Black Tea can both increase testosterone and reduce serum DHT. It blocks 5-alpha reductase.

From the Journal of Clinical Nutrition Zhou et al. 133 (2): 516. (2003):

Mice treated with black tea tended to have a greater serum testosterone concentration (34.4%, P = 0.50) and had a 72% lower DHT concentration than controls (P < 0.05), suggesting that black tea may contain components that inhibit the activity of 5-reductase, an enzyme that converts testosterone to the more bioactive DHT

Why would you, however, want to reduce serum DHT?

Generally, one wants to reduce DHT in the skin/scalp and the prostate.

Finasteride reliably reduces serum DHT around 60% when given at 5 mg daily doses. But the more important reduction is in the prostate and scalp, which are not reflected by serum levels.

Similarly, Saw Palmetto doesn’t affect serum DHT but reduces prostate DHT, and can block androgen receptors.

When on testosterone replacement, DHT is bound to increase depending on the mode of replacement (e.g. transdermal vs. injectable) and a person’s genetically determined 5-alpha-reducatase production. The higher the dose of testosterone, the higher the DHT production.

The question would be what to do, if anything, with the DHT.

There would be two areas to generally consider: Male Pattern Hair loss and Prostate Health (either growth or risk of cancer).

Sal Palmetto appears to concentrate its effects on DHT in the prostate (which has the enzymes to can convert adrenal hormones to DHT).

Finasteride can target scalp and prostate DHT production. There is a moderate decline in DHT in the blood. Prostate cancer, itself, starts in 100% of men at the age of 25. Other factors, such as immune system function, diet (e.g. iodine, vitamin D) help keep it controlled. In recent studies, the risk, overall, of uncontrolled prostate cancer is reduced with Finasteride.

Some use transdermal Progesterone applied to the scalp to help reduce hair loss. Progesterone may somewhat block alpha-reductase.

There are a multitude of compounds used to reduce inflammatory signaling and reduce DHT signaling/production in the scalp. It would be best to refer to sites such as http://www.regrowth.com for more information.

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These are some usual ranges for various signals:
Dihydrotestosterone (men): 25-75 ng/dL
Estradiol (men): 3-70 pg/mL – though within this range, some men clearly have suboptimal or excessive estradiol signaling.
SHBG (male): 7-49 nmol/L
Testosterone: 300-1000 ng/dL

When many levels are either too low or too high, the questions that come to mind are:
Why are so many so high or low? Is the treatment actually helpful?
Or is it causing downsides or frank harm?
Why keep a supraphysiologic level of testosterone when it causes significant problems with the rest of the hormones – e.g. excessive DHT, excessive estradiol, etc.
If supraphysiologic testosterone is contributing to problems, why not reduce the dose to a lower, physiologically more optimal range for health, particularly when problems are occurring across the system?

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If estradiol is low yet SHBG is high, the questions that come to mind are:
Is the person on an aromatase inhibitor given estrogen’s role in increasing SHBG?
If so, is the body compensating for the aromatase inhibition by increasing the production of other estrogens – resulting in a higher estrogen load despite having low Estradiol?
If so, is it useful to use an aromatase inhibitor since the body is circumventing it by producing higher amounts of other estrogens?
Would a dose reduction in testosterone be a better solution?

Hi Dr. Mariano,

First off, I would like to thank you for all of the time and effort that you invest in providing deep and concise explanations on your discussion forum. It is quite useful and educational.

I’m a long term finasteride sufferer who took finasteride for a very short period of time(2 months) and never recovered..It’s been many years and the only thing that makes me feel somewhat better is taking supplements like: 5-HTP, Mucana Prurines, and Yohimbe. Even with high normal testosterone, I’m still not recovered unless I take those supplements(which gets me to 50% of where I was pre-finasteride).. I do not understand why my body has not recoverd(I’m in my late 20’s….)

I truely believe our problem could be neurological in nature(dopamine/serotonin imbalances/NE/Epinerphine) and was curious if you are familiar with tetrahydrobiopterin deficiency. I heard this type of deficiency can lead to many imbalances(hormones, neurological, thyroid & adrenals). The drug prescribed to treat it is called BH4 which helps breaks down the molecule phenyalaline. Would testing Phenyalaline dictate if one has a tetrahydrobiopterin deficiency, and if this states true, would the drug Kuvan(Sapropterin) help correct this condition?

Here is an interesting article on Tetrahydrobiopterin Deficiency: http://emedicine.medscape.com/article/949470-print

Of note is that BH4 (Tetrahydrobiopterine) Defiency is generally rare (1 in a million people), is genetically based (e.g. mutations in the involved enzymes in producing BH4), and generally causes mental retardation.

Thus, if a person is bright enough to post to a web-site, the chances of having a primary BH4 deficiency is very very very unlikely.

Some nutrient deficiencies, however, can affect BH4 production. For example, a central nutrient in BH4 production is folic acid. This is one reason folic acid can have antidepressant properties. It leads to BH4 production, which then increases serotonin, norepinephrine, and dopamine production. Other nutrients affecting BH4 production include iron, selenium, etc. etc. etc. etc. I would say the vast majority of people have problems in these nutrients causing BH4 production problems rather than having an actual primary BH4 deficiency.

Hello Doctor Mariano.
I’ve just found this forum and I was thrilled! always liked your old meso posts, you seem to be a very knowledgeable about hormones, and a very good doctor. I’m going through a rough time right now and I was wondering if you could help me out a little bit.

I’m a healthy 28 year male from Portugal that took 1mg/day finasteride for 10 months to combat hair loss.

Before starting the treatment my baseline value was:
TT: 906 ng/dl (241 – 827)

6 weeks after stopping the treatment my levels were:
TT: 556 ng/dl (241 – 827)
FT: 9.6 pg/ml (9 – 47)

15 months after stopping the treatment my levels were:
TT: 343 ng/dl (241 – 827)
FT: 8.5 pg/ml (8.7 – 54.5)

In your opinion, can the use of finasteride alone cause hypogonadism by increasing T and peripheral aromatization to estradiol, therefore increasing the negative feedback on the hypothalamus and pituitary ?

I’m suffering from hypogonadism symptoms that I have never experienced until my finasteride use. Your input would be priceless and extremely appreciated.

don’t mean to go high jack HAN’s post, but i guess this a good place to ask such question.

Thank you so much for reading this,
kind regards
Zossima,