Questions For Anthony Roberts

[SWALE]

Here are a few of your published ideas, taken directly from your posts and papers. Can you explain them to us, please:

1. SERM'S lower estrogens.

2. "take baths in spironolactone",

3. Use of finasteride for PCT.

4. HCG stimulates thyroid hormone production.

We are hoping for logical, reasonable discussion of the above topics. If you require financial compensation for same, please let us know.

[DocJ]

Mmmmm...this could get interesting

[Deacon]

finasteride for PCT - now there is a dumbass theory if I ever hear one

[MANWHORE]

Originally Posted by Deacon

finasteride for PCT - now there is a dumbass theory if I ever hear one

what about Aromasin?

[Beefy]

bump

[jb55638]

This COULD get interesting, but SWALE scared off Anthony "Bill" Roberts.
He won't respond to this post b/c they already spent 14 pages on the same subject two weeks ago. Sill funny, though. MANWHORE--you always crack me up........"what about Aromasin"..........just egging them on, LOL.
What happened to the sexy angel; I can't get my dick up with out looking at it.......now what am I supposed to do??

[MANWHORE]

Originally Posted by jb55638

"what about Aromasin"..........just egging them on, LOL

Yes i could see myself doing something like that but i was being serious. I didn't know Hooker was Bill R. shit i didn't even know .. put 2 and 2 together and even knew Bill was back. Bill is short for Anthony? Yes i am in my own world and basically just see what i want to .. anyway,i was reading Mr. Roberts article about Aromasin on another board i go to which is basically all Vets and is very private. What ever Swale and Bill have going on is up to them,but i did like Bills article and has me thinking about other PCT options. .. There is even a source that has mixed up a PCT with Aromasin in it and guys (not newbees either) are really into it

[SWALE]

The "Bill" Roberts I respect has been around for years. I met him when I considered T-Mag home. He has a background in the sciences, and was working on his PhD in Biochem or Pharm or some related topic at the time. An extremely knowledgeable individual, he is also quite a gentleman.

This "Anthony" Roberts has no training whatsoever in any of the related topics. He obviously has never even read about any of them, nor does he know how to act.

Let's not insult Bill Roberts by confusing him with this character.

[MANWHORE]

O OK .. was that the BILL Roberts i use to talk to way back on Meso? .. the one you know? .. I didn't really talk to him,i would just ask questions about some PCt products and he would answer ... Now who is the guy mentioned in Anabolics 2002 as the steriod researcher (something like that)? that isn't this guy? It's the Bill you know?

[hooker]

Originally Posted by SWALE

Here are a few of your published ideas, taken directly from your posts and papers. Can you explain them to us, please:

1. SERM'S lower estrogens.

2. "take baths in spironolactone",

3. Use of finasteride for PCT.

4. HCG stimulates thyroid hormone production.

We are hoping for logical, reasonable discussion of the above topics. If you require financial compensation for same, please let us know.

Please find the exact article where I said the comments in blue, link us to them (by post) and re-post it, highlighted. Just so I know the context you are referring to....

Also...you're under the mistaken assumption that I read this board regularly, I see. I can't imagine why you think that. I participate on boards where I get a direct benefit from said interaction. This isn't one of them.

I said to switch to Prop at the end of a cycle, and use finasteride, becase in this study (animal), finasteride prevented LH-suppression caused by testosterone propionate...here's a chart from the study:


that chart shows the baseline level of LH in male sheep given a 5-Alpha-Reductase inhibitor (Finasteride), then a chart showing the LH levels in sheep given testosterone propionate, and finally a chart showing LH levels of sheep given testosterone propionate + the inhibitor (graph 3 in the series). You’ll note that although using the inhibitor alone produced no remarkable effects on LH at all, when administered with testosterone, it seems to have allowed LH pulsality to continue very much unaffected (slightly affected, but still very close to baseline) even though exogenous testosterone propionate was administered...all three are from reference...

Reference:Effect of inhibiting 5 alpha-reductase activity on the ability of testosterone to inhibit luteinizing hormone release in male sheep.
Biol Reprod. 1994 Jun;50(6):1244-50

HCG and stimulation of thyroid:

In this study, HCG produced hyperthyroidism:

Endocrinology. 1986 Apr;118(4):1558-66.Related Articles, Links

Thyrotropic activity of acidic isoelectric variants of human chorionic gonadotropin from trophoblastic tumors.

Mann K, Schneider N, Hoermann R.

