A while back I posted about yamanaka reprogramming factors restoring epigenetic topography. Turns out there's a company pursuing this very technology and estimating clinical trials in 5-6 years.
Article about them: [removed]
Their website: [removed]

Also, found this over at solvepfs: http://www.bbc.com/news/health-43435868
I know stem cell transplants have been talked about before in forums, its nice to know that they are becoming more widespread and accepted. I have wondered for a while why these types of treatments have not been advanced upon for some time, especially in diseases where an ill acting immune system is known. Apparently bone marrow transplant patients, a procedure that's been going on for decades, are recommended to get re-vaccinated for everythingafter their procedures. Seems to me developing safer and more effective stem cell transplant treatments is a no brainier for MS and a host of other autoimmune disorders.

Between these two treatments, these have got to do something for us right?

edit:
Only other thing that crosses my mind for the future is a group of us and the pfs people getting some of those new/upcoming $1000 epigenome assaying devices and getting a good pool of data to analyze and send to researchers to analyze. Then CRISPR? @flynnI'm with you now, when I think about the situation I'm in it doesn't seem that far out of an idea anymore.
All this has been brought up before hasn't it. Ha! Shows where my mind is.
And then there's the ever going Baylor study. When?!

8 hours ago, Frage said:

Between these two treatments, these have got to do something for us right?

I would think you would have to have a pretty good formal diagnosis for a type of treatment that kills the immune system with chemo drugs and replaces it with stem cells.
Speaking of something like MS, most if not all patients DO show real evidence of this on brain MRIs.
Other than hormone levels what has anyone found?
Seems like alot of subclinical symptoms that get brushed off as coincidence.

As far as genome testing is there anything out there that is really a better value then 23andme at this point?
For example I looked at Genos that cost 500 dollars and does whole exome sequencing, but wasnt even as thorough as 23andme and 23andme posted a lot more results that had meaning in promethease.
is seems like looking at whole genetic sequencing and mutations wouldn't mean much without some data to back up what could be considered a pathogenic mutation.
Speaking of that you have done 23andme I assume, and have promethease?

I would like to know some opinions on Fchawks post on page 613 in relation to brain damage.

You guys who are into gene info - do you not believe theres any brain damage post tane, is that why youre looking into gene info?

Id hate to think some answers are staring us in the face yet we ignore it and spend the next few years looking into genes etc when we should have spent time looking at something else....

Keen to hear more discussion on Fchawks post 2 pages back. Thanks

On 18.3.2018 at 12:03 AM, Colinboko said:

Also have any of you guys realized (before Accutane) that when you would get sick/fluyour acne would noticeably clear up...?

Cause mine did. So it just adds into my theory I guess. No wonder my skin looks amazing, if my damn immune system is in overdrive.

Yes, I actually do. I remember telling people about this when I was in high school and they thought I was imagining things. But I got next to no new pimples when I was sick for a week or two, when otherwise I'd get a new one every day.

This is the title of the Baylor study,
"Genetic and Epigenetic Studies on Post-Finasteride Syndrome Patients."
Absolutelyno information on it since its launch in 2013. This seems a little dead in the water to me.
They mention just one researcher, he is also a doctor that can be contacted.
Someone could possibly even make a appointment.
Dr. Mohit Khera. He has a email and phone number listed.

What are they looking at?

• This study will evaluate parameters of peripheral sexual function in patients with PFS.

• This study will uncover the underlying biological mechanisms related to the wide array of symptoms in PFS patients which closely match those of the androgen deprivation syndrome.

• This systematic investigation will help identify the genetic footprint of PFS and the array of deregulated androgen dependent functions.

• This study will elucidate the hormonal, genetic and epigenetic molecular mechanisms of the PFS.

• This study will provide leads for the development of mechanism-specific therapeutic strategies.

