Experiences and Questions: Personal Experiments with Oral Native Testosterone Base & Enclomiphene (TRT+)

[dirkdigglr]

Hi,

Since Maximus TRT+ (oral native Testosterone with enclomiphene) isn't available here, I created my own version using micronized native testosterone powder dissolved in 30g of olive oil, combined with enclomiphene. I've conducted two separate experiments:

Baseline / Context:

• Healthy male, athletic, non-obese, late 30s
• Daily exercise: ~40 min running, 30 min full-body training (rack, Olympic barbell)
• Total cholesterol: ~100 (on low-dose statin + ezetimibe), lipoproteine(a) 121 nmol/l (reference: <75 nmol/l)
• Diet notable for high consumption of broccoli and cauliflower (potentially lowering E2?)
• No thyroid issues, values normal

Baseline Hormonal Levels:

• Total T: ~500 ng/dl
• LH: 4.9 IU/L
• Estradiol (E2): 20.2 pg/ml
• SHBG: 42 nmol/l
• Free Testosterone (calculated): ~76 pg/ml (1.49% of total T)
• Albumin: 4.27 g/dl

Experiment 1 (Enclomiphene only, 6 mg every 3 days for 3 months):

• Total T: ~850 ng/dl
• LH: ~13 IU/L
• Estradiol (E2): 43.6 pg/ml
• SHBG: 80.5 nmol/l
• Free Testosterone (calculated): ~101 pg/ml (1.23% of total T)
• DHEA: 10.9 ng/ml (1.33 - 7.78 ng/ml)
• DHEA-sulfate: 430,0 µg/dl (88,9 - 427 µg/dl)
• Albumin: 4.76 g/dl

This protocol felt significantly better than my baseline.

Experiment 2 (4 weeks of micronized Native Testosterone Base):

• Morning dose: 600 mg Testo Base in 30g olive oil + 6.25 mg enclomiphene
• Afternoon dose (approx. 6 hours later): 600 mg Testo Base in 30g olive oil + 6.25 mg enclomiphene

Resulting Hormonal Levels (measured 5.5 hours after morning dose):

• Total T: ~1070 ng/dl
• LH: 11.8 IU/L (note: not suppressed, despite high T and enclomiphene)
• FSH: 9.5 IU/L
• Estradiol (E2): 14.9 pg/ml (significantly lower compared to enclomiphene-only and baseline)
• SHBG: 34.2 nmol/l
• Free Testosterone (directly measured): 42.35 pg/ml (reference: 7.00 – 22.70 pg/ml)

Initially, native Testo Base felt very stimulating and beneficial. However, currently, I experience:

• Low motivation
• Exhaustion and depressive symptoms
• Emotional numbness
• Short-term memory issues
• Sleep disturbances (particularly more wakefulness and sometimes waking up around 4 AM, possibly cortisol-related)

I've tried taurine, ashwagandha, and melatonin to help manage these sleep disturbances, with some improvement noted.

I suspect the symptoms might be related to significantly reduced Estradiol (E2) levels (currently 14.9 pg/ml, compared to 43.6 pg/ml on enclomiphene-only).

I've experimented yesterday once with ingesting 0.25-0.5 mg of micronized 17β-estradiol, though unsure about its efficacy as I dont have any scale for such tiny amounts.

Additionally, I considered potential dopamine overload or tolerance reactions due to initial positive effects followed by rapid decline in mood and motivation.

EDIT: I was taking L-tyrosine at 2 × 250 mg daily. After discontinuing it yesterday, I've noticed significant improvement in my symptoms today. It appears this was a major contributor to my issues. I'm now less certain about estrogen being the sole cause. However, I'll continue supplementing with DHEA to potentially increase estrogen levels, as it's likely a combination of factors.


DHEA Intervention:

• I've started taking 50 mg micronized DHEA with oil over the last two days, but haven't observed improvements yet. (EDIT: changed it now to 50mg evening dose without oil)
• Would DHEA be more effective without oil to enhance aromatization in the liver?
• How much DHEA should I optimally take?
• Does DHEA reliably increase Estradiol (E2)? What E2 levels should I aim for?

I previously felt much better emotionally and in terms of sleep quality on enclomiphene-only despite lower testosterone levels. My goal now is to dial in the Estradiol levels appropriately while maintaining the benefits of higher free testosterone.

Any input or advice is appreciated! thx!

See attached PDF for detailed blood values from Experiment 2. Note that this was only a brief, interim blood panel conducted due to emerging symptoms and the need for quick intervention.