Previous studies have indicated that hCG has a weak intrinsic thyroid-stimulating activity. Differences in the molecular composition and biological activity of hCG in patients with trophoblastic diseases and pregnant women occur, but are not well defined. Therefore, we have studied the effect of serum samples and purified hCG preparations from patients with trophoblastic diseases on T3 release from human and porcine thyroid slices in vitro. We examined 30 serum samples from 13 patients with nonseminomatous testicular germ cell tumors, 3 from women with choriocarcinoma, and 5 from patients with hydatidiform moles. In all but 1 serum sample from the tumor patients, but in none of 11 serum samples of pregnant women, T3-releasing activity was found. Two patients with testicular cancer and 1 patient with molar pregnancy experienced episodes of frank hyperthyroidism. Isoelectric focusing on polyacrylamide gels of tumor sera (n = 15) revealed substantial amounts of acidic isoelectric variants, pI 3.3-3.9, which were only barely detectable in pregnancy sera. The percentage of acidic hCG variants with pI 3.3-4.0 to total hCG with pI 3.3-5.2, as determined by hCG (+hCG beta) RIA of the eluted fractions of polyacrylamide gel isoelectric focussing, varied from 12-45% in sera of tumor patients and from 0-4% in pregnant sera. We purified the acidic variants of hCG with pI 3.6-3.8 (hCGav) from the urine of our patients. The beta-subunit of purified hCGav had a slightly higher mol wt (35,750) than that of hCG CR 119 (34,190) on polyacrylamide gel electrophoresis. The hCGav showed a dose-dependant stimulation of T3 release and cAMP generation from human thyroid slices, whereas the other hCG fractions on isoelectric focussing had no thyrotropic effect in similar dose levels. The TSH-like activity of hCGav could be roughly estimated as 10 mIU TSH/IU hCGav. Anti-hCG (+hCG beta) antiserum, but not anti-hTSH antiserum, neutralized the biological activity of hCGav. These findings strongly suggest that acidic hCG variants act as functional stimulators of the human thyroid in vitro. Since these molecular variants of hCG can exist in patients with trophoblastic diseases in significant amounts, they could be responsible for some cases of hyperthyroidism in trophoblastic diseases.

PMID: 3004921 [PubMed - indexed for MEDLINE]
Hyperthyroidism due to secretion of human chorionic gonadotropin in a patient with metastatic choriocarcinoma.

Meister LH, Hauck PR, Graf H, Carvalho GA.

Servico de Endocrinologia e Metabologia, Hospital de Clinicas da UFPR, 80060-240 Curitiba, PR. ludimylameister@yahoo.com.br

A 26-year-old pregnant woman presenting with repeated episodes of vaginal bleeding, weight loss, and shortness of breath was diagnosed with choriocarcinoma with metastases to both lungs. Chorionic gonadotropin levels (hCG) were >2.5 x 10(6)mU/mL. Consistent with hCG-induced subclinical hyperthyroidism, she had a suppressed TSH of 0.037 mU/L (0.49 - 4.67), a T4 of 18.1 microg/dL (4.9 - 10.7), and T3 of 136 ng/dL (45 - 137). Chemotherapy with a combined regimen with etoposide, methotrexate, and dactinomycine was started. The initial course was complicated by urosepsis with respiratory distress requiring endotracheal intubation for 3 days. She then improved rapidly, and her thyroid function tests were within normal limits by day 12. Six months later, after ten cycles of chemotherapy, the patient was in remission without signs of residual tumor or hCG-induced paraneoplastic activity.

: Gynecol Endocrinol. 2004 May;18(5):269-77.Related Articles, Links

The human chorionic gonadotropin molecule from patients with trophoblastic diseases has a high thyrotropic activity but is less active in the ovary.

Kato K, Mostafa MH, Mann K, Schindler AE, Hoermann R.

Department of Obstetrics and Gynecology, University of Essen, Essen, Germany.

To examine the pathogenesis of hyperthyroidism in women with trophoblastic diseases, the biological activity of human chorionic gonadotropin (hCG) molecules in women with normal pregnancy (n = 85) and in women with trophoblastic diseases (vesicular mole, n = 30; and choriocarcinoma, n = 12) was compared. Hyperthyroidism (thyroid stimulating hormone (TSH) < 0.3 mIU/l) was observed more frequently in women with trophoblastic diseases. All the sera were then subjected to Chinese hamster ovary cells transfected with the human TSH receptor (CHO-hTSHr cells) and cAMP production was compared. Sera from the women with choriocarcinoma showed the highest cAMP production. Interestingly, significant correlation between serum hCG level and cAMP production in CHO-hTSHr cells was observed only in women with trophoblastic disease. All the sera were then applied to CHO cells transfected with hCG/luteinizing hormone (LH) receptor (CHO-hCG/LHr cells). In contrast to the findings with the TSH receptor, sera from the women with normal pregnancy showed the highest cAMP production in these cells. Correlation between serum hCG level and cAMP production in CHO-hCG/LHr cells was significant only in normal pregnancy. These results indicate that the hCG molecule from women with trophoblastic diseases displays enhanced thyrotropic activity.