You have a newer study. What are they looking at?
[Edited link out]
SOMERSET, N.J., Jan. 29, 2018 ThePost-Finasteride Syndrome Foundationtoday announced Phase II of the clinical research on post-finasteride syndrome (PFS) being conducted at the University of Milano.

behavioral parameters, and alterations in neurogenesis, neuroinflammation and neurotransmitter pathways involved in the control of sexual function, as well as possible epigenetic changes in 5alpha-reductase. Possible changes of the gut microbiota composition will also be considered.

Reported symptoms include: loss of libido, erectile dysfunction, depression, suicidal ideation, anxiety, panic attacks, Peyronies disease, penile shrinkage, gynecomastia, muscle atrophy, cognitive impairment, insomnia, severely dry skin and tinnitus.

possible epigenetic changes in the 5-alpha reductase enzyme.

Sounds all too familiar.

Good post guitarman.

Im no scientist but my point in saying that theres brain damage implies brain inflammation.

I know calling it brain damage scares people off, call it brain interference if that helps but I believe thats what weve gotta deal with.

Pointless really going and just getting inflammation blood tests, get to the bottom of the brain damage and youll resolve the inflammation....thats my thought.

Has anyone looked at sorghum as a supplement?

looks like it holds many benefits, keen to know if anyone has tried it.

Sorry for this being so big, will try to keep my ideas more concise next time. Just hard sometimes

I think its been established that us accutane patients likely have some form, or something similar to, brain damage. However, the question is if brain damage is the reason for the persistence of our side effects. I don't think it is solely to blame at all. Because for example, the observation that there has been many PFS and PAS persons who have felt completely back to normal after using a 5ari like saw p or finasteride, or persons who have felt completely back to normal after using aromatase inhibitors. Of course, this was almost always temporary for these persons and often resulted in further worsening of symptoms long term, but I think it shows that the persistence of our side effects comes more from altered neurosteroids and hormones resulting from altered expression of 5ar enzymes/ androgen receptors/ something relating vs brain damage being the root cause. Here's another thing, arent there stories of people taking like one pill and immediately crashing with full blown PFS? I dont feel TBI's match these symptom timelines. Alot of our symptoms are also felt by people who take fin and accutane but go away after discontinuation just like roche and merck say. Even in these studies focusing on the brain altering effects of isotretinoin, the groups focused on were not post-tane groups. In fact, studies like this one even claim that psychiatric symptoms left after discontinuation too. These studies may not necessarily be representing us post-tane patients. There is something more going on than just a TBI, not that forms of brain damage are not plaguing us too, just that I don't think this is what is causing the bulk of persistent side effects. It doesn't fit the bill in my head.

The baylor study keeps getting postponed due to significant findings, this does not mean its exactly dead in the water. Part of me feels its not so smart to dismiss these relatively unbiased and even PHD level researches.

Whats obvious is that there is some kind of memory in our body causing the persistence of our symptoms. Epigenetics? Immune related? Apoptosis? Those are the three I've seen put about. Any others? TBI would fit under apoptosis if viewed as the root cause for most of our symptoms, but again I don't see the evidence that it is the major driving force of our symptoms. TBI's also arent the only conditions with symptoms similar to ours. CFS patients have a lot of similar symptoms for example. Do these three general categories of action encompass the possibilities of our disease? I feel we need to at-least establish the broad categories of damage that could be.

I am also worried that no one will ever figure the exact metabolic course that caused this in us. Metabolism and feedback systems and etc in the body are very complex and hard to investigate. Us PFS/PAS/PSSD patients have very little resources to throw around as well. I don't see diseases in the near future being cured do to more intimate knowledge of the interactions and metabolism of drugs, hormones, neurosteroids, enzymes, receptor expression, vitamins, proteins, aminos, etc. It is all just too complicated. This knowledge is of course needed, but only helpful to a point.

Instead, I think therapies that can correct diseases due to very root or general methods of action, like stem cell therapies for the immune system, reprogramming factors to the epigenome, or targeted CRISPR, will be much more successful. Therapies that could help us even if we only knew the broad type of damage we have.