 

[FunkOdyssey]

I suspect the symptoms might be related to significantly reduced Estradiol (E2) levels (currently 14.9 pg/ml, compared to 43.6 pg/ml on enclomiphene-only).

This is quite plausible. Your absolute level of E2 is low, the ratio of T & DHT / E2 is very high, and you have enclomiphene antagonizing estrogen receptors on top of that.

I would rather take less of something in this situation than add another compound to increase estradiol. Reducing the dose of oral testosterone would bring up the E2, reduce androgens somewhat, and improve the androgen/estrogen ratio. Reducing or removing enclomiphene would remove the estrogen antagonism and may improve symptoms even if it doesn't significantly change your levels.

If you are committed to trying to make things work without doing either of those things, you probably need to find a way to increase your E2. Taking DHEA with oil is going to promote lymphatic absorption and bypass the liver, which is not what you want to do if you are trying to maximize conversion into estrogenic metabolites. You'd better achieve that goal by taking it on an empty stomach and sending it straight to the liver.

Bear in mind, DHEA can dramatically increase androstenedione, E1 (estrone), and 7-hydroxy and 7-keto metabolites (in addition to some minor testosterone/DHT) at the same time that you are trying to increase E2. DHEA is often poorly tolerated even by men who appear to be deficient in DHEA, probably due to this propensity to metabolize into a random and unpredictable assortment of downstream hormones. It is not by any means a clean or targeted way to increase E2.

If it were me trying to fix this, without adjusting the oral T or enclomiphene, I would either use hCG to increase my E2, or simply inject some estradiol cypionate or valerate (never oral).

 

[Guided_by_Voices]

Hi,

Since Maximus TRT+ (oral native Testosterone with enclomiphene) isn't available here, I created my own version using micronized native testosterone powder dissolved in 30g of olive oil, combined with enclomiphene. I've conducted two separate experiments:

Baseline / Context:

• Healthy male, athletic, non-obese, late 30s
• Daily exercise: ~40 min running, 30 min full-body training (rack, Olympic barbell)
• Total cholesterol: ~100 (on low-dose statin + ezetimibe), lipoproteine(a) 121 nmol/l (reference: <75 nmol/l)
• Diet notable for high consumption of broccoli and cauliflower (potentially lowering E2?)
• No thyroid issues, values normal

Baseline Hormonal Levels:

• Total T: ~500 ng/dl
• LH: 4.9 IU/L
• Estradiol (E2): 20.2 pg/ml
• SHBG: 42 nmol/l
• Free Testosterone (calculated): ~76 pg/ml (1.49% of total T)
• Albumin: 4.27 g/dl

Experiment 1 (Enclomiphene only, 6 mg every 3 days for 3 months):

• Total T: ~850 ng/dl
• LH: ~13 IU/L
• Estradiol (E2): 43.6 pg/ml
• SHBG: 80.5 nmol/l
• Free Testosterone (calculated): ~101 pg/ml (1.23% of total T)
• DHEA: 10.9 ng/ml (1.33 - 7.78 ng/ml)
• DHEA-sulfate: 430,0 µg/dl (88,9 - 427 µg/dl)
• Albumin: 4.76 g/dl

This protocol felt significantly better than my baseline.

Experiment 2 (4 weeks of micronized Native Testosterone Base):

• Morning dose: 600 mg Testo Base in 30g olive oil + 6.25 mg enclomiphene
• Afternoon dose (approx. 6 hours later): 600 mg Testo Base in 30g olive oil + 6.25 mg enclomiphene

Resulting Hormonal Levels (measured 5.5 hours after morning dose):

• Total T: ~1070 ng/dl
• LH: 11.8 IU/L (note: not suppressed, despite high T and enclomiphene)
• FSH: 9.5 IU/L
• Estradiol (E2): 14.9 pg/ml (significantly lower compared to enclomiphene-only and baseline)
• SHBG: 34.2 nmol/l
• Free Testosterone (directly measured): 42.35 pg/ml (reference: 7.00 – 22.70 pg/ml)

Initially, native Testo Base felt very stimulating and beneficial. However, currently, I experience:

• Low motivation
• Exhaustion and depressive symptoms
• Emotional numbness
• Short-term memory issues
• Sleep disturbances (particularly more wakefulness and sometimes waking up around 4 AM, possibly cortisol-related)

I've tried taurine, ashwagandha, and melatonin to help manage these sleep disturbances, with some improvement noted.

I suspect the symptoms might be related to significantly reduced Estradiol (E2) levels (currently 14.9 pg/ml, compared to 43.6 pg/ml on enclomiphene-only).

I've experimented yesterday once with ingesting 0.25-0.5 mg of micronized 17β-estradiol, though unsure about its efficacy as I dont have any scale for such tiny amounts.

