Got Testosterone?

[Flankenstein]

I've read very negative things about it and very positive things as well. There are quite a few doctors who go that route before TRT as well. I'd be interested in what your thoughts are when you have more time.

Ok, I'll poke back in here after work with less brevity. I'll say this though- If I were going to take anything before TRT it would be hCG not clomid.

[WillBrink]

Ok, I'll poke back in here after work with less brevity. I'll say this though- If I were going to take anything before TRT it would be hCG not clomid.

I'm unclear how/why you'd come to that conclusion, so I'll be interested to see your thought process and or data on that conclusion.

[Irish]

Basic duplication of Will's post.

[Flankenstein]

I'm unclear how/why you'd come to that conclusion, so I'll be interested to see your thought process and or data on that conclusion.

I'm surprised that it is unclear to you. If I'm understanding Irish correctly, he is looking to "kick start" endogenous testosterone production before diving head first into TRT. If that is the case, hCG (w/ low dose arimidex depending on hCG dose and lab work) will do a better job than clomid. Again, excuse my brevity and lack of explanation/links to research.

[Irish]

I'm surprised that it is unclear to you. If I'm understanding Irish correctly, he is looking to "kick start" endogenous testosterone production before diving head first into TRT. If that is the case, hCG (w/ low dose arimidex depending on hCG dose and lab work) will do a better job than clomid. Again, excuse my brevity and lack of explanation/links to research.

That's the case for myself. I am not a "science guy" but I've been doing lots of reading and research. I thought hCG would be primarily used on TRT to keep the testicles functioning and Clomid would be better for a kick start.

I may be off base but I was also under the impression that hCG would mimic LH and possibly reduce the body's own natural output afterwards whereas Clomid would not have the same effect. Again, I'm a layman, trying to understand a lot of this and there is conflicting information throughout from doctors to scientists to end users.

[Irish]

DAA covered HERE if interested.

What are your thoughts regarding this quote in relation to that paper?

From the intro,

"... the nutrition/sport supplement industry has attempted to take advantage of this information by manufacturing D-ASP–containing products with the intent of these products increasing endogenous testosterone levels, presumably by activation of the HPG axis. Furthermore, these products are being marketed on the premise that increases in endogenous testosterone will result in increases in muscle mass, especially when ingested in conjunction with a resistance training program."

So clearly these guys were going to use real DAA correct? At least analyze what they purchased to make sure if conformed to DAA. Surely one would do that... correct? What did they use?

"The PLC group consisted of the oral ingestion of 4 capsules daily containing 3 g of guar gum, whereas the DAA group involved 4 daily capsules containing 3 g of D-ASP (Better Body Sports, Ventura, CA, USA), based on company guidelines for D-ASP and because the dosage was previously shown effective at increasing endogenous testosterone [2]."

Here is the exact product that was used -> Better Body Sports D-Aspartic Acid 120 Capsules

So the study shouldn't be about DAA but should be about "Better Body Sports D-Aspartic Acid". Well I'm sure they tested blood for DAA. Right? Turns out yes. They tested before the program and after (Day 0 and Day 29). The resistance training and Better Body Sports D-Aspartic Acid program was a 28 day program.

"In the DAA group, there was an increase in the serum levels of D-ASP that was not significantly greater than the levels of day 0 or significantly different from PLC (placebo). For serum DDO, when compared with PLC, there was a significant increase in the levels of DDO at day 29 in the DAA group."

What about estrogen?

"The provision of D-ASP has been shown to increase estrogen levels. There are in vitro data from boar [20] and lizard [8] testes demonstrating that endogenous testicular D-ASP enhances gonad aromatase activity. Therefore, based on the possibility that D-ASP supplementation may increase endogenous estrogen levels, thereby altering the testosterone/estrogen ratio, we assessed the levels of estrogen. However, our results showed estrogen levels to be unchanged by D-ASP supplementation, thereby indicating no effectiveness of D-ASP supplementation on up-regulating aromatase activity."

Is that a failure of DAA or Better Body Sports D-Aspartic Acid?

Well let's go back to the test at day 29 for D-ASP and DDO in blood? Only the DDO was significantly raised. What is that?

"The degradative role of DDO is to catalyze the oxidative deamination of d-amino acids to generate the corresponding 2-oxo acids, along with hydrogen peroxide and ammonia (or methylamine). In rodents, the administration of D-ASP was shown to increase DDO activity [22] and [23], suggesting that DDO activity is induced by increased levels of D-ASP. Based on this information, in the present study, it is possible that because of the higher baseline levels of testosterone, as a means of androgen-regulated feedback of the HPG axis, the level of serum D-ASP induced by supplementation was conceivably being degraded by DDO at a rate that rendered it unable to effectively activate the HPG axis."

By the time they start talking about this in the discussion they are looking for reasons why DAA didn't work in raising testosterone. Could be a good rationale. Could be some good reasoning in there. Sounds so good even bright minds adopted one of them there reasons. Hell we are all bright fellows... but why couldn't they test the OTC supplement product they received to see what exactly it was? How pure is it? How is the structure? Couldn't they have at least tested blood levels for DAA throughout? Sure a raised DDO indicates that there is probably is some DAA in that product. But not necessarily. This enzyme participates in alanine and aspartate metabolism. As an example of what DDO acts on and would presumably be raised in response thereto, "One enzyme was D-aspartate oxidase acting on acidic D-amino acids such as D-aspartate and D-glutamate" - Production, purification and characterization of D-aspartate oxidase from the fungus Trichoderma harzianum SKW-36, Shigekazu Yano, Advances in Bioscience and Biotechnology, 3, 7-13 2012

Anyway... I have no problem with the study as it relates to Better Body Sports. As for conveniently substituting DAA for Better Body Sports... I think that greatly weakens this study... and it makes me look sideways at anyone who wants to trumpet "Ah HA! I knew this stuff was worthless or is only worthwhile in XYZ populations."

