Deca (nandrolone) added to trt and wow!!

I recently had my TRT Dr approve a 10 week cycle of Deca to my 200 MG per week TRT. Took about 6 weeks to kick in but I feel really good. Sex drive off the hook and getting very strong and muscular. I do in the same Syringe 45mg T/35mg Deca e3d and take .25mg of Anastrozole 24 hrs after injection. Comes out to 225Mg of T and 175 Mg deca per week. I was told to make sure T is a tad higher then deca. anyone else adding deca to their TRT?

 

Is there any independent support for this concept, along with proposed mechanisms? And isn't the notion of variable SHBG binding affinity contradicted by the good agreement between Tru-T and the accurate free T tests?

I just don’t think dr Lichten would lie. I’ve been following him for a long time, and all the information he puts out is top notch if you’ve ever listened to him. He has a bunch of podcasts he put out back in 2012. If he’s been prescribing HRT successfully for many years, why would he lie and say he puts his patients on a low dose of deca to increase free T? He says that deca binds to SHBG, which consequently decreases how much SHBG can bind to testosterone, which increases free T.

Have you watched the recent video he did with Danny bossa talking about deca?

Im not taking a stance one way or the other. I don’t get married to any ideas. I just always try to keep an open mind. What do you think about this proposed idea that deca can free up testosterone, not by lowering SHBG, but by preventing SHBG from binding to as much testosterone?

 

I just don’t think dr Lichten would lie. I’ve been following him for a long time, and all the information he puts out is top notch if you’ve ever listened to him. He has a bunch of podcasts he put out back in 2012. If he’s been prescribing HRT successfully for many years, why would he lie and say he puts his patients on a low dose of deca to increase free T? He says that deca binds to SHBG, which consequently decreases how much SHBG can bind to testosterone, which increases free T.

Have you watched the recent video he did with Danny bossa talking about deca?

Im not taking a stance one way or the other. I don’t get married to any ideas. I just always try to keep an open mind. What do you think about this proposed idea that deca can free up testosterone, not by lowering SHBG, but by preventing SHBG from binding to as much testosterone?

To clarify, SHBG is not binding to nandrolone decanoate (Deca-Durabolin)—it's binding to the nandrolone after it's been freed from the ester. The Wiki page on SHBG says that testosterone has 19 times the binding affinity of nandrolone. To me this suggests that you'd have to have an awful lot of nandrolone to make much difference via competitive inhibition. Mesterolone (Proviron) has 440 times the binding affinity of nandrolone, so, setting aside legality and availability, why not prefer it for freeing up testosterone? It would take a lot less to do the job, potentially offsetting its—possibly undesirable—greater androgenic effects.

Your new paraphrasing of Dr. Lichten seems more equivocal, possibly only referring to competitive inhibition. Can you provide any direct quotes from him saying that nandrolone is influencing the actual binding affinity of nandrolone? People, myself included, say incorrect things all the time without intentionally lying. On this particular point I think madman has the stronger case, but his counterproductive ad hominem attacks distract from the science-based arguments.

 

To clarify, SHBG is not binding to nandrolone decanoate (Deca-Durabolin)—it's binding to the nandrolone after it's been freed from the ester. The Wiki page on SHBG says that testosterone has 19 times the binding affinity of nandrolone. To me this suggests that you'd have to have an awful lot of nandrolone to make much difference via competitive inhibition. Mesterolone (Proviron) has 440 times the binding affinity of nandrolone, so, setting aside legality and availability, why not prefer it for freeing up testosterone? It would take a lot less to do the job, potentially offsetting its—possibly undesirable—greater androgenic effects.

Your new paraphrasing of Dr. Lichten seems more equivocal, possibly only referring to competitive inhibition. Can you provide any direct quotes from him saying that nandrolone is influencing the actual binding affinity of nandrolone? People, myself included, say incorrect things all the time without intentionally lying. On this particular point I think madman has the stronger case, but his counterproductive ad hominem attacks distract from the science-based arguments.

Wow, you said that so intelligently and rationally that I agree 100% with you lol. I also believe he has a stronger case. I’m just not ruling anything out, and am very intrigued at possible options to increase the free T to E2 ratio without having to increase total testosterone. Deca seems like a compound that could potentially do this, as well as coming with quite a few other beneficial properties. Such as its anti-inflammatory and joint lubrication properties. Here’s the video where dr Lichten goes into detail about why he uses deca with with his HRT patients.

