Dht lowering medications

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Well here I go again,with another testimonial about another doctor appointment gone wrong. Yesterday I went to see a urologist,who told me I have a slightly enlarged prostate. I asked him about the effects of dht, and if there are any drugs to combat it. He told me there are a couple but they have bad side effects .Furthermore he said they don't stop the growing of the prostate. He wrapped up by giving me a follow up appointment in 1 year ,and an x-ray in one year. I asked for an MRI sooner but he refused. I want to ask if anyone has or us currently taking effective medicine for both?
 
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No my doctor actually said there were no drugs to reduce dht. He said it is something I have to live with as I get older. I get up 2-3 times a night,but in truth I drink over a gallon of green tea water around 5 hours before I go to bed. When I don't drink it,I get up 2 times
 
Oh,my psa was2.50 in June. The reason I wanted an MRI is it is more accurate in assessing size of prostate . I wanted a more objective test,rather than a generalization by the doctor
 
Thank you,appreciate it. Guess just reduce 5 alpha reductase enzyme
I came into all this with PFS. 5AR does a lot more than just turn test to DHT. Plenty of guys are fine with it but the ones that aren’t, like me, are really, really, life alteringly not fine with it in ways that never go back to normal.
 
Ya like @Anonymon said, reducing the 5ar enzyme with a synthetic drug is NEVER a good idea. It does a lot more than just reduce the conversion of test into DHT, again like he said.

And like @Vais5 said, I’ve also seen positive anecdotes of guys using progesterone cream on their taint to reduce enlarged prostate symptoms. This is the route I would try first if I were u. U have nothing to lose by trying it, and it would also be very cheap to give it a shot
 
You guys are saying finasteride does a lot more than reduce DHT ?

 
You guys are saying finasteride does a lot more than reduce DHT ?
What else does it do ?
Finasteride just blocks the 5ar enzyme. So it’s gonna mess with any processes that involve the 5ar enzyme to convert one molecule into another. The two main conversion processes that im aware of have to do with DHT and progesterone. Here’s a pretty good Reddit article talking about it

 
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Finasteride blocks 5AR type 2, not both 1 and 2. Here are the full list of conversions:

Cholestenone → 5α-Cholestanone
Progesterone → 5α-Dihydroprogesterone
3α-Dihydroprogesterone → Allopregnanolone
3β-Dihydroprogesterone → Isopregnanolone
Deoxycorticosterone → 5α-Dihydrodeoxycorticosterone
Corticosterone → 5α-Dihydrocorticosterone
Cortisol → 5α-Dihydrocortisol
Aldosterone → 5α-Dihydroaldosterone
Androstenedione → 5α-Androstanedione
Testosterone → 5α-Dihydrotestosterone
Nandrolone → 5α-Dihydronandrolone

I’m not entirely sure how type would affect what converts what, but there appears to be at least some substantial overlap because dutasteride inhibits type 1 and type 2 and reduces DHT even further than finasteride despite finasteride still hitting it pretty hard. Could also be dose related I suppose, but that’s less likely. Plenty of guys like me with PFS have documented issues with allopregnenolone and cortisol and testosterone, and things that overlap with that, such as thyroid levels. If you mess up any one of those hormonal axises you can easily throw the others off.

5AR seems self perpetuating, so if someone starts on test to a super high level and uses it, they seem to be a lot more protected from it, like bodybuilders. Maybe not all but many.

If any of the above get thrown off, you can also cause other issues to form that are further complications of it, and things can cascade from there, as it did with me. It’s not something to be taken lightly. The old wisdom used to be that if it messed something up it’d be your testosterone, so you’d just hop on gear and be fine. That’s decidedly not true and in many people makes things worse.

In general, 5AR’s amazing and if I could do anything it’d be to increase it.
 
Thank you,appreciate it. Guess just reduce 5 alpha reductase enzyme


The most common side effects of 5-ARIs include impotence, decreased libido, ejaculatory disorders, and gynecomastia.14 Less common side effects that have been reported include infertility, breast tenderness, depression, anxiety, dementia, and suicide. 15-18



*Changes in neuroactive steroids following 5-ARI use can lead to dysfunction of the dopaminergic system, reduction of hippocampal neurogenesis, an increase in neuroinflammation, alterations of the HPA axis, and epigenetic modification. Moreover, the alterations of the neuroactive steroids, especially AP, are also linked to the alteration of central nervous system receptor functions including dopaminergic receptors, GABA-A receptors, estrogen receptors, and androgen receptors



*The term post-finasteride syndrome was coined by some men to describe the persistent symptoms (sexual and non-sexual) that they developed in the setting of using or stopping finasteride. The most commonly reported symptoms include low libido, erectile dysfunction, loss of penile and scrotal sensitivity, decreased ejaculatory force and volume, reduction in penile size, anhedonia, depressive symptoms, anxiety, decreased concentration, reduced muscle mass, and fatigue.3

*According to the public dashboard of the FDA’s Adverse Event Reporting System, as of June 2021, there were 10,295 serious adverse events for finasteride. It is well established that most adverse medication events are grossly underreported.8 Importantly, three of the four most common reaction types are related to sexual dysfunction: erectile dysfunction, sexual dysfunction, and decreased libido




