Finasteride causes glutathione depletion and leads to CFS?

[mehhhhh]

The link to the article would be helpful…

m.qjmed.oxfordjournals.org/conte … 8/519.long

[bluejaysfan]

@droit

Finatruth,

The impact of a halted Methylation Cycle is massive. The most alluring aspect of this theory is the explanation of how you get to PFS, how it describes our symptoms and how it is persistent:

Get from Finasteride to a Methylation Block

1. Androgen deprivation leads to high oxidative stress (6)
2. Finasteride blocks neuronal oxidative stress protection (6)
3. DHT is needed for glutathione utilization (7)
4. DHT is an antioxidant, blocking it reduces protection to oxidative stress (4)

The accumulation of these effects overcomes your glutathione stores.

How it’s persistent:

1. A high oxidative stress environment reduces 5-alpha-reductase activity, thus preventing androgens from returning creating a circle of androgen deprivation and high oxidative stress (8)
2. A high oxidative environment destroys B12, which is the substrate of the initial Methylation cycle enzyme, thus blocking the methylation cycle and consequently blocking glutathione synthesis. (5)

jrheum.com/subscribers/07/02/341.html

[droit]

@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…

mehhhhh,

The frequencies in the normal population are publicly available. The spreadsheet I posted has the frequencies of mutations in the normal population, and a link to the general population data for each SNP.

viewtopic.php?f=27&t=7178&start=180#p72902

We do have high mutation frequencies at some important sites. For example, the frequency of a mutation at MTHFR C677T in the normal population is 36%, but it is 57% in our small data set.

Also, with BHMT, here are the frequencies of the general population vs our data set.

BHMT-02 rs567754 36% 58%
BHMT-04 rs617219 39% 67%
BHMT-08 rs651852 49% 67%

While we’re higher in MTHFR, I think the more important statistics is that everyone has some debilitation at MTHFR. Whether it be C677T P39P or A1298C, everybody has at least one and most have 2 mutations.

Further, the most dramatic pattern we are seeing is the frequencies of combination mutations. The frequency of a fully mutated BHMT-02 & BHMT-04 & BHMT-08 in the normal population is: 6.9%. In our dataset it is: 26%. And if you just look at the short term people (basically remove me who took Fin for 7 years), the probability is 45%. If this keeps up, the statistics will be undeniable.

I do have a hypothesis on why BHMT is important, but its too early to speculate.

But as I’ve said before, we don’t have the dataset to make any public claims.

[droit]

@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.

mehhhhh,

Chronic Fatigue and Fibromyalgia are now officially collapsed into one clinical term: ME/CFS. The MS ‘white spots’ that show up in MRIs, show up in those with ME/CFS.

Lange G, et al. Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome. J Neurol Sci. 1999 Dec 1; 171(1):3-7.

So this thread is already maintaining all three are collapsed into PFS. And the theory of ME/CFS condition is glutathione-depletion leads to a block in the methylation cycle. Which is exactly what we are raising awareness of here. Here’s my sound bite:

Androgen Deprivation via Finasteride causes high oxidative stress. Which, in the genetically susceptible, overcomes glutathione stores and glutathione production leading to persistent state of oxidative stress (OS), glutathione-depletion and consequently a halted methylation-cycle.

You should go back and listen to the podcast and video linked in the first few posts.

[mehhhhh]

Yeah, I’ve read through the thread and have been following along. I understand the general hypothesis. I just thought it was interesting that autonomic dysfunction is found among a large number of CFS patients. Issues with vascular control could explain issues such as hard flaccid and ED that we have been experiencing. Actually a category in evaluating autonomic function in men is erectile function.

Is it your contention that we actually have chronic fatigue syndrome or a condition that has a similar etiology as CFS?

[droit]

@mehhhhh

Yeah, I’ve read through the thread and have been following along. I understand the general hypothesis. I just thought it was interesting that autonomic dysfunction is found among a large number of CFS patients. Issues with vascular control could explain issues such as hard flaccid and ED that we have been experiencing. Actually a category in evaluating autonomic function in men is erectile function.

Is it your contention that we actually have chronic fatigue syndrome or a condition that has a similar etiology as CFS?

I’m trying to learn from what other communities who have established this as a core issue.

[droit]

Methylation Block and Androgen Dysfunction (post 2 of 2): Androgen Receptor and oxidative stress

Review of thread

Theory Again: Finasteride (androgen deprivation) causes oxidative stress (5) which, in the genetically susceptible, overcomes glutathione stores and glutathione production leading to persistent state of oxidative stress (OS), glutathione-depletion and consequently a halted methylation-cycle.

