Comment · Sat, September 2, 2023 · Nootropics Depot & Natrium Health
High Testosterone and High Prolactin
Original post in this thread
xxrbexx · 38 points
I’m a 44(M) and I’ve been taking Tongkat Ali and fadogia agrestis for 7 months now. I used Let’s Get Checked and my Testosterone is high and so is my Prolactin. They were both high with the last test in April too. Anything I search has nothing about both being high at the same time, only that when one is high the other is low.
What they were answering
thespaceageisnow · 1 points
From 2019:
“Strong accumulation of pyridoxine (PN) in CSF of PLP-treated patients was observed, suggesting the existence of a PN-forming enzyme. Our in vitro studies show that all cell lines reduce PL to PN in a time- and dose-dependent manner.”
https://www.sciencedirect.com/science/article/pii/S0304416519300753
Pyridoxal 5′-phosphate can convert to Pyridoxine in the body. It personally happened to me after long term exclusive P5P supplementation I developed peripheral neuropathy.
It’s not worth the risk seriously. B6 is shit at treating almost anything except a deficiency anyways.
u/MisterYouAreSoDumb · Nootropics Depot & Natrium Health
That study was not testing peripheral neuropathy patients. It was testing a handful of children taking P5P as treatment for other issues.
B6 is shit at treating anything anyways.
Literally in the study you linked, some of the children were keeping their seizures under control with P5P supplementation! This is on top of anemia and nausea and vomiting during pregnancy, and ironically, neuropathy... If it was shit at treating anything, why are doctors prescribing it to millions of patients? Saying P5P is shit at treating anything is just ignorant. Moreover, they have given P5P to people experiencing peripheral neuropathy from high pyridoxine supplementation, and it treated them! That's because peripheral neuropathy from high doses of pyridoxine manifests as B6 deficiency, because it is about pyridoxine inhibiting P5P in the body.
As I quoted above, 96% of case reports of peripheral neuropathy were from pyridoxine supplementation. I will quote again.
Hence, not only the dose, but also the vitamer present in the vitamin B6 supplements is important for the development of such adverse health effects. This is also presented by the data from Lareb, showing that more than 96 % of the reports is due to the use of PN in the supplements. The fact that the vast majority of the available vitamin B6 supplements contain PN must be taken into consideration here.
This is scientific research, not anecdotes online. Could the remaining 4% have some specific mutation that means they react differently? Sure, that is possible. That doesn't mean we go around trying to convince the other 96% of people to stop taking P5P!
PDXK mutations cause polyneuropathy responsive to pyridoxal 5′-phosphate supplementation
So perhaps certain mutations play a role in the response to P5P supplementation. However, the data is clear. P5P does NOT cause peripheral neuropathy in the vast vast majority of people. In fact, it treats it! My neighbor is a physician that has been treating peripheral neuropathy for the past 20 years, and he gives P5P to all his patients. He sees significant improvement in 95% of them. Telling people experiencing peripheral neuropathy to stop taking P5P is ill-advised for the vast majority of people.
There is evidence that not getting enough protein in your diet plays a role in whether you get toxicity from B6 supplementation.
Pyridoxine \(Vitamin B6\) Neurotoxicity: Enhancement by Protein-deficient Diet
In that study, they only saw toxicity from pyridoxine in the animals fed low protein diets. Moreover, they injected large doses of P5P and did NOT see any toxicity at all, even in the low protein diet group. They discuss the factor of protein binding on the toxicity of pyridoxine as well. There is also evidence that pyridoxine toxicity to sensory neurons is due to a lowering of P5P centrally, likely through inhibition of PDXK, which results in disrupted GABA signaling. This is likely because l-glutamic acid decarboxylase is a pyridoxal 5′-phosphate-dependent enzyme responsible for the formation of GABA. Taking too much pyridoxine can inhibit P5P formation, which then goes to lower GABA concentrations, causing glutamate toxicity. Again, taking P5P solves this. This is the prevailing theory right now. Could a very small number of people have some specific mutation we have not discovered yet, which leads to issues from P5P supplementation? Sure, anything is possible. We are complex organisms. However, the preponderance of the data is clear. B6 toxicity is caused by taking too much pyridoxine in the vast majority of cases, and in those cases, taking P5P can help counteract it. Saying that nobody should be taking P5P is unscientific and dangerous, and you should stop doing it.