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Can Finasteride/Propecia Cause Neurological Disorders?

Ever since I have stopped taking finasteride (early 2018 and now as of April 2019), I have been very fascinated with the research that I’ve found online from various scientific articles, forums, and various opinions from doctors and users. I’m sure that there’s a lot of people who are cautious and hesitant when considering taking finasteride, and since this usage of this drug for MPB is so controversial, I like to talk about it and hear from both sides. As you are aware, I stopped taking finasteride early April of this year. Just to be clear, I did NOT have any of the known side effects while taking finasteride for 4 months (back in 2018). Some of the most common side effects include sexual dysfunction, depression, congnitive function, brain fog, decreased libido, and shrinkage in the sex organs. I did stop taking finasteride due to the information that I have gathered online and studying about various effects on neuro-hormones finasteride alters in the central nervous system. Now, I am not trying to convince anyone to take or not to take finasteride. Taking this drug is elective and each person is obligated to do what he feels is necessary when introducing drugs to their body. This video is simply based on my very own research done from available sources online, so please take it with a grain of salt.

So finasteride inhibits two 5-alpha reductase isoenzymes (types II and III). 5AR1 is found mainly in the brain, muscle, liver, and sebaceous glands. 5AR2 can be found in the prostate, seminal vesicles, liver and hair follicles. A lot of people are under the misconception that since finasteride doesn’t inhibit type 1 (which is found in the brain), it doesn’t affect the brain. However, 5AR2 is also expressed in very significant amounts in spinal cord motor neurons, in similar amounts found in the prostate.

The isozymes of 5AR converts Testosterone -> Dihydrotestosterone and Progesterone -> Dihydroprogesterone.

The conversions are inhibited by finasteride and so the production of neuroactive steroids is inhibited, since their metabolic pathway continues like this:

Dihydroprogesterone -> Allopregnanolone

These converions are catalyzed by an enzyme called 3-alpha hydroxysteroid dehydrogenase (3-alpha HSD).

Now we come to the REAL issue: The inhibition of Allpregnanolone production. Although Allopregnanolone (ALLO) can be produced in the brain by 5AR1, the CNS is also dependent on peripheral 5AR2.

Finasteride inhibits allopregnanolone production in spinal chord motor neurons where mainly 5AR2 is present and also reduces allopregnanolone levels in the brain and other parts of the CNS since these parts are dependent on peripheral 5AR2 conversion of progesterone to dihydroprogesterone which is then converted to allopregnanolone by 3-alpha HSD.

So why is ALLO so important? Well, allo increases neurogenesis, improves performance of learning and memory, regulates emotions, enhances myelination, and having the proper level of serum ALLO can prevent neurodegeneration which can lead to many neurological disorders.

The question is what the result of long-term allopregnanolone depletion is as ALLO has vital function in the myelination of neurons and how progressive loss of neurosteroid synthesis may contribute to neurodegeneration. According to research done by reseachers at John Hopkin’s, pregnant women with low levels of ALLO experienced mood disorders such as anxiety and depression, which seems to correlate with some of the side effects of finasteride. Low levels of ALLO can be observed in patients suffering from neurological disorders such as Multiple Scroleris, Parkinson’s and Alzheimer’s. Now, while low levels of ALLO are found in patients suffering from the said neurological disorders, there is no direct link between the use of finasteride and these disorders. (it’s also in the same sense that people suffering from MS/heart disease also have low levels of vitamin D; having low levels of vitamin D does not mean you will get MS, although it can definitely increase your chances of getting certain illnesses over someone who has normal levels of vitamin D). However, we can merely speculate that this is a possibility since low levels of ALLO can be seen in finasateride users and in people suffering from various neurological problems, and structural alternations of myelin, whether by genetics or through the environment or medication, might occur in early stages of neurological diseases.

Some studies demonstrate that neuroactive steroid production (neurosteroids like allopregnanolone, which is vital for myelination) is increased when the spinal cord is injured. This is the body’s reaction to the damage (in this case demyelination in the grey matter in the spinal cord). Usually this works perfectly in a healthy man in order to prevent such an advanced irreparable demyelination.

While using finasteride, you not only can possibly cause neurological damage by inhibition of neuroactive steroids but you don’t let your body recover by a natural response of increased neurosteroid production by 5AR2 because you are inhibiting what is meant to heal you!

Since nobody has really studied the long term neurological effects of finasteride, users are merely test subjects on what unknown effects finasteride can lead to due to allopregnanolone depletion. Another thing to consider is what levels are considered dangerous for allopregnanolone and if discontinuation of finsateride can result in reversing the allopregnanolone depletion in the CNS. Obviously we need more research done on long-term finasteride users and how it can affect the CNS as neurological diseases can take decades to develop. Although there is no concrete evidence, we can only speculate that due to this, some people are experiencing slurred speech, balance and cognitive awareness as well as brain fog and it’s good to speculate and see how these issues can perhaps be tied with the use of finasteride.

The difficulty about long-term research on the use of finasteride is that it is costly and there’s so many strict criteria that research studies have to adhere to. There can be issues with people who take other forms of medication that can alter the research, or defects in their genetic make-up that can skew the studies, so it really is difficult to get a true understanding of finasteride’s effects. And while there are long term studies done on finasteride, they don’t research the nuerological effects in the CNS.

 If you are someone who has discontinued the use of finasteride, omega 3s (fish oil – helps with neuronal growth and repair), antioxidants such as grapes, blueberries, pomegranate juice, and regularly exercising appear to be beneficial. It may also be a good idea to get an MRI done to see the extent, or lack of, damage done to the spinal cord. But in another video, I will talk about how you can increase your allopregnanolone levels through food and supplements. The good news is that, based on my research, nobody has suffered from MS, Parkinson’s/Alzheimer’s based on the use of finasteride.

In conclusion, there is no concrete evidence that the use of finasteride and depletion of allopregnanolone leads to any neurological disorders. However, we can only speculate from the given information and research done and attempt to piece together how it CAN affect the CNS and to understand why some people suffer from neurological symptoms when taking the drug due to hormonal imbalances in the body. Ultimately, If you are tolerating the medication and feel that the potential benefits outweigh the potential risks, then stick with it. And if the benefits are not sufficient to outweigh the alteration in your body’s chemistry, then I would say less (aka no medication) is better… I wish there was a clear answer, but in situations like this, it’s up to you, your comfort level and your needs.

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