Test results backing up this theory:

100% of the 4 forum members who have tested for markers of Oxidation stress, have shown extremely high OS. As always, I am posting research in an effort to generate interest in this theory and get more testing in this area so we can determine with some statistical significance that PFS is or isn’t this. Once we have compelling evidence, we can focus on the protocol to get out of this state.

Androgen Dysfunction

A theory on this forum isn’t complete without ties to Androgen Dysfunction.

In the last Androgen Dysfunction post (propeciahelp.com/forum/viewt … =60#p71331), I summarized research that showed methylation of Androgen Receptor (AR) is essential AR’s activity. When the researches mutated a site of methylation, AR’s activity was reduced by at least 50%.

In the work summarized here is of Alexandra Fajardo. Dr. Fajardo published one paper during her Ph.D and had 2 other papers worth of work in her dissertation (see citations).

Simple summary of research

In the work of Fajardo, it is demonstrated that under high oxidative stress, Androgen Receptor expression is significantly reduced. This effect is particularly pronounced in vivo when glutathione is depleted (Yes, they literally run an experiment with Glutathione knocked down - how convenient).

Oxidative Stress down-regulates Androgen Receptor

In this work, the researchers used two chemicals to simulate oxidative stress (Alpha-tocopherylquinone and ca27). Upon application of oxidative stress, there is a reduction in AR receptor expression. Figure 4 (2a) shows a total obliteration of AR upon oxidative stress treatment - proportional to the concentration of OS and the time.

Oxidative Stress down-regulates Androgen Receptor responsive gene mRNA levels

Further, the paper looks at PSA expression in response to OS. PSA is a sensitive indicator of androgenic response. After applying oxidative stress, there is a 9 fold decrease in PSA expression. However, Vitamin E, an antioxidant increased expression of PSA. Suggesting combating oxidation improves androgen receptor (2b).

Table 2, has a more comprehensive list of AR target genes and the effects of oxidative stress showing down regulation of AR target mRNAs (2c).

Antioxidants attenuate OS driven ablation of AR this effect.

When the authors applied anti-oxidants NAC and Vitamin E during the application of oxidative stress, the AR down-regulation was reversed (2g).

This effect of antioxidants is upfront, or during the application of oxidative stress. They don’t measure whether or not AR can be rescued after 1 day of oxidative stress with NAC. So NAC is not the cure to PFS, but it may have been helpful while taking Fin.

How does this happen

What the authors show is: the OS driven AR protein down-regulation is independent from proteasomal degradation. And AR protein down-regulation is only slightly dependent on down regulated mRNA expression.

So the cell still makes AR mRNA, albeit a reduced number of mRNAs. But the reduced mRNAs does not explain the massive reduction in AR protein (2e).

Either the AR protein doesn’t get made or its made an quickly degraded.

In the discussion it is suggested that depleted glutathione (the reduced/good form is called GSH) can cause protein misfolding. When proteins get misfolded, the cell’s ‘unfolded protein response’ is involved

The paper demonstrates that OS up regulates proteins in the ‘unfolded protein response.’ So the author is suggesting AR protein is made, but it’s misfolded, so it gets chewed up (2f).

Second, and more important, Androgen receptor is dysfunctional in the presence of oxidative stress:

The author reduces glutathione directly in cells using a ‘glutathione ligase,’ then measures AR expression before and after exposure to OS. Essentially the experiment shows that (2d):

1. In the presence of low glutathione, AR is expressed normally

2. In the presence of low glutathione and OS, AR is expressed significantly lower than when OS is applied alone.

3. ‘The Curcumin Analog ca27 Down-Regulates Androgen Receptor Through an Oxidative Stress Mediated Mechanism in Human Prostate Cancer Cells,’ ncbi.nlm.nih.gov/pmc/articles/PMC3309160/

4. “NOVEL MECHANISMS OF ANDROGEN RECEPTOR DEGRADATION BY
   ALPHA-TOCOPHERYLQUINONE AND CURCUMIN ANALOG 27,” https://repository.unm.edu/bitstream/handle/1928/20817/Fajardo%20Dissertation%202011%2012-13-11.pdf?sequence=1