PMID: 15346663 [PubMed - indexed for MEDLINE]

1: J Clin Endocrinol Metab. 1994 Apr;78(4):933-8.Related Articles, Links
Interaction of human chorionic gonadotropin (hCG) and asialo-hCG with recombinant human thyrotropin receptor.

Hoermann R, Broecker M, Grossmann M, Mann K, Derwahl M.

Medical Department II, Klinikum Grosshadern, University of Munich, Germany.

hCG is a putative thyroid stimulator. The present studies were undertaken to examine its interaction and that of its desialylated variant asialo-hCG with recombinant human TSH (hTSH) receptor (hTSHr). To this end, we transfected a human thyroid carcinoma cell line (HTC) lacking endogenous TSHr with the full-length cDNA of the hTSHr. Unlike the wild type, the transfected cells, termed HTC-TSHr cells, were able to bind bovine TSH (bTSH) with high affinity and increase cAMP production in response to bTSH stimulation. Of the hCG forms, intact hCG displayed a weak activity to inhibit [125I] bTSH binding to HTC-TSHr cells, with 100 mg/L (2.6 x 10(-6) mol/L) producing maximally a 20% inhibition, whereas asialo-hCG achieved half-maximum binding inhibition at a concentration of 8 mg/L (2.3 x 10(-7) mol/L). The inhibitory constant (Ki) of asialo-hCG for recombinant hTSHr was calculated from saturation experiments in the presence of variable doses of bTSH and a fixed concentration of asialo-hCG to be approximately 8 x 10(-8) mol/L. The interaction of asialo-hCG with TSHr was further assessed by studies of the direct binding of the radioactively labeled hormone to both HTC and HTC-TSHr cells. [125I]Asialo-hCG binding to HTC-TSHr cells was 4.7%, compared to 1.5% in the wild-type cells lacking TSHr and was displaceable by bTSH (0.1-100 IU/L), indicating specific binding of the tracer to TSHr. Functionally, hCG (up to 100 mg/L; 2.6 x 10(-6) mol/L) proved unable to evoke any significant cAMP response over basal values in HTC-TSHr cells, as did asialo-hCG. Asialo-hCG, but not hCG, inhibited bTSH-stimulated adenylate cyclase activity in the cells in a dose-dependent manner. In conclusion, the present data show that intact hCG binds only weakly to HTC-TSHr cells and produces no significant cAMP stimulation, which is at variance with data obtained in FRTL-5 and Chinese hamster ovary-TSHr cells, but in good accord with previous findings in human thyroid membranes. Asialo-hCG, on the other hand, strongly binds to recombinant TSHr and inhibits the cAMP response to bTSH in HTC-TSHr cells, indicating that the desialylated hCG variant directly interacts with the receptor and truly is an antagonist of the hTSHr.

PMID: 8157724 [PubMed - indexed for MEDLINE] Making you look stupid is almost too easy. But I'll take my usual per-article fee for it. Contact the board owner for payment details.

[SWALE]

We'll ignore your impression that being financially compensated by the owner of this Board isn't a "direct benefit", and also the fact you have had plenty of time to respond with insults or to try to promote yourself here amidst posts. I guess that is why I, and all others here, think you read this Forum.

1. "SERM's increase estrogen". This is a quote from you, taken directly from a thread on this very Board, on the "Articles" Forum, where you were supposing yourself sufficiently expert to lecture ME. It is there for all to see. Now, please explain why you think drugs such as Nolvadex and Clomid increase estrogen.

Does someone want to post that quote for the rest of us?

2. Several members have emailed me that you wrote somewhere else there is an appropriate application of topical spironolactone where it is basically applied to the entire body. If you now wish to deny you ever made any such ridiculous recomendation, then please just say so.

3. This concept demonstrates a profound lack of understanding of the physiological processes involved; plus simply a total lack of experience with the medication being recommended. It also sheds light on what you consider a valid thought process. More on that later.