Chemotherapy drugs do seem risky, after all accutnae is also used for chemotherapy. However, with the history of how accutane has affected me (and knowing that this is probably not because of its chemotherapy effects but its 5ar/anti-androgenic affects like fin or ssris), it is something I would consider. I'm in real bad condition right now, and I'm just a year post. I'm in pain all day every day, joint pain, bone pain, stomach pain, nausea, psychosis, headaches, tinnitus... Im slowly getting addicted to opioids, gaba drugs, booze, ssris, smokes and more just to cope You know its like, what do I got to lose?

Another thing, I actually take and do, and have done for a while, a large amount of the things listed by Fchwak. Lots of people have done similar protocols with very mixed results. Some with good results. Why the mix? Who will ever know. The methods of action of a lot of these things are too complicated to really understand.

All I know after 20 years is this:

Time wont heal you - dont count on time working it out for you, if youve got issues post tane, youre stuck with them till theres a cure - thats my experience.

Gut - dont expect a Gastroenterologist to help - they cant find anything wrong - fact!!

Liver - you might have a fatty liver, aside from that I dont think anyone has found any conclusive info that our problems stem from liver. At this stage if you think its liver, like me youd be speculating, happy to be proven wrong.

Hormone: how much more testing as a group can we possibly do?? So many mixed results with no certain outcome.

So whats left? Blood flow and Brain function as far as Im concerned. Cant speak for everyone but after that I cant think what else to look into, other than speaking to a psychiatrist about the fucking shear joy of this unnecessary journey....absolutely mind boggling to say the least...

So I got my sed rate back....

it was 2....

the range is 0-15

So since there cant be a negative sed rate, I decided to look up the causes of a lower measurement. What pops up? Hyperviscosity of the blood. TONS of CFS sufferers have sed rates ranging from 0-3 and a lot are forced to believe its a result of really thick, sticky blood. This would explain a lot in my opinion.

I had an abnormal protein spike on my electrophoresis. Not entirely sure which protein was spiked but I was diagnosed with MGUS and need to get checked up on every six months to make sure it doesnt turn into anything more serious (cancer etc). Wanna know what causes Hyperviscosity? High plasma proteins in the blood. What causes high proteins? Not entirely sure. Certain infections, immune dysfunctions have been known to set them off. But having high amounts of plasma proteins means high antibody rate.. which would explain my immune system issues. Certain forms of low grade inflammation are also not detectable by CRP or ESR my doctor said. I think my symptoms are a result of the constant stream of antibody release mixed with poor blood flow due to Hyperviscosity. Even though I cant find the exact cause as to what triggered these plasma proteins to become overactive, calming them down with an immunosuppressant seems like the next best thing until we can figure out how to remove the root problem. Thought this was super interesting. Anyone else have lower sed rates?

Slowly but surely piecing this together.

On 3/22/2018 at 12:22 PM, TrueJustice said:

All I know after 20 years is this:

Time wont heal you - dont count on time working it out for you, if youve got issues post tane, youre stuck with them till theres a cure - thats my experience.

Gut - dont expect a Gastroenterologist to help - they cant find anything wrong - fact!!

Liver - you might have a fatty liver, aside from that I dont think anyone has found any conclusive info that our problems stem from liver. At this stage if you think its liver, like me youd be speculating, happy to be proven wrong.

Hormone: how much more testing as a group can we possibly do?? So many mixed results with no certain outcome.

So whats left? Blood flow and Brain function as far as Im concerned. Cant speak for everyone but after that I cant think what else to look into, other than speaking to a psychiatrist about the fucking shear joy of this unnecessary journey....absolutely mind boggling to say the least...

I agree, I find it highly improbable that this problem relates to the gut, liver or hormone levels. There is far too much variation here, and many people have no issues with any of these who have some of the major symptoms of PAS.

This certainly relates to the brain. One school of thought think this is due to brain damage. But there are other reasons. I think there has been a downregulation of key genes encoding enzymes like 5 alpha reductase 1, leading to a deficiency of steroids such as DHT and neurosteroids in the brain. This leads to reduced activity of neural pathways such as dopaminergic pathways which explains most of the mental side effects and also explains changes in blood blow/activity.

