Finasteride causes glutathione depletion and leads to CFS?

[dgreene]

I know deprenyl is being looked at since light at the end recovered and used it (we don’t know exactly what made him recover). Maybe a higher dose is necessary for other people.

Searching for substances that up-regulate dopamine or dopamine receptors.

Sulbutiamine

en.wikipedia.org/wiki/Sulbutiamine

“Although its clinical efficacy is uncertain,[3] it is the only compound used to treat asthenia that is known to selectively target the areas that are involved in the condition.[4] In addition to its use as a treatment for chronic fatigue, sulbutiamine may improve memory, reduce psycho-behavioural inhibition, and improve erectile dysfunction.”

Citicoline

en.wikipedia.org/wiki/Citicoline

Studies suggest that CDP-choline supplements increase dopamine receptor densities,[1] and suggest that CDP-choline supplementation helps prevent memory impairment resulting from poor environmental conditions.[2] Preliminary research has found that citicoline supplements help improve focus and mental energy and may possibly be useful in the treatment of attention deficit disorder.[3][4] Citicoline has also been shown to elevate ACTH independently from CRH levels and to amplify the release of other HPA axis hormones such as LH, FSH, GH and TSH in response to hypothalamic releasing factors.[5]

Thats very interesting.

Inositol supposedly up-regulates dopamine receptors, trying to find a paper that proves it. I’m wondering if the severely affected people have severely reduced dopamine receptors and thats why deprenyl doesn’t work. Light at the end was hitting the gym a week or so after his crash. I was so sick I couldn’t do anything for a month. I always suspected he was not affected as much as some of us were.

Good think we have the Italians helping us out. There are so many studies on finasteride and dopamine conducted in Italy.

[droit]

@droit

I am posting the 23AndMe Methylation Cycle related data.

sdrv.ms/14UBS2F

The format is in number of mutations (different from ‘wild type’). A 1 means the person is heterozygous for a mutation, and a 2 means homozygous for a mutation.

We don’t have to dataset to run formal statistics yet, but the challenge with something like this is that you don’t need any one mutation to have a debilitated methylation capacity. It is the combination of events that makes things more sever. For example: everyone has

1. MTHFR and BHMT

or

2. MTHFR and CBS.

The short-coursers seem to have MTHFR, BHMT and CBS. We will have to think about what statistics we will need to express this with larger data.

If you guys want to see how each of these genes fit into the cycle, there is a great diagram here:

autismpedia.org/wiki/images/ … -cycle.jpg

There is a good discussion going on about VDR-TAQ, but I don’t think there is any anomaly there. The proportion of mutations in the normal population is 58% and in our data set it is 63%. So its already a common mutation and if this proportion keeps up as we get more data, there won’t be anything significant there.

The more interesting things are in the combination of events of the enzymes that introduce and keep metabolites in the methylation cycle. The short coursers tend to have MTHFR, BHMT and CBS. If things up this way, there will be some strong statistics there.

[Cap]

I’ve suspected an issue with dopamine as well. I’ve noticed when I go without sleep or drink caffeine, my symptoms temporarily improve. Both of those things raise dopamine, I think.

[Finatruth]

Don’t know if you need to suspect it, the Italy results indicated drastically low levels of dopamine

[Cap]

Oh. Well alright then.

[Cap]

@dgreene

Citicoline

en.wikipedia.org/wiki/Citicoline

Studies suggest that CDP-choline supplements increase dopamine receptor densities,[1] and suggest that CDP-choline supplementation helps prevent memory impairment resulting from poor environmental conditions.[2] Preliminary research has found that citicoline supplements help improve focus and mental energy and may possibly be useful in the treatment of attention deficit disorder.[3][4] Citicoline has also been shown to elevate ACTH independently from CRH levels and to amplify the release of other HPA axis hormones such as LH, FSH, GH and TSH in response to hypothalamic releasing factors.[5]

This one especially sounds very promising. Is there any way to get ahold of it?

[dgreene]

Its an over the counter supplement, you should be able to get it pretty easily.

[Cap]

I’ll definitely try it out. I’m secondary hypo so it sounds like it increases exactly what I’m missing. We’ll see, I guess.