2a. Citation 2, Figure 4, page number 80

2b. Citation 2, page number 81-82

2c. Citation 2, page number 82-84

2d. Citation 2, page number 88-90

2e. Citation 2, page number 86-87

2f. Citation 2, page number 151

2g. Citation 2, page number 94-101

3. “Testosterone protects cerebellar granule cells from oxidative stress-induced cell death through a receptor mediated mechanism,” sciencedirect.com/science/ar … 9300031553

4. “Androgen treatment of neonatal rats decreases susceptibility of cerebellar granule neurons to oxidative stress in vitro,” ncbi.nlm.nih.gov/pubmed/10103123

5. propeciahelp.com/forum/viewt … one#p70973

Consider reading. Loss of Androgen Receptor in Aging and Oxidative Stress through Myb Protooncoprotein-regulated Reciprocal Chromatin Dynamics of p53 and Poly(ADP-ribose) Polymerase PARP-1, ncbi.nlm.nih.gov/pmc/articles/PMC2606006/

[mariovitali]

Hi Guys,

I am Back with an update. First of all i feel great, i dare to say that my erections are as hard like 15 years ago even more frequently (but not always). I stopped taking NAC (in search of the root of my problems) and after reading my 23andme data i dropped TMG, B6 (P-5-P) and MethylCobalamin B12. I am using only Metafolin (800), Cyanocobalamin B12 (not methylated, due to my COMT mutations) 1000 mcg per day and i added to my regimen some new things. Speed on achieving an erection remains the same (=not as fast as i used to)

Before i move on i just wanted to remind that :

1. i would feel much better and have harder erections by eating Cholesterol-rich foods. (Check my old posts)
2. I have High Cholesterol
3. I am hypothyroid (sub-clinical) and also have secondary hypogonadism

So i decided to re-visit my hypothesis about Cytochrome P450scc. I already knew potential inducers and one was Forskolin. I then saw this on Wikipedia for Forskolin entry which i have missed:

Forskolin (also called Coleonol) is a labdane diterpene that is produced by the Indian Coleus plant (Coleus forskohlii). Forskolin is commonly used to raise levels of cyclic AMP (cAMP) in the study and research of cell physiology. Forskolin resensitizes cell receptors by activating the enzyme adenylyl cyclase and increasing the intracellular levels of cAMP. cAMP is an important signal carrier necessary for the proper biological response of cells to hormones and other extracellular signals. It is required for cell communication in the hypothalamus/pituitary gland axis and for the feedback control of hormones.

I saw an earlier thread on Forskolin and i decided to give it a good try this time. So i added :

-100mg Forskolin to induce cAMP, which in turn induces P450scc which in turn cleaves Cholesterol to generate steroids (including the much wanted Allopregnanolone for neuronal repair).
-approx 12 mg of Clomid every other day (This is needed because Forskolin raises E2)

It seems that my neurologic problems are significantly better. Erections to the full as discussed. For some reason though i do not sleep as i used to but i am trying to find a solution with GABA which seems to also help towards a calm attitude plus it inhibits neuronal over-excitation. No Tinnitus (which now it seems to me that occurred due to over-excitation because of Glutamate/GABA imbalance but i cannot be sure).

I am really positive for this regimen. Also, memory is getting better for the first time. I know that this thread is about Methylation but i wanted to tell you the good news.

I will have Blood tested for Free T, Cholesterol, E2, TSH, T3, Ammonia and Taurine on Friday. If Free T, TSH and Cholesterol are normal then the theory of downregulated CYP11A1 (P450scc) in my case will be confirmed.

[droit]

mariovitali,

Great work leveraging your genetics to optimize you protocol. Quick comments:

1. A lot of people have CBS mutations, which speeds up the enzyme. B6 would speed it up more, so I’m glad you have done what I have done and cut B6.

2. Most don’t recommend cyano-B12. You have to work hard to pull the cyanine off, then you need a glutathione molecule to detox it. Its counter productive.