Additionally, I considered potential dopamine overload or tolerance reactions due to initial positive effects followed by rapid decline in mood and motivation.

EDIT: I was taking L-tyrosine at 2 × 250 mg daily. After discontinuing it yesterday, I've noticed significant improvement in my symptoms today. It appears this was a major contributor to my issues. I'm now less certain about estrogen being the sole cause. However, I'll continue supplementing with DHEA to potentially increase estrogen levels, as it's likely a combination of factors.


DHEA Intervention:

• I've started taking 50 mg micronized DHEA with oil over the last two days, but haven't observed improvements yet. (EDIT: changed it now to 50mg evening dose without oil)
• Would DHEA be more effective without oil to enhance aromatization in the liver?
• How much DHEA should I optimally take?
• Does DHEA reliably increase Estradiol (E2)? What E2 levels should I aim for?

I previously felt much better emotionally and in terms of sleep quality on enclomiphene-only despite lower testosterone levels. My goal now is to dial in the Estradiol levels appropriately while maintaining the benefits of higher free testosterone.

Any input or advice is appreciated! thx!

See attached PDF for detailed blood values from Experiment 2. Note that this was only a brief, interim blood panel conducted due to emerging symptoms and the need for quick intervention.

Thanks for posting this. One of the big problems with what I'll call the Minimally Suppressive Testosterone/SERM approaches is the lack of publicly available discussion on the results of such experimentation, so it's interesting to see your results. I had never heard of L-Tyrosine creating those issues, but I've been feeling a little off recently and I take it for its sun-protective affects, so I will stop it for now and see if my energy levels increase.

 

[dirkdigglr]

This is quite plausible. Your absolute level of E2 is low, the ratio of T & DHT / E2 is very high, and you have enclomiphene antagonizing estrogen receptors on top of that.

I would rather take less of something in this situation than add another compound to increase estradiol. Reducing the dose of oral testosterone would bring up the E2, reduce androgens somewhat, and improve the androgen/estrogen ratio. Reducing or removing enclomiphene would remove the estrogen antagonism and may improve symptoms even if it doesn't significantly change your levels.

If you are committed to trying to make things work without doing either of those things, you probably need to find a way to increase your E2. Taking DHEA with oil is going to promote lymphatic absorption and bypass the liver, which is not what you want to do if you are trying to maximize conversion into estrogenic metabolites. You'd better achieve that goal by taking it on an empty stomach and sending it straight to the liver.

Bear in mind, DHEA can dramatically increase androstenedione, E1 (estrone), and 7-hydroxy and 7-keto metabolites (in addition to some minor testosterone/DHT) at the same time that you are trying to increase E2. DHEA is often poorly tolerated even by men who appear to be deficient in DHEA, probably due to this propensity to metabolize into a random and unpredictable assortment of downstream hormones. It is not by any means a clean or targeted way to increase E2.

If it were me trying to fix this, without adjusting the oral T or enclomiphene, I would either use hCG to increase my E2, or simply inject some estradiol cypionate or valerate (never oral).

Hi,

Thanks a lot for your reply – it has been extremely helpful in clarifying some mechanisms I didn’t fully understand before. I’ve got some follow-up questions and thoughts regarding LH, estradiol action, absorption timing, and also how much of my symptoms may stem from dopaminergic overstimulation.

---

1. LH Levels under Enclomiphene + Oral T Base

What surprised me is that my LH is still elevated (~11.8 IU/L) even though I’ve been taking two doses of 600 mg micronized testosterone base in 30g olive oil per day. I had expected LH suppression due to high free T. But Enclomiphene seems to be maintaining LH even with supraphysiological T levels.

From the Maximus white paper, I thought LH would stay roughly flat – but mine is almost as high as on Enclomiphene monotherapy (~13 vs 11.8 now). So my question is:

• Is it usual that Enclomiphene so effectively overrides the negative feedback of oral testosterone? (In the Maximus study, Enclomiphene kept LH stable but didn’t increase it to such levels.)
• Is this increase in LH actually driving additional endogenous T (or E2) production?

---

2. Enclomiphene’s Estrogen Receptor Antagonism

I hadn’t realized before that Enclomiphene not only tricks the hypothalamus into thinking there’s an E2 deficiency, but also acts as an ER antagonist throughout the body.

This raises several questions:

• Does it significantly blunt E2’s action in the brain, bone, or other tissues?
• Could this antagonism itself explain part of the mood/cognitive flattening?
• Is this antagonism in some contexts a desired feature (e.g., to feel more androgen-dominant), or always an unwanted side effect?

