivores.
https://www.ncbi.nlm.nih.gov/pubmed/21118604
Oral creatine monohydrate supplementation improves brain performance: a double-blind, placebo-controlled, cross-over trial.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691485/
Dietary supplement creatine protects against traumatic brain injury.
https://www.ncbi.nlm.nih.gov/pubmed/11079535
Three weeks of creatine monohydrate supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players.
https://www.ncbi.nlm.nih.gov/pubmed/19741313
Fish oil 3g x2 per day. It has very strong neuroprotective effects, and has been shown to control epilepsy in children. In animals it has been show to increase testosterone and improve sperm count
Fish Oil Intake and Seizure Control in Children with Medically Resistant Epilepsy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4525390/
Effect of Long-Term Fish Oil Supplementation on Semen Quality and Serum Testosterone Concentrations in Male Dogs
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4948075/
Effect of dietary fish oil on mouse testosterone level and the distribution of eicosapentaenoic acid-containing phosphatidylcholine in testicular interstitium.
https://www.ncbi.nlm.nih.gov/m/pubmed/28955915/
Zinc 30mg elemental/day Has been shown to have neuroprotective effects, improve male hormone profile, and improve liver health. If also taking iron supplements take at a different time of the day, because zinc can hinder iron absorption
Zinc status and serum testosterone levels of healthy adults.
https://www.ncbi.nlm.nih.gov/pubmed/8875519
Effect of zinc and selenium supplementation on serum testosterone and plasma lactate in cyclist after an exhaustive exercise bout.
https://www.ncbi.nlm.nih.gov/pubmed/21744023
Effect of zinc supplementation on neuronal precursor proliferation in the rat hippocampus after traumatic brain injury.
https://www.ncbi.nlm.nih.gov/pubmed/
Example treatment routine
Creatine - increases Dihydrotestosterone (DHT) and testosterone, which is very important for PFS sufferers especially, while also increasing muscle power and improves neuroplasticity
Fish Oil - improves joint pain, helps heart disease, reduces seizure incidence and promotes neurogenesis
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
Multivitamin - makes me less likely to be malnourished.
Ketogenic Diet: Improves body composition, can help ED, has been known to cure depression and anxiety, and improves neuroplasticity. I tried it for a
Hyperbaric oxygen therapy: If this therapy is accessible to you I would also take advantage of it, though I havent done it. Many studies show it strongly promotes neuroplasticity
Olive Oil: Improves hormones, displays neuroprotective effects, helps with constipation and antioxidents, improves wound healing and skin health, helps with depression and anxiety
Extra virgin olive oil improves learning and memory in SAMP8 mice.
https://www.ncbi.nlm.nih.gov/pubmed/21955812
Neuroprotective effect of olive oil in the hippocampus CA1 neurons following ischemia: Reperfusion in mice
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724295/
Olive oil-enriched diet reduces brain oxidative damages and ameliorates neurotrophic factor gene expression in different life stages of rats.
https://www.ncbi.nlm.nih.gov/pubmed/26168701
Extra-virgin olive oil preserves memory, protects brain against Alzheimer's
https://www.sciencedaily.com/releases/2017/06/170621103123.htm
It also helps joint pain
https://www.ncbi.nlm.nih.gov/pubmed/25294776
Anti-inflammatory and joint protective effects of extra-virgin olive-oil polyphenol extract in experimental arthritis.
Depression and anxiety
Role of Monoaminergic System in the Etiology of Olive Oil Induced Antidepressant and Anxiolytic Effects in Rats
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725699/
Constipation and antioxident profile
The short-term effects of olive oil and flaxseed oil for the treatment of constipation in hemodialysis patients.(only 4ml a day)
https://www.ncbi.nlm.nih.gov/pubmed/25238699
Antioxidant activity of olive polyphenols in humans: a review.
https://www.ncbi.nlm.nih.gov/pubmed/20209466
Alternative treatment routines
Things that might help, but are on the riskier side and I am unlikely to attempt myself, but possibly would help
The regulation of adult rodent hippocampal neurogenesis by deep brain stimulation.
https://www.ncbi.nlm.nih.gov/pubmed/18173322
High-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
Deep 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].
Conclusion
Remember, there will be scars remaining from your specific syndrome, but thismay help withbrain fog, erectile dysfunction, depression, anxiety, injury-susceptiblility, and the continuous and inevitable deterioration of health that the doctors can't seem to pinpoint the cause of, and instead it will be merely the scars, such as back pain, eye floaters, the occasional sore joint, low T, and unlike before, your body will be able to respond and heal so even those scars may fade a little. Good Luck everyone!
EDIT:*I've recently talked to others who's post accutane syndrome makes mine pale in comparison. For me, it was completely life changing, I thought about ending it, but I could still live. Before recovery, I could still live a life, if I lowered my expectations low enough, dropping out of Uni and accepting I would never have a sexual relationship, and that I would never be particularly happy or successful, while post recovery, I I think I can now achieve a good life, going to Uni and dating, etc. However, for others, it affects them a lot harsher than it did me, life is not liveable in any sense, and so for promising a cure, I feel like a fraud. I'm going to leave it up, because I know it can still help SOME people regain control of their life, but for plenty of people, who accutane his much harder than myself, it may not bring much respite, and so I apologise for any whom I gave false hope,though I still encourage everyone to give it a go