Let's consider what the hormone DHT does for adult males. Better yet, let's think about what happens when it is suppressed with finasteride. In a significant number of men--and those who were not even suffering elevated levels of same to start with---this very often results in weakness, fatigue, fat gain, depression, lack of libido, and frank impotence. Does that sound to anyone like what we are trying to AVOID with PCT? When you add in the overall effects of this very problematic list of negative side effects on our training, and therefore muscle size, we come to the conclusion that you are recommending a drug during PCT which CAUSES all the negative side effects of NOT doing PCT.

A good analogy would be for you to recommend unprotected, promiscious sex to prevent AIDS.

I have several dozen patients who now suffer PERMANENT ill side effects after taking low-dose finasteride for even a short period of time. Did it not ever occur to you to actually learn about the drugs you want people to take?

I see how you have come up with the wacky ideas you write about: you read somewhere that doing this or that elevates LH, so you, in an effort to make a name for yourself by coming up with some new idea, begin writing about using it somewhere in steroid use. Most often the study you have read, and reference as "proof" of your concept, either is not an appropriate use of reference, or simply has no bearing on the topic at all. Simply, you do not understand how to read a study. You made a comment in this very thread which offers even more proof of that fact.

You never consider the overall action of the therapy you propose. This is because you simply cannot, as you have never studied physiology, biochemistry, pharmacology or endocrinology. Even moreso, I see constant abandonment of simple common sense: recommending a drug which causes the symptoms of hypogonadism while trying to treat same. For these resons, you have shown that you cannot even begin to fathom the overall results of what following your advice will bring. This is all just plain lazy.

4. Here we have the same lack of knowledge, experience and common sense from the last example.

The first study discusses a VARIANT of HCG (NOT that found in a bottle from a pharmacy) produced by CANCER cells under very specific conditions. THIS is "evidence" from you?

The second study is also from a cancer patient. As is the third. No cogent application whatsoever.

Reread the abstract from the fourth study you reference. Do you REALLY think this study backs your idea?

While the beta subunit of HCG shares common moiety (electrostatics and sterics) with the beta subunit of TSH, HCG does not promote thyroid production in any useful manner. As soon as I can lay my hands on the PI from a box of HCG, I will provide a quote directly from same. That might have been the first place you thought to look before writing what you have.

Why do you think the "fat farms" abandoned HCG therapy for weight loss 30 years ago?

The article you posted, at Mind and Muscle if memory serves, was a situation where you were advising a female to use HCG as part of PCT. There are more issues involved with that recomendation than just thyroid hormone production, including use of an androgen-inducing substance during PCT. More of the lack of knowledge, and common sense, demonstrated by this "expert".

Were I you, I would hold off on giving anyone any more advice until you spend a couple of years actually learning some of the science necessary to develop even a rudimentary understanding of these topics. Of course, that would put you amongst the very academics you so profoundly despise. Then actually get some field experience--what you have bragged about so far impresses no one (an "almost Mr. Tennessee" who magically became "Mr. Tennesse" a few days later). Your time spent coaching soccer, or whatever else it is you do, has failed you miserably where learning science is concerned. Until then, you are hurting people naive enough to follow your advice. These are serious matters, indeed.

[hooker]

Originally Posted by SWALE

We'll ignore your impression that being financially compensated by the owner of this Board isn't a "direct benefit", and also the fact you have had plenty of time to respond with insults or to try to promote yourself here. I guess that is why I, and all others here, think you read this Forum.

1. "SERM's increase estrogen". This is a quote from you, taken directly from a thread on this very Board, on the "Articles" Forum, where you were supposing yourself sufficiently expert to lecture ME. It is there for all to see. Now, please explain why you think drugs such as Nolvadex and Clomid increase estrogen.

Does someone want to post that quote for the rest of us?

2. Several members have emailed me that you wrote somewhere else there is an appropriate application of topical spironolactone where it is basically applied to the entire body. If you now wish to deny you ever made any such ridiculous recomendation, then please just say so.

3. This concept demonstrates a profound lack of understanding of the physiological processes involved; plus simply a total lack of experience with the medication being recommended. It also sheds light on what you consider a valid thought process. More on that later.

Let's consider what the hormone DHT does for adult males. Better yet, let's think about what happens when it is suppressed with finasteride. In a significant number of men--and those who were not even suffering elevated levels of same to start with---this very often results in weakness, fatigue, fat gain, depression, lack of libido, and frank impotence. Does that sound to anyone like what we are trying to AVOID with PCT? When you add in the overall effects of this very problematic list of negative side effects on our training, and therefore muscle size, we come to the conclusion that you are recommending a drug during PCT which CAUSES all the negative side effects of NOT doing PCT.

A good analogy would be for you to recommend unprotected promiscious sex to prevent AIDS.