I originally thought Enclomiphene simply enabled higher endogenous production – but now I’m wondering whether its ER-blocking activity is part of what’s making me feel off.

---

3. Kinetics of Micronized T Base in Olive Oil

I’ve been taking micronized T base (600 mg in 30g olive oil) twice per day, usually on an empty stomach in the morning and ~6 hours later. I typically go for a run right after the morning dose.

I’m curious:

• How fast does this olive oil formulation absorb compared to the Maximus tablets?
• Is it possible that the absorption is too fast due to micronization + empty stomach → leading to dopamine spikes / fast drop-offs?
• Is there any data on how fat-based vs food-based absorption affects serum T curves?

I’ve read that Maximus suggests taking it with food (not oil) to slow absorption. Would this lead to a smoother curve with fewer peaks and crashes?

---

4. Cognitive Effects of Peaks vs Stable Exposure

This is important to me: Do the mental benefits (drive, clarity, motivation) require T to be stable for many hours? Or does a short-lived high T level leave lingering effects throughout the day?

I’m asking because I felt like the initial weeks on oral T were great. But now, the effects feel more blunted – almost like a dopaminergic tolerance or instability. The peaks may be too intense and short, leading to dysregulation rather than stable enhancement.

I’m wondering:

• Would lowering the per-dose amount (e.g., to 2x 300–400 mg) help avoid overstimulation?
• Or should I switch to a different base/vehicle to reduce the peak/trough amplitude?

---

5. Estradiol Microdosing

I’ve now taken 0.25–0.5 mg/day of micronized 17b-estradiol in 80% isopropanol + 20% PG (1 mg/ml). I’ve noticed subtle improvements so far.

I’d love to know:

• Should E2 effects be noticeable within 1 day, or does it build up over several days?
• How quickly does transdermal ethanol-based E2 wear off?

I’m assuming I’ll need a few days of consistent application to see stable benefits. If so, I’ll likely continue with 0.25 mg/day for now.

Also, one thing that still confuses me: why does estradiol drop that much in the oral T + Enclomiphene protocol? In my case, it dropped below my drug-free baseline (~20 pg/ml) to 14.9 pg/ml. That’s a significant difference, and I’m wondering what drives it.

• Is it due to enzymatic saturation?
• Is the duration of elevated T too short for effective aromatization?
• Or does the presence of high androgens + Enclomiphene suppress aromatase activity indirectly?

I had assumed that splitting the T base into two daily doses might create enough time-above-threshold for aromatization to occur, but this clearly didn’t happen.

---

6. Dopamine Overload Hypothesis

I’m beginning to suspect that I’ve been stacking too many dopaminergics: oral T peaks, Alpha-GPC, Acetyl-L-Carnitine, Uridine, and previously L-Tyrosine (500 mg x2). Removing L-Tyrosine already made a noticeable positive difference.

It’s possible that this whole setup triggered a kind of dopamine overstimulation → tolerance → emotional dullness and sleep issues. Kind of like what Maximus describes with “dopamine fasting.”

I actually like the Acetyl-L-Carnitine and Alpha-GPC stack, as it makes my mind clear pretty quickly. I saw that you had mentioned somewhere else that Alpha-GPC can cause depression and posted a study about nicotinic agents. What are the effects for you if you take Alpha-GPC?

Would love to hear your take on this. Especially whether transient T spikes could produce dopaminergic rebounds or fatigue.

All in all, I suspect it's a mix of things: maybe transient spikes that are too high, some dopamine overload effects, and likely also a low estrogen ratio – and the combination of these may be driving the symptoms.

Really appreciate you taking the time to read all this and share your perspective – it's been incredibly helpful to have input from someone who understands the nuances.

 

[FunkOdyssey]

Is it usual that Enclomiphene so effectively overrides the negative feedback of oral testosterone? (In the Maximus study, Enclomiphene kept LH stable but didn’t increase it to such levels.)

Yes, but the negative feedback from oral native testosterone is minimal to begin with. We have internal data showing, on average, men's LH only dropped by 0.8 IU/L (non-significant and within margin of error) when using a single 600 mg dose of native oral T daily.

Is this increase in LH actually driving additional endogenous T (or E2) production?

Yes, it certainly is, unless you have primary hypogonadism.

• Does it significantly blunt E2’s action in the brain, bone, or other tissues?
• Could this antagonism itself explain part of the mood/cognitive flattening?
• Is this antagonism in some contexts a desired feature (e.g., to feel more androgen-dominant), or always an unwanted side effect?