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Back on topic, those arguing the low doses of nandrolone (Deca is just one ester) are a cardio risk also need to factor in that if a reduction in joint pain allows one to do significantly more conditioning (basketball, running , biking swimming, hiking, whatever) and load- bearing exercise, then that in itself is likely cardio-protective and could very well out-weigh any (likely low) risk assuming low doses, as in under 100mg per week.

 

Back on topic, those arguing the low doses of nandrolone (Deca is just one ester) are a cardio risk also need to factor in that if a reduction in joint pain allows one to do significantly more conditioning (basketball, running , biking swimming, hiking, whatever) and load- bearing exercise, then that in itself is likely cardio-protective and could very well out-weigh any (likely low) risk assuming low doses, as in under 100mg per week.

The Deca has helped my tennis elbow immensely. I had to do two shots of cortisone at the beginning of the year. It wasn’t just affecting “listing heavy” it limited me from swimming, racket sports, working on the computer, and would shoot pain when picking up something as mundane as a gallon of milk.

So far so good with Deca. No complaints. I do think people try to make too many “rules” about TRT, much like they do with nutrition where there really no long term studies and people use their own experiences and belief systems to dictate to others how they must do x, y, or z and must administer on a, b, or c, et al.

 

The Deca has helped my tennis elbow immensely. I had to do two shots of cortisone at the beginning of the year. It wasn’t just affecting “listing heavy” it limited me from swimming, racket sports, working on the computer, and would shoot pain when picking up something as mundane as a gallon of milk.

So far so good with Deca. No complaints. I do think people try to make too many “rules” about TRT, much like they do with nutrition where there really no long term studies and people use their own experiences and belief systems to dictate to others how they must do x, y, or z and must administer on a, b, or c, et al.

Well said. Here’s some things I wrote down and saved a while ago on this topic.

-Reasons why new ideas are not often accepted initially
Fear of leaving the comfort and treading a new uncertain path. Human beings seek stability and comfort. New ideas are first accepted as unstable.

All truth passes through three stages.
First, it is ridiculed.
Second, it is violently opposed.
Third, it is accepted as being self-evident (obvious)

It’s basically just human behavior to fear/ judge things that are unfamiliar. It must have to do with evolution and survival. So I try not to take too much offense when people ridicule new ideas, like using other AAS compounds in HRT. It’s just human behavior. They’re just victims of their own biology.

 

Oh great, so they’re going to use a testing method that doesn’t match up with symptoms? Very smart.

All those compounds lower SHBG, I’m talking about things that decrease binding affinity, like deca. If there’s things that decrease binding affinity, that means that everyone that has a SHBG of 30, is going to have different free T levels, even with the same total T, due to everyone’s SHBG binding at different rates. You’ll never understand this because you’re too caught up in studies, instead of what actually happens in the real world.

And you’re clearly saying that you are smarter than dr Lichten when you state that there’s no such thing as someone’s SHBG binding more or less to testosterone, even at the same level, when he’s saying that deca, for example, can decrease SHBG’s binding affinity without actually lowering the number. Have fun spreading false information to everyone on here and telling every guy that SHBG is just a number. No formula is going to accurately tell you your free T level based of of a total T and SHBG. You’re never going to get it, and I feel bad for guys that listen to you and continue to be symptomatic just because you tell them their free T is “in range”.

when you state that there’s no such thing as someone’s SHBG binding more or less to testosterone, even at the same level,


After testicular secretion, a small proportion of testosterone undergoes activation to two bioactive metabolites, estradiol and DHT.

The amplification pathway converts roughly 5-10% of T--->DHT and roughly (~0.2-0.3%) of T--->estradiol.

Keep in mind that the amplification pathway converts ~4% of circulating testosterone to the more potent, pure androgen, DHT and DHT circulates at ~10% of blood testosterone concentrations, due to spillover from the prostate and nonprostatic sources.

Regarding RBA (relative binding affinity) of steroids to SHBG.....dihydrotestosterone (DHT)>testosterone>androstenediol>estradiol.

DHT binds to SHBG with about 5 times the affinity of testosterone and about 20 times the affinity of estradiol.