The people in your position, including me, take Hydroxy-B12. Perque is the typical one:

perque.com/products-page/dig … 2-guard-2/

Or people take:

holisticheal.com/hydroxy-b12-mega-drops.html

@mariovitali

Hi Guys,

I am Back with an update. First of all i feel great, i dare to say that my erections are as hard like 15 years ago even more frequently (but not always). I stopped taking NAC (in search of the root of my problems) and after reading my 23andme data i dropped TMG, B6 (P-5-P) and MethylCobalamin B12. I am using only Metafolin (800), Cyanocobalamin B12 (not methylated, due to my COMT mutations) 1000 mcg per day and i added to my regimen some new things. Speed on achieving an erection remains the same (=not as fast as i used to)

Before i move on i just wanted to remind that :

1. i would feel much better and have harder erections by eating Cholesterol-rich foods. (Check my old posts)
2. I have High Cholesterol
3. I am hypothyroid (sub-clinical) and also have secondary hypogonadism

So i decided to re-visit my hypothesis about Cytochrome P450scc. I already knew potential inducers and one was Forskolin. I then saw this on Wikipedia for Forskolin entry which i have missed:

Forskolin (also called Coleonol) is a labdane diterpene that is produced by the Indian Coleus plant (Coleus forskohlii). Forskolin is commonly used to raise levels of cyclic AMP (cAMP) in the study and research of cell physiology. Forskolin resensitizes cell receptors by activating the enzyme adenylyl cyclase and increasing the intracellular levels of cAMP. cAMP is an important signal carrier necessary for the proper biological response of cells to hormones and other extracellular signals. It is required for cell communication in the hypothalamus/pituitary gland axis and for the feedback control of hormones.

I saw an earlier thread on Forskolin and i decided to give it a good try this time. So i added :

-100mg Forskolin to induce cAMP, which in turn induces P450scc which in turn cleaves Cholesterol to generate steroids (including the much wanted Allopregnanolone for neuronal repair).
-approx 12 mg of Clomid every other day (This is needed because Forskolin raises E2)

It seems that my neurologic problems are significantly better. Erections to the full as discussed. For some reason though i do not sleep as i used to but i am trying to find a solution with GABA which seems to also help towards a calm attitude plus it inhibits neuronal over-excitation. No Tinnitus (which now it seems to me that occurred due to over-excitation because of Glutamate/GABA imbalance but i cannot be sure).

I am really positive for this regimen. Also, memory is getting better for the first time. I know that this thread is about Methylation but i wanted to tell you the good news.

I will have Blood tested for Free T, Cholesterol, E2, TSH, T3, Ammonia and Taurine on Friday. If Free T, TSH and Cholesterol are normal then the theory of downregulated CYP11A1 (P450scc) in my case will be confirmed.

[Raberduck]

@mariovitali

-approx 12 mg of Clomid every other day (This is needed because Forskolin raises E2)

Clomid will raise your E2 even more, because it is not an aromatase-inhibitor (like Arimidex) but and selective estrogen-antagonist, that blocks estrogen-effects in your brain, leading to more testosterone production.

[mariovitali]

@Raberduck

@mariovitali

-approx 12 mg of Clomid every other day (This is needed because Forskolin raises E2)

Clomid will raise your E2 even more, because it is not an aromatase-inhibitor (like Arimidex) but and selective estrogen-antagonist, that blocks estrogen-effects in your brain, leading to more testosterone production.

How on earth did i miss that, Thanks Man.

[droit]

Someone asked me about the different genetic tests, so I figured I should post the comparison publicly.

23AndMe

I am personally an advocate for 23AndMe. For $99 you get a full dataset of 960,000 SNPs and a subscription to their site, which analyzes your data and gives you basic traits about your genetic data. They even show you your ancestry. Because the dataset is so big, you can mine your data as you read more papers that discuss various mutations.

Some people think there are accuracy concerns. With any high volume experiment, there is a rate of error. It’s probably small if any.

With 23AndMe, you can send your raw data through a Genetic Genie wizard and get a Methylation specific view of your genotypes, like we’ve been gathering here:

sdrv.ms/14UBS2F

It is starting to be undeniable that a pattern is emerging. AJ72 just gave me more of his data, and he has all the hallmarks: Mutations at all BHMT sites, CBS and something at MTHFR.

There are also other 3rd party wizards out there.

I am personally interested in recruiting more 23AndMe data so we continue exploring the angle in this thread. I’m the only long term user and have a genetic different profile than the others.

Plus, Awor has specifically requested any data from forum members to contribute to the foundation (viewtopic.php?f=27&t=7178&start=160&hilit=snps#p72753). So for very cheap, you can have some fun and help the foundation in a profound way.

Dr. Yasko

Has a methylation specific gene test for $495 (holisticheal.com/health-test … ic-testing).

