So both increase dopamine levels in the brain yet one increases receptors while the other decreases them? I dont disagree with those statements but I dont think they tell the whole story either.
I agree that somehow our dopamine production/sensitivity may have been affected so I took this test about a week ago:
The NeuroAdrenal-Basic from this page that tests dopamine, GABA, Serotonin etc…through saliva and urine. I ordered through a local physician so Im not sure how to order from the site but it was about 250 dollars. I have no idea how accurate these things are so I might do it a few times to see if I can establish consistency, or maybe even some progress. Meanwhile, I should get the results back in a week or so…
You realize your source comes from an anti-marijuana campaign that is run by the government? There has been a lot of marijuana misinformation created by the government for the express purpose of frightening kids away from it, classifying it as a schedule 1 drug just the same as HEROIN, COCAINE, AND METHAMPHETAMINE. Overloading dopamine is the way they get kids to fear “drugs”, because kids understand what dopamine is. In fact the cannaboid system is much more complicated than this and marijuana has many active cannaboids (something like 400+). It is just beginning to be studied. So you cannot boil this down to dopamine alone, especially when researchers without government anti-drug agendas suggest the opposite. Keep in mind this is the same government that approved FINASTERIDE as a safe and legal drug for our use and got us into this mess in the first place.
Here’s a link and a graph of some properties of cannaboids (many more exist if you want further info):
To the second point, I have seen the same symptoms on a number of other sites. Stopthethyroidmadness has some similar ones. Not all of white collar america is suffering as bad as we are, but many are searching these things online and not broadcasting it to the world. I have a relative that works at the department of health and human services. He said one of the statistics that was brought to his attention when he joined is the high amount of self and fad internet diagnosis. And no wonder, people feel worse and most doctors are arrogant pill-pushing idiots. Just because you were the anti-thesis of these symptoms pre-fin doesn’t mean that the general population is healthy and mirroring your experience. Obesity is constantly rising. The number one calorie source in the USA comes from high-fructose corn syrup in beverages. There are a lot of people out there on “maintenance” medications which slowly wear out the body. I’ve seen a stat that says 1/5 but cannot find it. Before fin I wouldn’t mind discussing society’s ills but honestly I don’t have the energy anymore.
You’re right. Dopamine’s importance cannot be understated. I’m feeling like everything’s importance cannot be understated though. My point is how little we really know. If you find dopamine as a cure and it works for you I’m on it. However I took tyrosine and didn’t get cured. It made me feel good and a little high for a week then it stopped working too. It was very similar to when I first took magnesium. However it didn’t give me full functionality back like marijuana did. I don’t think fin just fucked our dopamine system. I think it went deeper and altered enzyme production that gives the body the ability to make, use, and store energy. It also interrupted our natural hormonal loop which got stuck on the wrong level.
Regarding exercise, I’ve reached a point where the more exercise I do the tighter my muscles get. If it is supposed to upregulate dopamine receptors, why is long term moderate exercise making me feel as if the dopamine is leaving my body?
The biggest problem we all have was a minor knowledge of the human physiology. We took this knowledge and used it not knowing the consequences. Now we’re trying to figure it out by looking at individual solutions when in fact finasteride could have blocked multiple enzymes we don’t even know about down to the cellular level leaving us with ignorance and inability to test.
still new to this, but i think learning quickly. i got on the dopamine idea because of my high prolactin levels. ie. high prolactin usually accompanied by low dopamine, when its not high enough to be a prolactinoma, just the general lack of joy or feelings from anything and because my body wants to smoke cigarettes more than ever and i am happier when i have a drink or two (have stopped all together now) than i used to be from drinking. All points to low dopamine.
Anyway, Just asked Dr. Jacobs to write me a script for this test so i can get it done locally.
Wondered if you got results back and what they were etc?
I did and quite a few of the results got my attention. This test was pretty comprehensive however it did not include the inhibitory neurotransmitter taurine. The NeuroAdrenal-Expanded panel which I just ordered does. Also, it tests for dopamine and serotonin metabolites to assess receptor activity.
Results:
All descriptions were condensed from either my provider or the neurorelief website.
Excitatory Neurotransmitters:
All are low range or below
Epinephrine: 7.5 {7-12} All units are microg/gCr unless specified
A bit low but not notably so. Supports stress adaptation, sustained energy level, and mood.
Norepinephrine: 21.8 {30-45} Low
Helps with stress adaptation while supporting energy levels and mood again. Low Epinephrine and Norepinephrine contribute to fatigue, low stress adaptation, low mood, lack of focus/concentration, and poor memory. Low levels of Norepinephrine specifically contribute to feeling overwhelmed and subsequent anxiety.
Phenylethylamine (PEA): 37.6 {30-70} nMol/gCr
Supports mood and again, helps sustain energy levels.