I am trying to discuss each theory in depth with evidence. I am just starting to talk about brain damage theory. Would be good if people could sig up and contribute in any way they can. Post blood results, opinions, things which have helped etc. - [removed]

On 3/23/2018 at 12:21 AM, flynn said:

I agree, I find it highly improbable that this problem relates to the gut, liver or hormone levels. There is far too much variation here, and many people have no issues with any of these who have some of the major symptoms of PAS.

This certainly relates to the brain. One school of thought think this is due to brain damage. But there are other reasons. I think there has been a downregulation of key genes encoding enzymes like 5 alpha reductase 1, leading to a deficiency of steroids such as DHT and neurosteroids in the brain. This leads to reduced activity of neural pathways such as dopaminergic pathways which explains most of the mental side effects and also explains changes in blood blow/activity.

I am trying to discuss each theory in depth with evidence. I am just starting to talk about brain damage theory. Would be good if people could sig up and contribute in any way they can. Post blood results, opinions, things which have helped etc. - [removed]

If its a 5AR problem then why do some of us have normal DHT levels?

40 minutes ago, Colinboko said:

So I got my sed rate back....

it was 2....

the range is 0-15

So since there cant be a negative sed rate, I decided to look up the causes of a lower measurement. What pops up? Hyperviscosity of the blood. TONS of CFS sufferers have sed rates ranging from 0-3 and a lot are forced to believe its a result of really thick, sticky blood. This would explain a lot in my opinion.

I had an abnormal protein spike on my electrophoresis. Not entirely sure which protein was spiked but I was diagnosed with MGUS and need to get checked up on every six months to make sure it doesnt turn into anything more serious (cancer etc). Wanna know what causes Hyperviscosity? High plasma proteins in the blood. What causes high proteins? Not entirely sure. Certain infections, immune dysfunctions have been known to set them off. But having high amounts of plasma proteins means high antibody rate.. which would explain my immune system issues. Certain forms of low grade inflammation are also not detectable by CRP or ESR my doctor said. I think my symptoms are a result of the constant stream of antibody release mixed with poor blood flow due to Hyperviscosity. Even though I cant find the exact cause as to what triggered these plasma proteins to become overactive, calming them down with an immunosuppressant seems like the next best thing until we can figure out how to remove the root problem. Thought this was super interesting. Anyone else have lower sed rates?

Slowly but surely piecing this together.

Thats super interesting and a great find.

So you just ask for a Sed rate blood test do you?

Also, did your Dr maybe suggest going on a blood thinner while you try to find the root cause?

28 minutes ago, TrueJustice said:

Thats super interesting and a great find.

So you just ask for a Sed rate blood test do you?

Also, did your Dr maybe suggest going on a blood thinner while you try to find the root cause?

Ordered it through walk-in for like 30 bucks! And had it faxed to my GP! And yeah, he did say there were a few routes I could take. But I think the cause of my Hyperviscosity is from the amount of immuno proteins floating around in my system. So maybe an immunosuppressant could help. I also just want to trial out some prednisone regardless, considering it helped some people like significantly. And a person with a igM protein spike was able to bring it down by dosing prednisone. 

It™s like the puzzle is slowly coming together. For me at least. Having that spike in immunoglobulins and then this... 

18 hours ago, Frage said:

The baylor study keeps getting postponed due to significant findings

Is this what you are referring to? I found this in the PFS Foundations annual address 2017. This is absolutely the only information I could find. Unless you know more and would like to share, which would be greatly appreciated.
http://www.pfsfoundation.org/news/2016-pfs-foundation-annual-address-2/
"Meanwhile, our clinical study at Baylor College of Medicine continues to progress steadily. The moment its published, well announce the results."

