My doctor mentioned a new theory last week - that Finasteride might have damaged the mitochondria.
He found a paper stating that mitochondria are involved in Finasteride metabolism, and other papers discussing drug-induced mitochondrial damage. Finasteride was not listed as a drug which does this, but the range of drugs is pretty huge.
Most of the info I’ve read about mitochondrial damage so far relates to fatigue and CFS. Although this caught my attention:
“… damage caused by mitochondrial failure such as immune disturbances resulting in allergies and autoimmunity, poor digestive function, hormone gland failure, slow liver detoxification.” drmyhill.co.uk/wiki/CFS_-_The_Ce … al_Failure
There is no doubt this is happening in PFS, but I am not sure it is because of Finasteride metabolism in the mitochondrial.
Mitochondrial membranes get eaten up by oxidative stress/free-radical damage, which is normally maintained by glutathione (1,2 and many many more).
You will have to read the Methylation-Cycle/Glutathione thread (viewtopic.php?f=27&t=7178&start=240#p74980, we’ve gotten one more since this post) which clearly show a shift in the glutathione levels (reduced ‘GSH’ vs. oxidized ‘GSSH’).
The ratio of GSH to GSSH is a direct indicator of the oxidative environment of the cell. Depleted GSH and elevated GSSH means an oxidative environment, which is what we are seeing on this test.
These measurements have massive consequences on many things touched on in the thread including basic enzyme biochemistry in the cell and, as you’ve said cell/mitochondrial membrane health.
Since your doctor sounds engaging, you may want to tell him that: a handful of people on our forum have consistently, with very little standard deviation, found they have dysfunction in the methylation cycle and depleted glutathione.
You can tell him about the Methylation Protocol we’ve borrowed from the CFS community, but we are looking to extend it for us. He may have a colleague that is interested in this area and may be able to help.
“Mitochondrial impairment as an early event in the process of apoptosis induced by glutathione depletion in neuronal cells: relevance to Parkinson’s disease,” sciencedirect.com/science/ar … 5297006473
if one of the problems is oxidative stress in the mitocondria why do I have a mini crash after taking antioxidants for a few days?
In my case, I experienced mini crashes with these supplements taken one at a time: fish oil, astaxanthin, and Ubiquinol QH. At first I thought it was because of inhibiting the DHT, but my lab test show a high DHT, and Ubiquinol is not an 5ar inhibitor. I repeated the experiment with Ubiquinol QH alone and I crashed again after a few days.
Any idea?
I see, “Antioxidant paradox” is when supplementation of antioxidants does little or nothing to cure oxidative diseases. In our case though, supplementation of antioxidants does not only nothing but makes things worse. Has it always been the case for you or did you have ups and downs? I only had downs so far with antioxidants.
Maybe the autolysis that happens during a serious fasting would help restoring the mitocondria to an optimal status, but it’s just an hypothesis.
Thanks for the summary of your research and pointing me towards your thread.
Mitochondrial damage could certainly be caused by reduced glutathione, rather than directly by Finasteride metabolism.
I’ve actually been taking a few of the supplements in the Methylation Protocol for a while.
I had low serum B12 (356) back in December and took a sublingual B12 supplement for 3 months - “Biotics B12 2000” containing 2000 mcg hydroxocobalamin. This didn’t raise my B12 level so I switched to a different sublingual product for another 3 months - “Jarrow Formulas Methyl B12 5000” containing 5000 mcg methylcobalamin. This raised my level to 1355 (range 200 - 835). I haven’t tested methylmalonic acid yet, so I could still have a functional B12 deficiency.
I was also low in CoQ10 and began supplementing in January with “Bio Life Co-Q10”. My initial level was 614 (range 670 - 990) and it increased to 927 after 3 months. I stopped supplementing and it dropped back down to 405. I’m now taking it again.
My current regimen includes Pure Encapsulations B-Complex Plus (which contains Metafolin L-5-MTHF) and BioCare B6 which provides the active form pyridoxal-5-phosphate.
I’ll email my doctor about your findings and get his thoughts. I might try and get the Methylation Panel test myself too.
Thank you for your update. That’s pretty cool that you have been taking this protocol incidentally. If you want to see what the others have been taking there is a thread dedicated to this here:
Its valuable to hear of the effectiveness in Jarrow’s B12 in raising serum levels. Just make sure to consider my note here about the vagueness of serum levels:
I’ll add that CoQ10 is synthesized by the Methylation Cycle. I think I’ve cited a paper figure at one point in the theory thread showing those reactions.
I would expect someone with a methylation block to have low CoQ10 for this reason. However, AnnonXXX was one anomaly in that he had normal CoQ10 per a Metametrix test then later took the Methylation Panel and showed the classic methylation block/glutathione depletion.
I would have to ask him what he was taking that could have masked this indirect marker. He also had normal methylmalonic acid.
You can read a summary of his pre-Methylation Panel tests here:
Also, make sure to experiment and note your experience with B6. I’m unsure what is right for our population. B6 is the coenzyme for the enzyme (CBS) that drains metabolites from the methylation cycle.
From the genetic data, many of us already have up-regulating mutations in that enzyme so providing more co-enzyme worries me.
You can probably tell in a couple of days whether stopping or restarting it makes you feel better. It personally makes me tired.
Speaking to medical professionals about any relevant data is very valuable. The conventional practitioners typically don’t know much about this stuff, but who knows this Dr may have resources in this area. I am excited to hear what you dig up.
Please update us with any data on the Theory or treatment thread depending on what is appropriate and let me know if you need anything.