The RBA of DHT let alone testosterone and even estradiol to SHBG would trump the majority of various AAS (anabolic androgenic steroids) let alone nandrolone.

If anything the only steroid which would have a stronger RBA to SHBG than DHT, testosterone or even estradiol would be mesterolone (Proviron).

So as I stated previously.....You are lost on this one when you stated..... "Plus the fact that you don’t understand that all SHBG isn’t created equal"


*The current algorithm and the experimental data reported here were generated using wild type SHBG which is present in nearly 98% of Caucasians. Genome wide association studies have revealed several SHBG polymorphisms, two of which have been reported to affect testosterone binding to SHBG (28).


So if anything regarding SHBG:T binding unless you fall into the 2% which may have an SHBG polymorphism.....and only 2 have been reported to affect T binding to SHBG or you are using mesterolone (Proviron) added to trt than it is highly unlikely that someone’s SHBG binding more or less to testosterone, even at the same level would happen.....hence FT level would not be different with the same TT/SHBG/Albumin level.....let alone to any significant degree.

Also regarding the TruT algorithm it has been shown that:

Effects of Estradiol and Dihydrotestosterone (DHT). Addition of estradiol 17β in concentrations ranging from 10 to 500 pg/mL had no significant effect on percent free testosterone. Similarly, free testosterone concentrations in men treated with graded doses of testosterone enanthate plus placebo whose DHT concentrations extended from physiologic to supraphysiologic range did not differ from those treated with testosterone enanthate plus dutasteride whose DHT concentrations were very low (Bhasin et al 2012), indicating that DHT over the range of concentrations relevant in male and female physiology has little effect on percent free testosterone.


The new dynamic model leads to the reconsideration of several dogmas related to testosterone's binding to SHBG and has important physiologic and clinical implications. First, the fraction of circulating testosterone which is free is substantially greater (2.9±0.4%) than has been generally assumed (% cFTV 1.5±0.4%). Second, percent FT is not significantly related to total testosterone over a wide range of total testosterone concentrations. However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, SHBG is able to regulate FT levels in much larger dynamic range.


Let me state this again:

Second, percent FT is not significantly related to total testosterone over a wide range of total testosterone concentrations. However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, SHBG is able to regulate FT levels in much larger dynamic range.


Key point being....."Due to the allostery between the two binding sites, SHBG is able to regulate FT levels in much larger dynamic range"

Again let's top it off with the fact that this is what you are truly not understanding when it comes to SHBG:T binding.

Relation between Percent FT with Total Testosterone and SHBG. Intra-dimer complex allostery suggests that SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated. Indeed, it was found that percent FT calculated using the new model changed very modestly over a wide range of total testosterone concentrations. In contrast, the Vermeulen's equation suggests a negative relation between percent FT and total testosterone. Furthermore, as SHBG concentrations increase, percent FT calculated using our new model shows only a modest decline in contrast to the marked decline in percent FT calculated using Vermeulen's equation.


Too make it clearer to you of the significance here:

* SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated.

 

@Gman86

Regarding the so called "stupid" TruT calculator as you say.....tread lightly!

We are not dealing with amateurs here.



About Function Promoting Therapies

Function Promoting Therapies, LLC, and Tesvgen, the commercialization arm of FPT, LLC, were established in 2012. The company’s goals are to provide:

• Advanced diagnostic algorithms that improve accuracy in the diagnosis of male reproductive disorders
• Enabling tools to enhance compliance and improve treatment outcomes for male reproductive disorders
• Advanced tools for dosimetry to optimize testosterone therapy

FPT has focused its initial efforts at developing the TruT product line and its Men’s Health franchise. The Company strives to innovate at a high level, maintain our access to academic research and pre-eminence in this content area, and to optimally balance research and commercial success.

We are based in the heart of Boston within reach of some of the most renowned endocrine research and clinical centers in the world. Our research partners are spread throughout USA and we have research ties with leading institutions in Europe. These networks provide us the opportunity to share and validate our findings and enable us to leverage from a global palette of resources.

Our access to a network of academic experts at leading academic institutions also means that we are in tune with the upcoming changes in treatment patterns or recommendation of professional societies.