Histamine: 9.4 {14-24} Low
Has the function of “pacemaker” in the brain. Regulates levels of Epinephrine and Norepinephrine.
Glutamate: 15.5 {15-32} microMol/gCr
Primary excitatory neurotransmitter responsible for most neurotransmission. Essential for thinking and memory. Low levels associated with “fuzzy thinking”, slower cognitive processing, fatigue, and inborn amino acid metabolism errors.
Inhibitory Neurotransmitters:
All are elevated save one.
GABA: 7.7 {4.7-7.0} microMol/gCr High
The infamous GABA. Major inhibitory neurotransmitter in the brain.
Glycine: 1133.2 {455-980} microMol/gCr High
Inhibitory neurotransmitter much the same as GABA but operates primarily in brain stem and spinal cord.
Serotonin: 39.7 {120-185} Extremely Low
At one third of the low end my Serotonin was by far the most striking result. Essential in maintaining balance between excitatory and inhibitory neurotransmitters which is obviously offset. Depression, fatigue, anxiety, irritability, insomnia, decreased pain tolerance, impulsivity, hypoglycemia, and insulin resistance can all be attributed to low serotonin. Sugar can temporarily raise tryptophan (serotonin precursor) crossing blood brain barrier so a craving for sweets could be sign. GABA and Glycine are elevated to compensate for low serotonin (or vice versi).
Dopamine: 152.3 {115-175}
The only neurotransmitter that is solidly in range. Dopamine gets its own category because it is both inhibitory and excitatory depending on the region of the brain it is acting. Normal urine levels may not tell the whole story and true synaptic level could be lower because low Serotonin decreases Dopamine turnover and excretion. This will hopefully be assessed along with serotonin turnover by the expanded test. I would be very surprised if my dopamine processing is completely normal due to what I percieve to be decreased reward pathway sensitivity.
Adrenal Hormones:
All elevated in response to persistent stress.
Cortisol:
Morning: 14.7 {7.0-10} ng/mL High
Midday: 8.4 {3.0-6.0} High
Evening: 4.5 {2.0-4.0} High
Night: 2.3 {<1.5} High
Stress produces an increase in HPA activity however this increase in turn creates negative feedback where Cortisol turns down the HPA axis. Persistant high cortisol is neurotoxic in the hippocampus as well as other areas of the brain. Cortisol increases neuron excitation through interference with GABA receptor. GABA and Glycine are elevated further to compensate for this. From wikipedia excessive cortisol shuts down the reproductive system and reduces Serotonin and Glutamate in the brain. When HPA finally becomes dysfunctional cortisol drops but production will be unregulated throughout the day. This is a more advanced case of adrenal fatigue than my results show. Symptoms of elevated cortisol are fatigue, decreased energy, impaired memory, insulin resistance, insomnia, anxiety, impaired concentration, restlessness, and feelings of hopelessness.
DHEA: 672.0 {250-578} pg/mL High
The most important androgen in our bodies. Dont know if there can ever be too much but high level is another indicator of adrenal stress response. My body shouldn’t need to circulate this much and this level is probably unsustainable.
I should point out that these samples were taken about two months ago. Since then I have been following my providers instructions and have been supplementing with various amino acids and supplements. Specifically those that support the adrenals and Serotonin production as well as the standard multi-Vs etc…I should have results from the advanced profile in a couple of weeks.
The second study cited by the OP here indicates that increased GABA paradoxically increases Dopamine receptor sensitivity. This leads to me to wonder the following:
We are not low on dopamine, but our dopamine receptors have become desensitized due to decreased GABA levels caused by fin’s inhibition of progesterone to allopregnenalone.
Tyrosine may help in the short term, but its effects will fade as “supplemented” dopamine causes dopamine receptor downregulation.
PFS sufferers don’t lost zest for life because of dopamine, but low GABA causes anxiety, and secondarily, natural dopamine and supplemented dopamine to be ineffective.
Ineffective dopamine due to receptor desensitization creates longer refractory period (dopamine not as effective against prolactin, so even normal prolactin levels are problematic because dopamine cannot act properly).
Xyrem and other GABA modulators are may have more effect that initially thought.
Hey guys, long-time lurker, first time poster. I’ve never used Propecia, but was on TRT for 4 years, and gradually became tolerant to the effects of Testosterone, eventually ending up with complete loss of libido. This was despite all labwork returning normal (TT, Free T, E2, androgens, etc). I realize my situation may appear different from those on this board, but I am starting to believe that though the origin of my libido loss may be different, the underlying issue is the same–a mismatch of Dopamine levels and Dopamine receptors in the brain.
This is pure speculation of course, but reading this thread, a few personal observations seem to support the dopamine receptor downregulation hypothesis. I have been tolerant to the effects of supplemental Testosterone for a few years now. Not only libido, but even secondary sexual characteristics like muscle wasting, dry skin, etc. 2 years ago, I was taking 100mg/wk Testosterone injections as part of my TRT, and developed a temporary but strong coffee habit, consuming upwards of 15-20 cups a day for a month. I had a full caffeine tolerance at this point as well–I could drink as much coffee as I wanted and fall asleep right after.