[dgreene]

Be careful though. There are drugs out there that can cause priapism, if you notice an erection lasting longer than normal, go to the ER immediately. Not saying any of these will cause that, but you never know how we will react.

[dgreene]

@mariovitali

I am saying the above as a potential warning on what lies on the road ahead : Neurodegeneration. The good thing is that with time i managed to understand all of the unrelated symptoms i was getting from PFS.I started the methylation protocol as Droit suggested and waiting for the 23andme results. For some reason i am getting an almost immediate feedback (either positive or negative) to whatever i am trying so i think that the methylation protocol has not helped me (yet but of course this could change) in terms of my symptoms that point to neurodegeneration. OTOH, My “tinnitus-attacks” are completely gone.

I don’t see your logic here. Also, aren’t you the guy who had a full report with statistics regarding an auto-immune theory?

Lets not make any definitive conclusions until the doctors are done with the research.

[droit]

@Cap

I’ve suspected an issue with dopamine as well. I’ve noticed when I go without sleep or drink caffeine, my symptoms temporarily improve. Both of those things raise dopamine, I think.

No one would disagree with you in that there is dopamine dysfunction in PFS. But dopamine dysfunction is too shallow in the full canon of PFS. This thread proposes that dopamine dysfunction, whether it be at the dopamine production level or the receptor level, is just a symptom in a bigger picture of dysfunction.

If you want to investigate dopamine dysfunction in PFS in this thread, I recommend looking at the work of Richard Deth, who says dopamine D4 receptors work by binding to dopamine, then transferring methyl groups to membranes.

ncbi.nlm.nih.gov/pubmed/10395213
youtube.com/watch?v=z1L84EQ9S5k
books.google.com/books?hl=en&lr= … &q&f=false

His work is very complicated, but it is important work.

Or look at the BH4 cycle, which is connected to the Methylation cycle and synthesizes dopamine and serotonin.

autismpedia.org/wiki/images/ … -cycle.jpg

researchgate.net/publication … a9e8f2.pdf

[Cap]

I’m going to pick up choline along with a few other things after I get my latest bloods back in a couple weeks. I’ll let you know what benefits I get, if any. I’ll begin the methylation protocol then as well. It may make it difficult to figure out what I’m getting benefits from but I want to hit this thing from multiple angles at once.

[mariovitali]

@dgreene

[
I don’t see your logic here. Also, aren’t you the guy who had a full report with statistics regarding an auto-immune theory?
Lets not make any definitive conclusions until the doctors are done with the research.

I am not making any conclusions Dgreene, after all this is the “theories” thread isn’t it? Regarding the autoimmune disease theory i cannot be sure. I am writing in this thread because i realized that many of my problems were because of possible Glutathione depletion . The statistics i posted essentially showed that L-Cysteine food sources were helping me. As a result i saw that Glutathione boosting could be a solution and -for me- it was as i have stopped being depressed, i started sleeping normally and my erections came back (although it takes a lot of time to achieve one).

However i still have several other problems such as Constipation and at times pains at my arms and legs. At one point i accidentally bumped my funny bone and the electric shock sensation was not very intense as i would expect.

I am planning to have an MRI to assess any neuronal degeneration in the next month.

[droit]

A couple of people have asked for Dr. Yasko’s book, here it is for free:

dramyyasko.com/wp-content/fi … 2_file.pdf

She is a Naturopath that treats methylation cycle dysfunction in CFS and Autism patients. She has very good explanations of things.

[Livingdead]

I’m sort of in a rush right now and I haven’t been able to read all the tread and the links, but I wanted to know what protocol I can do if I don’t know if I have the gene mutation. I’ll be out of the country for a while and I’m not sure I’ll be able to get these things where I’m going, so I would need to buy the supplements right now. Is it safe to try Methylcobalamin B12, Phosphatidyl Serine and Trimethylglycine if I have the gene mutation without knowing it? And what about NAC? I had some improvements during the last months and I don’t want to scrap it all if there’s a real risk here. Of course, I don’t mean feeling bad a day or two, I’m talking about more serious damages that would leave me with more problems than those I have right now.