It doesn't speak to me that way.

ETA - From a letter to the guy who headed up the story.

I wanted to point out a serious potential flaw with the DAA study published August 15 of this year. Although you speculated that the lack of results and even lack of measurable blood levels were due to increased D-amino oxidase levels (a potential unknown homeostatic mechanism), which is insightful, I believe you may have overlooked another, simpler possibility.

The supplement industry as you know is unregulated. Often-times products are shipped en masse from overseas and COAs (certificates of analysis) are not included, contain errors, are forged, etc. The Ventura, CA supplier from whom you purchased is essentially a bargain bin provider.

I am suggesting that rather than a previously unknown DAA homeostatic mechanism that would require very high levels of D-amino oxidase type enzymes, a simpler "mechanism" (if you will) would be that the product used was weak, or even entirely counterfeit. There is plenty of precedent for such a suspicion.

I already did some footwork and emailed the company, Better Body Warehouse Supplements, and asked for a certificate of analysis under the auspices of making a purchase. The reply I received notified me that the product was no longer going to be carried, and that a new brand would be available soon. No COA was offered or mentioned. The web-page for the product went down immediately after I made the inquiry.

You can draw your own inferences from the above facts.

Seeing as the only significant change in the control vs the group given Better Body Warehouse DAA was serum DAAO, it's important to note that alanine and glutamate metabolism involve DAAO.

I would be very interested to know whether independent lab results were obtained by your team, or if a COA was given from Better Body. If not, I would suggest that the study be appended with a note or editor's note that the purity of the product was questionable and may have skewed results.

Hopefully if not, your team still has some of the product (since it's now discontinued) and would consider performing or funding independent tests of the purity and authenticity.

[Flankenstein]

That's the case for myself. I am not a "science guy" but I've been doing lots of reading and research. I thought hCG would be primarily used on TRT to keep the testicles functioning and Clomid would be better for a kick start.

I may be off base but I was also under the impression that hCG would mimic LH and possibly reduce the body's own natural output afterwards whereas Clomid would not have the same effect. Again, I'm a layman, trying to understand a lot of this and there is conflicting information throughout from doctors to scientists to end users.

Yes, hCG has many applications. Preventing testicular atrophy on TRT is certainly one of them.

[WillBrink]

]I'm surprised that it is unclear to you[/B]. If I'm understanding Irish correctly, he is looking to "kick start" endogenous testosterone production before diving head first into TRT. If that is the case, hCG (w/ low dose arimidex depending on hCG dose and lab work) will do a better job than clomid. Again, excuse my brevity and lack of explanation/links to research.

Oh, it's not unclear to me, but I don't agree fully either. HCG works at the T level HPTA and does not correct low T from suppressed HPTA acting as LH and does not kick start the actual HPTA to produce T. In fact, it will suppress it. Clomid works at the HP levels of the HPTA and is actually a better kick starter med for the HPTA. Yes, some docs may use HCG as a form of TRT, but the often need for the AI along with it (greatly increasing costs, need for lab work, etc) due to elevated E2, along with possibility of leydig cell desensitization due to long term use of HCG, and a few other issues, makes it a poor mono therapy choice in my view. If one is going to go on TRT, there's no reason to "kick start" it with HCG.

One can get good responses with Clomid and HCG combined to re start the HPTA*, and some will use small amounts of HCG and T (and AI if indicated) to keep the T part of the HPTA working. For men that want to maintain sperm counts and nad size, it's the way to go.

Studies (see linked already) have found Clomid modestly effective for raising T as mono therapy and it's working via the HP part of the axis vs just the T level, which may be the better option.

Neither are a good choice for TRT as mono therapy in my view.


* = Probably the smartest doc I know in this areas uses Clomid, HCG, and Tomox in a very specific doses and schedule that has excellent responses for suppressed HPTA due to long term AAS use or men who want to come off TRT for some reason. He finds all three, due to their different impact on the HPTA, is most effective.

[WillBrink]

That's the case for myself. I am not a "science guy" but I've been doing lots of reading and research. I thought hCG would be primarily used on TRT to keep the testicles functioning and Clomid would be better for a kick start.

You're correct.

I may be off base but I was also under the impression that hCG would mimic LH and possibly reduce the body's own natural output afterwards whereas Clomid would not have the same effect. Again, I'm a layman, trying to understand a lot of this and there is conflicting information throughout from doctors to scientists to end users.

You have a better handle on it than the majority of docs out there.

[WillBrink]

What are your thoughts regarding this quote in relation to that paper?

The entire thing can be summed up as: more research is needed. Taking the (essentially) worthless mouse studies, and combined with the US study done in humans, combined with some possible wrinkles added by what you posted, would at best, lead one to conclude more research is needed. I will say, lab work I have seen from users "in the wild" found nadda, and interest by users dropped sharply after that study and general lack of "real world" results by users. I'd also have to go back and look at the materials and methods of the study to see if they tested the product for purity and dose, which they often do.