She gets the stuff on the genetic genie output + 5 SNPs she thinks are important that 23AndMe doesn’t get. You can see the ones she gets in red here:

mthfrsupport.com/yaskos-comp … r-23andme/

Dr. Ben

I wasn’t aware that Dr. Ben sold a genetc test so I took a look. It looks like he’s selling SpectraCell’s test (spectracell.com/clinicians/p … enotyping/ - $195), which just looks at two MTHFR mutations, 677 and 1298 mutations (23AndMe gets these).

It does come with a clear report (seekinghealth.com/media/mthf … report.pdf), but you can do this research yourself, particularly with the Genetic Genie wizard, which highlights whether or not you have mutations.

[Finatruth]

Droit- can you put this is the contect of the new study released on depleted neurosteroids in the CNS?

[moonman1]

That weird reaction I got to NAC I also get from Red Marine Algae. This really makes me think its a detox/herx reaction.

[bluejaysfan]

As in a good reaction, moonman?

I took NAC a long time ago and felt some positives… tried it again recently and it started out good, but, then was a negative on my erections so I stopped.

I have been debating whether curcumin is safe or not for us. I think the plain kind is. I’ve recently started taking 3 Now brand curcumin three times daily to curb a little chronic inflammation and I’ve noticed easier, harder and a bit more sensitivity in erections. It’s only been about 2 days, but, it was a good enough improvement to mention.

My guess is despite having good response to b12/folate… I may have not got enough if a handle on inflammation. Apparently it is important to ease that to get the most out of methylation. As far as I can tell, curcumin seems to work better than fish oil, or maybe would be a good addition.

I dont want to take ibuprofen and Tylenol is a complete no no.

I’ll see how this 3 a day curcumin holds up and report again towards the end of the week.

[chelated]

When you take fish oil (Omega 3) against inflammation and not for every day health maintenance you need at least (!) 10 capsules a day. Ideally double that. Just FYI.

[Xhorndog]

Just FYI, a fervently anti-omega 3 supplementation point of view:

raypeat.com/articles/articles/fishoil.shtml

excerpts:

Some of the important antiinflammatory effects of fish oil result from the oxidized oils, rather than the unchanged oils (Sethi, 2002; Chaudhary, et al., 2004). These oils are so unstable that they begin to spontaneously oxidize even before they reach the bloodstream. The most popular way of arguing that fish oil will prevent heart disease is to show that it lowers blood lipids, continuing the old approach of the American Heart Association’s “heart protective diet.” Unfortunately for that argument, it’s now known that the triglycerides in the blood are decreased because of the fish oil’s toxic effects on the liver (Hagve and Christophersen, 1988; Ritskes-Hoitinga, et al., 1998). In experiments with rats, EPA and DHA lowered blood lipids only when given to rats that had been fed, in which case the fats were incorporated into tissues, and suppressed mitochondrial respiration (Osmundsen, et al., 1998).

Considering that this thread centers on reducing oxidative stress, and fish oils are readily oxidized, it may be prudent to challenge the notion that Omega-3s are beneficial.

The belief that eating cholesterol causes heart disease was based mainly on old experiments with rabbits, and subsequent experiments have made it clear that it is oxidized cholesterol that damages the arteries (Stapran, et al., 1997). Since both fish oil and oxidized cholesterol damage rabbits’ arteries, and since the lipid peroxides associated with fish oil attack a great variety of biological materials, including the LDL lipoproteins carrying cholesterol, the implications of the rabbit experiments now seem very different.

Another way of arguing for the use of fish oil or other omega-3 fats is to show a correlation between disease and a decreased amount of EPA, DHA, or arachidonic acid in the tissues, and to say “these oils are deficient, the disease is caused by a deficiency of essential fatty acids.” Those oils are extremely susceptible to oxidation, so they tend to spontaneously disappear in response to tissue injury, cellular excitation, the increased energy demands of stress, exposure to toxins or ionizing radiation, or even exposure to light. That spontaneous oxidation is what made them useful as varnish or paint medium. But it is what makes them sensitize the tissues to injury. Their “deficiency” in the tissues frequently corresponds to the intensity of oxidative stress and lipid peroxidation; it is usually their presence, rather than their deficiency, that created the disposition for the disease.

[Xhorndog]

@bluejaysfan

I have been debating whether curcumin is safe or not for us. I think the plain kind is. I’ve recently started taking 3 Now brand curcumin three times daily to curb a little chronic inflammation and I’ve noticed easier, harder and a bit more sensitivity in erections. It’s only been about 2 days, but, it was a good enough improvement to mention.