Partners and Collaborations

We continue to work with collaborators in academia and the wider industry for exciting new applications and further development of TruT™. Some of our existing partnerships include:


Johns Hopkins University ‐ Diagnosis and management of hypogonadism in HIV and co-infections.

The Mayo Clinic ‐ Personalized algorithm and therapy development.

Karolinska Institute ‐ Dynamics of free testosterone levels after surgical interventions in men and women.

regionh.dk - Examining population reference ranges of free testosterone for Danish cohorts.

UCLA School of Nursing ‐ Examining the dynamic role of multiple hormones in altering transport and bioavailability.

Boston IVF ‐ Developing a novel platform for rational treatment and management of in-vitro fertilization interventions.

Myosyntax ‐ Dynamics of testosterone bioavailability during caloric restriction.




Ravi Jasuja, Ph.D.
Chief Scientific Officer

Dr. Jasuja serves as the Chief Scientific Officer of the Function Promoting Therapies, LLC and is an expert in the use of biophysical techniques for investigating the interactions of steroid hormones with their cognate receptors and binding proteins. He led innovative research that uncovered the mechanistic origin of errors in the current model of testosterone binding to SHBG and provided the insight that led to the generation of the new TruT™ method for determining free testosterone concentration.



As I stated before there are three heavy weights in the field behind the invention of TruT.

Ravi Jasuja, Shalender Bhasin and Mikhail N Zakharov.

If you seriously believe that factors which could affect SHBG:T binding were not taken into account during the development of the newer calculated TruT algorithm.....than you truly are senseless.

A significant amount of research, money and time have been invested since 2012.

 

I’m not saying it’s not accurate, I’m saying they can put in all the money and time they want, they’re leaving out the most important factor, symptoms. Without them factoring in guys’ symptoms, it means very little. They’re still behind the times, and are using sick individuals to extrapolate data from

 

But this isn’t really their concern, their concern is to come up with an accurate way to measure free T, which they’ve done. All that needs to happen is for these top doctors to start doing studies on men and focus on their free T related to their symptoms. Then all the tru-t calculator has to do is adjust its range.

 

I’m not saying it’s not accurate, I’m saying they can put in all the money and time they want, they’re leaving out the most important factor, symptoms. Without them factoring in guys’ symptoms, it means very little. They’re still behind the times, and are using sick individuals to extrapolate data from

Are you criticizing this distribution referenced by @madman?

"Based on the new data on the distribution of free testosterone levels in healthy men the target range of free testosterone has been determined to be 164 to 314 pg/ml (mean+/−1SD)"

I'd lean more towards @xqfq's interpretation:

Based on my reading of madman's post about the range, I believe it's the "16-31" range isn't a "95% of people fall into this" sort of range but rather the "therapeutic target" range. So it's something like, if you're in that 16-31 range, you may not have hypogonadal symptoms.

 

Got my bloodwork back after 5 weeks on Deca. Everything’s peachy. The only difference is my cholesterol creeped up from 122 to 139 which is still great. I’ve been eating more red meat for protein. My hemocrit bumped up from 48 to 49.8. PSA looks great, and TSH at 1.06.

Will run the 2nd five weeks as planned at 250 mg per week Deca on top of TRT.

 

Did your free T levels change or were these unaffected by deca?

 

Did your free T levels change or were these unaffected by deca?

Good question. I didn’t pay to have sex hormone panels run.

 

Wow, you said that so intelligently and rationally that I agree 100% with you lol. I also believe he has a stronger case. I’m just not ruling anything out, and am very intrigued at possible options to increase the free T to E2 ratio without having to increase total testosterone. Deca seems like a compound that could potentially do this, as well as coming with quite a few other beneficial properties. Such as its anti-inflammatory and joint lubrication properties. Here’s the video where dr Lichten goes into detail about why he uses deca with with his HRT patients.

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Having watched the video, do you guys know which pharmacies carry capsules/injections of Stanozolol? My TRT provider partners with Empower but I only see the cream on their website.

First lab before beginning TRT some months ago, my free T was at 6 with the bottom end of range approx 9. Unfortunately, SHBG was not checked on my first lab but I'll be sure to have it checked at next draw.

 

Got my bloodwork back after 5 weeks on Deca. Everything’s peachy. The only difference is my cholesterol creeped up from 122 to 139 which is still great. I’ve been eating more red meat for protein. My hemocrit bumped up from 48 to 49.8. PSA looks great, and TSH at 1.06.