While you don't have a Baylor study atm, You do have thethe Center for Clinical Investigation at the Brigham and Womens Hospitalstudy from 2016 that im sure some of you are aware of.
Characteristics of Men Who Report Persistent Sexual Symptoms After Finasteride Use for Hair Loss
https://academic.oup.com/jcem/article/101/12/4669/2765035

Objective:

To determine whether these persistent symptoms after discontinuation of finasteride use are due to androgen deficiency, decreased peripheral androgen action, or persistent inhibition of steroid 5-reductase (SRD5A) enzymes.

We found no evidence of androgen deficiency, decreased peripheral androgen action, or persistent peripheral inhibition of SRD5A in men with persistent sexual symptoms after finasteride use. Symptomatic finasteride users revealed depressed mood and fMRI findings consistent with those observed in depression.

The clinical implications of these findings are that symptomatic finasteride users are unlikely to benefit from treatment with testosterone, DHT, or any other androgen, because these patients do not have evidence of androgen deficiency, persistentSRD5Ainhibition, or androgen insensitivity.

BUT.
fMRI blood oxygen level-dependent responses to erotic and nonerotic stimuli revealed abnormal function in brain circuitry

Also.
It is possible that mood and cognitive complaints may be related to reduced neurosteroid production due to persistent local inhibition of SRD5A activity in specific brain regions (42), which was not reflected in changes in peripheral DHT levels.

Going forward it will be interesting to see how any future studies could hopefully expand from this.

4 hours ago, guitarman01 said:

Is this what you are referring to? I found this in the PFS Foundations annual address 2017. This is absolutely the only information I could find. Unless you know more and would like to share, which would be greatly appreciated.
http://www.pfsfoundation.org/news/2016-pfs-foundation-annual-address-2/
"Meanwhile, our clinical study at Baylor College of Medicine continues to progress steadily. The moment its published, well announce the results."

While you don't have a Baylor study atm, You do have thethe Center for Clinical Investigation at the Brigham and Womens Hospitalstudy from 2016 that im sure some of you are aware of.
Characteristics of Men Who Report Persistent Sexual Symptoms After Finasteride Use for Hair Loss
https://academic.oup.com/jcem/article/101/12/4669/2765035

Objective:

To determine whether these persistent symptoms after discontinuation of finasteride use are due to androgen deficiency, decreased peripheral androgen action, or persistent inhibition of steroid 5-reductase (SRD5A) enzymes.

Conclusions:

We found no evidence of androgen deficiency, decreased peripheral androgen action, or persistent peripheral inhibition of SRD5A in men with persistent sexual symptoms after finasteride use. Symptomatic finasteride users revealed depressed mood and fMRI findings consistent with those observed in depression.

The clinical implications of these findings are that symptomatic finasteride users are unlikely to benefit from treatment with testosterone, DHT, or any other androgen, because these patients do not have evidence of androgen deficiency, persistentSRD5Ainhibition, or androgen insensitivity.

BUT.
fMRI blood oxygen level-dependent responses to erotic and nonerotic stimuli revealed abnormal function in brain circuitry

Also.
It is possible that mood and cognitive complaints may be related to reduced neurosteroid production due to persistent local inhibition of SRD5A activity in specific brain regions (42), which was not reflected in changes in peripheral DHT levels.

Didnt know about this. Thank you for sharing!

Getting an MRI tomorrow. Results on Thursday. Will post here after.

Good luck Lamme.

is it an MRI we need over a Cat scan??

Im uncertain on this....

1 hour ago, TrueJustice said:

Good luck Lamme.

is it an MRI we need over a Cat scan??

Im uncertain on this....

doc sent me in for an MRI as I had told her about the pressure behind my right eye

@guitarman01
The assay device I was talking about: https://nanoporetech.com/resource-centre/publications/detecting-dna-methylation-using-oxford-nanopore-technologies-minion
It's called the minion and can read cpg islands.
With regards to what I'm talking about with the term 'significant findings', that's just the term I've heard thrown about on propeciahelp and solvepfs threads usually about why the study keeps being set back.
And yeah I know the harvard study is unfortunate to say the least.

Anyone else get a Malar type rash when laying out in the sun...?