I originally thought Enclomiphene simply enabled higher endogenous production – but now I’m wondering whether its ER-blocking activity is part of what’s making me feel off.

Yes, enclomiphene is blocking estrogen receptors throughout the body, and this may vary depending on its concentration in a particular tissue. This is less of a problem with enclomiphene monotherapy, because your pituitary gland is tuning your estradiol level appropriately to overcome enclomiphene's ER antagonism. Sometimes this antagonism may be desirable, when your estradiol is high enough to cause adverse effects, and you do not want to inhibit aromatase.

What you want to appreciate about enclomiphene: your estradiol on labs no longer accurately represents the amount of estrogen signaling that is occurring, and you need to factor this into your interpretation of labs. With enclomiphene monotherapy, your E2 may increase to 45 pg/mL, but your tissues are only perceiving 25 pg/ml worth of estradiol because enclomiphene is blocking some of it. In that scenario, you probably feel pretty good. When you have 14.9 pg/mL of E2, and it feels like you actually have 5 or 10 pg/mL because of the enclomiphene, you are not going to feel very good.

• How fast does this olive oil formulation absorb compared to the Maximus tablets?
• Is it possible that the absorption is too fast due to micronization + empty stomach → leading to dopamine spikes / fast drop-offs?
• Is there any data on how fat-based vs food-based absorption affects serum T curves?

I don't have this comparison data you are looking for. I do not think a fast spike and drop off is necessarily responsible for any adverse effect you are experiencing, as many forms of short-acting testosterone behave similarly and are well tolerated. It is an easy experiment for you to perform though, trying it both ways.

This is important to me: Do the mental benefits (drive, clarity, motivation) require T to be stable for many hours? Or does a short-lived high T level leave lingering effects throughout the day?

No, I do not believe the benefits require T to be stable for many hours. Every successful user of any form of oral T, or topical T, or testosterone propionate, or natesto, has levels that fluctuate wildly across a 24 hour period. The high peak levels are able to drive changes in gene expression and effects that persist despite the serum level dropping back down.

I’m asking because I felt like the initial weeks on oral T were great. But now, the effects feel more blunted – almost like a dopaminergic tolerance or instability. The peaks may be too intense and short, leading to dysregulation rather than stable enhancement.

I think this is a combination of a few things: honeymoon period is over, your estradiol is too low and amount of actual estrogen signaling is critically low, and you are taking too many supplements (discussed below).

Also, one thing that still confuses me: why does estradiol drop that much in the oral T + Enclomiphene protocol? In my case, it dropped below my drug-free baseline (~20 pg/ml) to 14.9 pg/ml. That’s a significant difference, and I’m wondering what drives it.

• Is it due to enzymatic saturation?
• Is the duration of elevated T too short for effective aromatization?
• Or does the presence of high androgens + Enclomiphene suppress aromatase activity indirectly?

We do not know for sure why the oral testosterone reduces E2. Our hypothesis is that the elevated DHT acts as a natural aromatase inhibitor. It would be interesting to understand the exact mechanism, but it is most important to simply understand that oral testosterone does reduce E2, and then make your adjustments accordingly.

Another thing oral testosterone does that we don't understand: it elevates DHEA-S dramatically based on some internal data. Test your DHEA-S with oral T and no supplemental DHEA and you may discover that is happening to you too.

I’m beginning to suspect that I’ve been stacking too many dopaminergics: oral T peaks, Alpha-GPC, Acetyl-L-Carnitine, Uridine, and previously L-Tyrosine (500 mg x2). Removing L-Tyrosine already made a noticeable positive difference.

You cannot possibly dial in a TRT protocol with all of these supplements complicating the picture. I would remove all of these going forward, and only considering adding them back, one-by-one, at some future date when you are finished adjusting your hormones.

I actually like the Acetyl-L-Carnitine and Alpha-GPC stack, as it makes my mind clear pretty quickly. I saw that you had mentioned somewhere else that Alpha-GPC can cause depression and posted a study about nicotinic agents. What are the effects for you if you take Alpha-GPC?

Absolute garbage is what I feel like with cholinergics, which includes acetyl-l-carnitine btw. You may want to research the catecholaminergic-cholinergic balance theory of depression, to appreciate why these supplements are not always benign. Here is a good paper on this: Cholinergic Regulation of Mood: From Basic and Clinical Studies to Emerging Therapeutics - PMC

Really appreciate you taking the time to read all this and share your perspective – it's been incredibly helpful to have input from someone who understands the nuances.

No problem. I'm not sure Maximus would appreciate me extending so much assistance to someone that went rogue and tried to copy our Oral T + Enclo protocol with UGL products, but I can't help myself.