[mariovitali]

Hey Guys,

Received my 23andme results. Here they are :

COMT V158M rs4680 AG +/-
COMT H62H rs4633 CT +/-
COMT P199P rs769224 GG -/-
VDR Bsm rs1544410 CT +/-
VDR Taq rs731236 AG +/-
MAO A R297R rs6323 G -/-
ACAT1-02 rs3741049 AG +/-
MTHFR C677T rs1801133 AA +/+
MTHFR 03 P39P rs2066470 GG -/-
MTHFR A1298C rs1801131 TT -/-
MTR A2756G rs1805087 AG +/-
MTRR A66G rs1801394 AA -/-
MTRR H595Y rs10380 CC -/-
MTRR K350A rs162036 AA -/-
MTRR R415T rs2287780 CC -/-
MTRR A664A rs1802059 AG +/-
BHMT-02 rs567754 CT +/-
BHMT-04 rs617219 AC +/-
BHMT-08 rs651852 CT +/-
AHCY-01 rs819147 CT +/-
AHCY-02 rs819134 AG +/-
AHCY-19 rs819171 CT +/-
CBS C699T rs234706 AG +/-
CBS A360A rs1801181 AG +/-
CBS N212N rs2298758 GG -/-
SHMT1 C1420T rs1979277 GG -/-

Droit and/or others,PM me if you have any comments. From the results i understand that i do have a serious MTHFR mutation and several other heterozygous ones.

I just wanted to say that i might have a solution regarding my neurological problems, plus my erections are even more harder. I will not say anything yet but we should keep in mind that the Methylation theory unveils some significant reasons for our problems but it does not -for now- explain other problems such as Hypogonadism, Hypothyroidism commonly associated with PFS.

For these problems, P450scc induction could be the missing link but i will not say anything more for now until i have some more concrete -personal- results.

[droit]

@mariovitali

Hey Guys,
Received my 23andme results. Here they are :

The data continues to be consistent. Mutations in MTHFR, mutations at every BHMT site and CBS. It is shocking that there are so many full mutations in BHMT.

You’re the first to have a compound heterozygous mutation in CBS. So far people have had just one or the other. And you’re also the first to have mutations in AHCY.

AHCY is the enzyme that converts SAH (SAMe with the methyl group used up) into Homocysteine.

autismpedia.org/wiki/images/ … -cycle.jpg

Those mutations prevent the flow to Homocysteine, so the system is totally bottle-necked off. This would impact generation of glutathione and recycling metabolites in the methylation cycle.

I wonder if that’s why NAC is been so good for you, you don’t have have any flow to the transsulfuration pathway, and thus limited cysteine.

Just a theory.

Is it possible to get some testing or see if there are methlyaltion doctors in your area? You can search Phoenix Rising to see if there is a doctor in your area .

forums.phoenixrising.me/index.ph … octors.32/

[mehhhhh]

I wondered if anyone could speak to the rate of these mutations in the general population. If we’re talking about 50%, this probably doesn’t mean much yet. If we’re talking about <25% it would seem like the statistics are more meaningful.

I will say that caffeine has had a fairly obvious, positive effect on my symptoms, both sexually and mentally. I know that CFS sufferers often turn to caffeine to function. Hard to say if that bolsters our connection to CFS or not though…

[mariovitali]

@mehhhhh

I wondered if anyone could speak to the rate of these mutations in the general population. If we’re talking about 50%, this probably doesn’t mean much yet. If we’re talking about <25% it would seem like the statistics are more meaningful.

I will say that caffeine has had a fairly obvious, positive effect on my symptoms, both sexually and mentally. I know that CFS sufferers often turn to caffeine to function. Hard to say if that bolsters our connection to CFS or not though…

Agreed, we should have a look at genomes of people that quitted Propecia without having any side effects. Tough call but this should be one of our Targets.

Caffeine gives me a nice mental boost as well but i do not know how good this is in the long run.

[mehhhhh]

Has anyone read this study? Autonomic dysregulation could explain most, if not all, of the symptoms we are dealing with. Caffeine has always had a vasoconstrictive effect on me. I wonder if that’s why the caffeine is affecting my hard flaccid…by acting on the vascular system, which is not regulating itself correctly due to a problem with the autonomic nervous system.

We keep talking about correlations with MS, CFS, fibro…this would connect them all, just with different etiologies for the ANS dysregulation in each, possibly leading to the variations in symtoms.