Im currently in Florida visiting family and I was laying by the pool and walked inside and was burnt from cheek to cheek and across my nose. But no where else significantly got red...

I believe the chemotherapy adjunct medication Isotretinoin has the potential to insult the PNS, as it is more susceptible to chemical injury than other regions (CNS or the brain directly), especially in those of developmental ages. As a result, the Autonomic nervous system can be affected. The PSNS for instance controls many regulations throughout the body, such as glandular function. Isotretinoin is marketed on its ability to shrink sebaceous glands, which are exocrine glands. I question how a chemical is able to discern between exocrine/endocrine, throughout the body, as its "effect" takes place. The drug has been remarked as having the ability to "make cancerous cells appear normal" in medical journals.

I urge people to look into their symptoms as it relates to the nervous system. Here is a photo, now recall our pattern of symptom commonalities in the a.reproductive region b. digestive region c. neurological region

I don't think it's far-fetched at all to make a PNS>ANS>Limbic System pathway of chemical toxicity, I think someone who actually knows about this stuff would say it's feasible, and if not, I'd like to hear why not.

I think people should focus their effort on a chemotherapy toxicity induced dysautonomia.

7 hours ago, macleod said:

I believe the chemotherapy adjunct medication Isotretinoin has the potential to insult the PNS, as it is more susceptible to chemical injury than other regions (CNS or the brain directly), especially in those of developmental ages. As a result, the Autonomic nervous system can be affected. The PSNS for instance controls many regulations throughout the body, such as glandular function. Isotretinoin is marketed on its ability to shrink sebaceous glands, which are exocrine glands. I question how a chemical is able to discern between exocrine/endocrine, throughout the body, as its "effect" takes place. The drug has been remarked as having the ability to "make cancerous cells appear normal" in medical journals.

I urge people to look into their symptoms as it relates to the nervous system. Here is a photo, now recall our pattern of symptom commonalities in the a.reproductive region b. digestive region c. neurological region

I don't think it's far-fetched at all to make a PNS>ANS>Limbic System pathway of chemical toxicity, I think someone who actually knows about this stuff would say it's feasible, and if not, I'd like to hear why not.

I think people should focus their effort on a chemotherapy toxicity induced dysautonomia.

I totally see what you™re getting at here, but how come other forms of chemo don™t leave patients riddled with this nasty disease like we are? What is so different about iso? And how would one treat chemo toxicity? I mean we would obviously just have to treat symptoms and find out what that chemo triggered right?

14 hours ago, macleod said:

I believe the chemotherapy adjunct medication Isotretinoin has the potential to insult the PNS, as it is more susceptible to chemical injury than other regions (CNS or the brain directly), especially in those of developmental ages. As a result, the Autonomic nervous system can be affected. The PSNS for instance controls many regulations throughout the body, such as glandular function. Isotretinoin is marketed on its ability to shrink sebaceous glands, which are exocrine glands. I question how a chemical is able to discern between exocrine/endocrine, throughout the body, as its "effect" takes place. The drug has been remarked as having the ability to "make cancerous cells appear normal" in medical journals.

I urge people to look into their symptoms as it relates to the nervous system. Here is a photo, now recall our pattern of symptom commonalities in the a.reproductive region b. digestive region c. neurological region

I don't think it's far-fetched at all to make a PNS>ANS>Limbic System pathway of chemical toxicity, I think someone who actually knows about this stuff would say it's feasible, and if not, I'd like to hear why not.

I think people should focus their effort on a chemotherapy toxicity induced dysautonomia.

It would be very interesting to see what Doctors recommend??

Google œsupplements for treating chemo toxicity and there™s nothing we all haven™t tried at some point.

B vitamins 
Co Q10
Fish oil
Ginseng
Antioxidants 
Curcumin

Fixing Chemo brain involves much more than just supplementing though:

Yoga
Qigong 
Rest
Meditation
Acupuncture
Brain games
Massage 

I dunno, is what I™m mentioning here completely different to addressing PNS issues??