My guess is despite having good response to b12/folate… I may have not got enough if a handle on inflammation. Apparently it is important to ease that to get the most out of methylation. As far as I can tell, curcumin seems to work better than fish oil, or maybe would be a good addition.

I dont want to take ibuprofen and Tylenol is a complete no no.

I’ll see how this 3 a day curcumin holds up and report again towards the end of the week.

Aspirin is an aromatase inhibitor. Peat has noted that both polyunsaturated fats and prostaglandins stimulate the expression of aromatase (testosterone into estrogen). Aspirin acts in opposition to estrogen by inhibiting COX enzymes (producers of prostaglandins), but also by suppressing inflammatory cytokines (which also increases aromatase) with salicyclic acid, a major component of aspirin.
Aspirin is an antioxidant that protects against lipid peroxidation and at high doses is able to “uncouple” mitochondria causing hyperpyrexia (increased body temperature; releasing energy as heat instead of ATP).
Aspirin decrease inflammatory cytokines (especially IL-6), which depresses thyroid, and increase prolactin, PTH, and estrogen.
Through a variety of mechanisms Peat has suggested that aspirin protects against the harmful effects estrogen, prolactin, serotonin, cortisol, histamine, and radiation.

Full article: dannyroddy.com/main/2012/1/6 … amide.html

More info: raypeat.com/articles/aging/aspir … ncer.shtml

I experimented a little with aspirin/k2, and it did help blood flow modestly.

[moonman1]

GeneticGenie.com has now added GSTT1 gene. Look like I may have a deletion on the entire gene. I suggest you guys run your 23andme data back through it and check out yours…

[i]

Glutathione S-transferase (GST) theta 1 (GSTT1) is a member of a superfamily of proteins that catalyze the conjugation of reduced glutathione to a variety of electrophilic and hydrophobic compounds. Human GSTs can be divided into five main classes: alpha, mu, pi, theta, and zeta. The theta class includes GSTT1 and GSTT2. The GSTT1 and GSTT2 share 55% amino acid sequence identity and both of them were claimed to have an important role in human carcinogenesis. The GSTT1 gene is located approximately 50kb away from the GSTT2 gene. The GSTT1 and GSTT2 genes have a similar structure, being composed of five exons with identical exon/intron boundari

[/i]

[droit]

As I’m sure everyone knows, cdnuts posted a recovery viewtopic.php?f=22&t=8271. It would appear that his regimen included: fasting (detox), clean diet/lifestyle, vitamins/supplements, and some kind of DHT supplementation/T-boosting.

I thought I would post an interpretation (with quotes from this post: viewtopic.php?f=22&t=8271&hilit=complex#p74297) in the context of this thread. This is of course a very narrow view and I am not advocating for using androgens.

@cdnuts

Take: B complex. Magnesium complex (the kind you dissolve in water works best) Fish oils. Take everyday at first, then go to every couple of days.

He took a B-Complex, which of course is core to the therapy we are borrowing from the CFS community.

@cdnuts

Meditate.

Meditation is relieving stress.

@cdnuts

Fast. Just once, for two weeks or more if you can.

Caloric restriction has been known to reduce oxidative stress.

nytimes.com/2009/07/10/scien … ction&_r=0
ncbi.nlm.nih.gov/pubmed/21109198

I think there may be some value in this in terms of clearing a very slow moving digestive system some of us have.

@cdnuts

****I also did several cycles of a DHT compound

One of the premises of the theory is that androgen deprivation causes oxidative stress. One of the observations we have on the labs and the neurosteroids papers is that 5-alpha-reductase is blocked up (I cited how OS could block 5AR here: viewtopic.php?f=27&t=7178&p=72779&hilit=reductase#p72779).

Its a reasonable leap that testosterone supplementation won’t convert to DHT in a PFSer… and I would worry if it would go down to estrogen. And I wonder if excessive testosterone would back up to estrogen. But DHT is not convertible to T or estrogen. I’ve wondered what effect DHT supplementation would have on relieving the oxidative stress.

Here is the most related paper:

“Effect of dihydrotestosterone on mouse embryonic stem cells exposed to H2O2-induced oxidative stress”

ncbi.nlm.nih.gov/pmc/articles/PMC2811836/

In this context, the methylation protocol banks on reducing oxidative stress will unblock 5-alpha-reductase. But there may be another vicious cycle, where lack of androgens causes oxidative stress, but oxidative stress keeps androgens down.