Will run the 2nd five weeks as planned at 250 mg per week Deca on top of TRT.

Why are you using at this dosage? And what is your Testosterone dosage? Are you having side effects on libido?

 

*The current algorithm and the experimental data reported here were generated using wild type SHBG which is present in nearly 98% of Caucasians. Genome wide association studies have revealed several SHBG polymorphisms, two of which have been reported to affect testosterone binding to SHBG (28).

Hey I'm trying to learn and follow along here: I always read that the it varied person to person, not just their shbg number, but also how strong the shbg was at binding. Is this research showing that 98 percent of Caucasian males have shbg that's basically the same as far as it's ability to bind to hormones?

 

Why are you using at this dosage? And what is your Testosterone dosage? Are you having side effects on libido?

A few reasons. First Nelson recommended running 200 mg. A 10 week protocol takes me to the 1st of the year when I want to cut a bit again, and I have a bottle of 2500 mg, so I chose 250 mg Deca. I’m on 150 mg per week TRT plus Cabergoline. My libido is the same, as are my erections. I have morning wood 5 days per week.

 

A few reasons. First Nelson recommended running 200 mg. A 10 week protocol takes me to the 1st of the year when I want to cut a bit again, and I have a bottle of 2500 mg, so I chose 250 mg Deca. I’m on 150 mg per week TRT plus Cabergoline. My libido is the same, as are my erections. I have morning wood 5 days per week.

SS, thanks for your contributions to this thread. Question: Did you experience any fluctuation in your HDL/LDL numbers after the first 5 weeks? I've read the HDL/LDL ratio is a primary factor in plaque buildup whereas total cholesterol is a sum of "good" + "bad" (debatable how "bad" LDL really is.. Tris are a different story).

We know that AAS cause a shift in HDL but impact is dose dependent. Any notable shift in your HDL so far?

If Nelson reads this, was your HDL always in normal range when you supplemented with Deca at 100 mg/wk?

 

SS, thanks for your contributions to this thread. Question: Did you experience any fluctuation in your HDL/LDL numbers after the first 5 weeks? I've read the HDL/LDL ratio is a primary factor in plaque buildup whereas total cholesterol is a sum of "good" + "bad" (debatable how "bad" LDL really is.. Tris are a different story).

We know that AAS cause a shift in HDL but impact is dose dependent. Any notable shift in your HDL so far?

If Nelson reads this, was your HDL always in normal range when you supplemented with Deca at 100 mg/wk?

When on trt the most commonly prescribed injectable esterified T is enanthate or cypionate.

As we know when starting trt or increasing/decreasing dose .....T levels are in FLUX during the following weeks leading up to when blood levels have stabilized.....as it will take roughly 5-6 weeks due to the enanthate or cypionate ester.....let alone 2-3 months at the new levels for the body to truly adjust.

When adding nandrolone decanoate to a trt regime it will take longer for blood levels to stabilize due to the decanoate ester.

Testosterone enanthate: 7-carbon ester side-chain
Testosterone cypionate: 8-carbon ester side-chain
Nandrolone decanoate: 10-carbon ester side-chain
Testosterone undecanoate: 11-carbon ester side-chain

Testosterone undecanoate has the longest duration of action and blood levels take much longer to stabilize compared to the enanthate or cypionate ester.

He is only 5 weeks in.....some what pointless to test lipids or hemoglobin/hematocrit at such time.....I would give it 8-12 weeks before testing bloods to truly gauge whether said dose/injection frequency has any impact on possibly lowering ones HDL or increasing hemoglobin/hematocrit.

It has been shown that when using higher doses of nandrolone as in 200 mg/week it can lower HDL and it has been shown that lower doses of 100 mg/week can increase hemoglobin/hematocrit.....but it is not a given as it comes down to how the individual responds to testosterone/AAS.

Short term use as in 5 weeks is minimal.....will be much more interesting to see blood work at the 8-12 week mark.

Regarding increased hemoglobin/hematocrit which is common on trt.....levels will increase within the first 1-3 months and can take up to 9-12 months to reach peak levels.

Longer use of higher doses of nandrolone would most likely have the same impact.