When I returned home, I went cold turkey. That resulted in 4 days of the worst migraines of my life, as my dopamine levels crashed (speculation). I also stopped Testosterone replacement at this time in order to do a reset of my HPA, as per my physician. I resumed Testosterone replacement with Androderm instead of injectable, to see if another form of delivery would affect libido. Well my libido skyrocketed higher than it had been in years. This lasted a month before dropping off.
Now this could easily be theorized that the libido increase resulted from the transdermal Testosterone delivery, which increases DHT much more than injectable form. But I had been on doses of injectable Testosterone as high as 300mg/wk, which should have resulted in higher DHT, yet never increased my libido at all. I had a full tolerance to supplemental Testosterone. It was only when I went through severe caffeine withdrawals that I had a sudden surge in libido.
I speculate that the caffeine withdrawal increased Dopamine receptor levels, which re-sensitized my brain to Testosterone, restoring libido temporarily. After a month, the surge in Dopamine levels from Testosterone may have once again downregulated the amount of Dopamine receptors, bringing me back to the old state of loss of libido. Again, this is pure speculation, as I didn’t do the proper blood testing to back up my anecdote with data, but it does offer a better explanation than has ever been offered to me by any Endocrinologist or physician.
Former, have you, or do you plan on experimenting with Xyrem or any other dopamine antagonist? I thought of Seroquel as well, since it is a Dopamine antogonist but which has a few benefits, including possibly not raising Prolactin levels too much. From Wikipedia:
Seroquel also has a short half-life of only 6 hours, making it perfect to take before bed (it is commonly used as a sleeping pill). I’m hypothesizing that if someone were to take a Dopamine antagonist during sleep repeatedly, it may increase Dopamine receptor levels and resensitize the brain to Dopamine, allowing Testosterone to have the proper effect on libido. I’m not suggesting anyone be the guinea pig on this idea, but maybe there have been studies done on this effect that we could look to for further confirmation.
We aren’t depressed but we do have a lot of symptoms of depression. I have the anhedonia part of depression without actually feeling depressed. I think depression comes in many flavors
I’ve been thinking about this theory, and i don’t think using an anti-psychotic would help increasing dopamine receptors. People with ADHD, are supposed to have less dopamine receptors, but using an anti-psychotic has never been something considered for adhd.
I took Seroquel and it helped me sleep, unsurprisingly. Made me feel like a zombie though, and put on a lot of weight. Didn’t help with any PFS symptoms at all, apart from reducing fatigue due to better sleep, for which I was initially grateful. I wouldn’t recommend it to anyone.
Yes I stopped feeling like even more of a zombie than I did with pfs.
It helped with sleep and fatigue and when I came off I managed to be able to sleep more or less a full night not long after. But I don’t think this can be attributed to the drug. No other benefits in brain fog or sexual sides.
Guys these thread is amazing, continue with it pls! I will look for dopamine antagonist. ( I just bought L-tyrosine before reading this thread!, Would be experiencing with it a litle )
all studies ive seen point to fact that during finasteride use, dopamine levels are altered and increased. i just read in a thread somewhere else here, someone mentioned that someone who took finasteride, their libido was 10/10 and stronger than it usually is. this would make sense if dopamine is increased while on the drug. however, once the drug is stopped from being used, one would think that the dopamine would be decreased. perhaps a dopamine “tolerance” was much higher than normal and that tolerance has not been adjusted after the drug has been discontinued. similar to how some recreational drugs increase dopamine, then the user needs the drug itself in order to “feel normal” again.
fasting (long talked about on this forum for it’s positive benefits) is one of the few things that increase dopamine receptors and help to normalize this system. i believe going carb free has a similar effect (2 recoveries, Chi & IHP both went carb free for long periods of time in order to treat and effectively cure PFS)
I have been on wellbutrin XL 300mg the whole time, it is a dopamine reuptake inhibitor and non-selective, also nueropenepherine, it is an amazing antidepressant. It is the only one I know of that always works and doesn’t make you numb and increases the libido, focus, makes you lose weight, gives you energy. If you take it just make sure to take brand name only or the generic that is a white round hard pill that looks just like the brand name one, the other generics do not work right at all. Not just my opinion, the opinion of zillions of people on the net, even the FDA recalled the oval generics, but they are back out there. Often when people have bad experiences with wellbutrin XL it is because they took the bad generic. If I take the oval shaped generic I feel like shit, I highly recommend this drug.
Yeah, 9 years on finasteride, towards the last 2 years of my use, I was incredibly horny, all I talked about was sex, the closer I got to crashing the higher my libido was, really incredible libido and then of course, penis goes dead, and PFS started.
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