*In a large series, we replicated Khera’s findings of persistent physical sequelae associated with changes in SF in men after DC FIN. While more research is needed, this population is young, ED is most often severe, and testing shows a high prevalence of vascular, neurologic, and hormonal pathologies



*Significant literature indicating that 5a-Rs and 3a/3bHSORs are widely expressed and distributed in various regions of the nervous system suggests a critical function of these enzymes in the effects exerted by testosterone and its metabolites. Indeed, 5a-Rs catalyze a key rate-limiting step in the formation of 5a-reduced neuroactive steroids and, therefore, is critical in maintaining the physiological function of the nervous system. Indeed, T and its metabolites are implicated in processes of neurogenesis, myelination and remyelination, neuroprotection, and attenuation of neuroinflammation. Furthermore, these metabolites play an important role in the reduction of stress responses and modulation of behavior





*Circulating testosterone is converted in many peripheral tissues to its two active metabolites, 5α dihydrotestosterone (DHT) and 17β estradiol (E2)

*In many androgen-responsive tissues, a family of steroid 5α reductase enzymes converts testosterone to DHT, and the aromatase enzyme, a product of the CYP19A1 gene, converts it to E2

*Many tissue-specific biologic effects of testosterone are mediated through DHT and E2

*The rates of conversion of testosterone to DHT and E2 vary among people due to polymorphisms of genes that encode the steroid 5α reductases and the aromatase enzyme as well as other host-specific factors that affect the activity of these enzymes

*It is not known how the circulating concentrations of testosterone’s metabolites – DHT and E2 – modulate the effects of testosterone on various outcomes and how their circulating levels rank in their contribution to the observed effects of testosterone treatment on physiologic outcomes
 
On the dopaminergic front, a lot of the things I’ve had success with are highly related to that, and the ones I haven’t done well with are at times noted to increase serotonin, which is your dopamine is too low isn’t great.

Pregnenolone can do a lot related to PFS but has studies showing a dose dependent increase in dopamine response to stimulus. I didn’t get much out of lower doses but on 400mg I like it. Selegiline, an MAO-B inhibitor, also helped immensely, particularly when combined with that, but I’d be careful with that one. Currently coming off it because it appears to interact poorly with my levothyroxine/T4, and was the cause of massive cramps and rapidly increased intestinal movement that was too much for me. Before getting T4 back it was all great, sans having to be careful not to get too caught up in trivial things since everything felt great. Without enough T3, I feel like crap, and without T4 alongside that, I have erectile dysfunction with retaining blood in my penis. Increasing ketones also helps and has similar theories behind it.

If it wasn’t for that, high dose pregnenolone and HCG and potentially selegiline together would probably work wonders for a lot of goes with PFS like me. Test helps a lot too of course.
 
On the dopaminergic front, a lot of the things I’ve had success with are highly related to that, and the ones I haven’t done well with are at times noted to increase serotonin, which is your dopamine is too low isn’t great.

Pregnenolone can do a lot related to PFS but has studies showing a dose dependent increase in dopamine response to stimulus. I didn’t get much out of lower doses but on 400mg I like it. Selegiline, an MAO-B inhibitor, also helped immensely, particularly when combined with that, but I’d be careful with that one. Currently coming off it because it appears to interact poorly with my levothyroxine/T4, and was the cause of massive cramps and rapidly increased intestinal movement that was too much for me. Before getting T4 back it was all great, sans having to be careful not to get too caught up in trivial things since everything felt great. Without enough T3, I feel like crap, and without T4 alongside that, I have erectile dysfunction with retaining blood in my penis. Increasing ketones also helps and has similar theories behind it.

If it wasn’t for that, high dose pregnenolone and HCG and potentially selegiline together would probably work wonders for a lot of goes with PFS like me. Test helps a lot too of course.
So ur currently off of Selegiline completely for the time being?
 
So ur currently off of Selegiline completely for the time being?
For now yeah. I really enjoyed almost every aspect of it but the intestinal cramps it seemingly was causing by having my organs contract too hard and pretty much any time I ate having to poop as T4 was building up in my system was too much. If I could get by with just T3 and have a functioning penis I’d have loved to stay on it. I was pulling my hair out trying to figure out what it was since nothing was helping but it’s looking like it was the interaction of those too things unfortunately. I started waking up at night with leg cramps from it. Makes my intestines really sensitive as T4 built up and even something with more fiber than I was used to would cause everything to flow through. Started losing weight too in a bad way from it.

I’ll probably play around with it again some day in very small doses in the anti aging range. I was on 2.5mg under the tongue every morning and quit cold turkey.

Avoid DHT lowering meds if you don’t want to gamble at potentially dealing with crap like this for the rest of your life.
 
Not a drug, but fenugreek lowered DHT by 9.42% in this study on resistance trained males.

 
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Oh,my psa was2.50 in June. The reason I wanted an MRI is it is more accurate in assessing size of prostate . I wanted a more objective test,rather than a generalization by the doctor
You can get an MRI if you are willing to pay for it. No health insurance company is going to cover the cost just to satsify your curiosity since the doctor does not see a medical reason. A PSA of 2.5 is good.
 
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