I have several dozen patients who now suffer PERMANENT ill side effects after taking low-dose finasteride for even a short period of time. Did it not ever occur to you to actually learn about the drugs you want people to take?

I see how you have come up with the wacky ideas you write about: you read somewhere that doing this or that elevates LH, so you, in an effort to make a name for yourself by coming up with some new idea, begin writing about using it somewhere in steroid use. Most often the study you have read, and reference as "proof" of your concept, either is not an appropriate use of reference, or simply has no bearing on the topic at all. Simply, you do not understand how to read a study. You made a comment in this very thread which offers even more proof of that fact.

You never consider the overall action of the therapy you propose. This is because you simply cannot, as you have never studied physiology, biochemistry, pharmacology or endocrinology. Even moreso, I see constant abandonment of simple common sense: recommending a drug which causes the symptoms of hypogonadism while trying to treat same. This is all just plain lazy.

4. Here we have the same lack of knowledge, experience and common sense from the last example.

The first study discusses a VARIANT of HCG (NOT that found in a bottle from a pharmacy) produced by CANCER cells under very specific conditions. THIS is "evidence" from you?

The second study is also from a cancer patient. As is the third. No cogent application whatsoever.

Reread the abstract from the fourth study you reference. Do you REALLY think this study backs your idea?

While the beta subunit of HCG shares common moiety (electrostatics and sterics) with the beta subunit of TSH, HCG does not promote thyroid production in any useful manner. As soon as I can lay my hands on the PI from a box of HCG, I will provide a quote directly from same. That might have been the first place you thought to look before writing what you have.

Why do you think the "fat farms" abandoned HCG therapy for weight loss 30 years ago?

The article you posted, at Mind and Muscle if memory serves, was a situation where you were advising a female to use HCG as part of PCT. There are more issues involved with that recomendation than just thyroid hormone production. More of the lack of common sense demonstrated by this "expert".

Thats for articles, not posts.

I notice you haven't posted the direct quote from me. Please do so, and stop stalling. Make your next post thoose 2 quotes from me, in quote tags, with a reference to the article or post where I made that claim. Lets see it. Stop stalling.

More studies showing that HCG stimulates thyroid production in rodents then one showing so in humans (albeit less strongly):

Horm Res. 1983;17(1):36-42.Related Articles, Links

Thyroidal responses to human chorionic gonadotropin in the chick and rat.

Pekary AE, Azukizawa M, Hershman JM.

The thyrotropic activity of human chorionic gonadotropin (hCG) has been examined in the chick and the rat. Uptake of 32PO4 by chick thyroid increased significantly with injection of bovine thyrotropin (bTSH) with a maximum response at 2.4 mU per chick. On the other hand, no significant stimulation of 32PO4 uptake was detected with injection of graded doses of highly purified hCG up to 0.25 mg per chick. 1 mg of partially purified hCG, equivalent in biological potency to the maximum dose of highly purified hCG used in the chick, did induce a significant increase in 32PO4 uptake. In rats, highly purified hCG stimulated a very significant release (p less than 0.001) of 125I from the thyroid and partially purified hCG had a thyrotropic activity equivalent to 0.42 microU bTSH/U hCG, identical to the value we reported in mice, 0.42 microU bTSH/U hCG. The duration of hCG action on thyroidal release of 125I in the rat was longer than that for bTSH, as it is in the mouse. hCG also induced a significant rise in the serum level of triiodothyronine in rats. We conclude that pure hCG is a weak thyrotropic substance in the rat but not in the chick. These results and other evidence suggest an inhibitory role for the densely glycosylated 30 amino acid residue C-terminal extension on the beta-subunit of hCG which limits, by steric hindrance, the interaction of the TSH-like hCG 'core' with thyrotropin receptors.

PMID: 6840670 [PubMed - indexed for MEDLINE]

J Clin Endocrinol Metab. 1978 Oct;47(4):898-901.Related Articles, Links

Effect of human chorionic gonadotropin on thyroid function in euthyroid men.

Sowers JR, Hershman JM, Carlson HE, Pekary AE.

The effect of large doses of commercial hCG on thyroid function was studied in eight men who received 100,000 or 150,000 IU hCG iv. These large doses of hCG produced definite thyroidal iodine release (TIR) responses in all eight men. The TIR after hCG administration was more delayed and of lesser magnitude than the TIR responses to TSH and TRH. There were no significant changes in serum T4, T3, or TSH for 48 h after hCG administration. No clinical side effects were noted in the subjects after iv administration of these large doses of hCG. The results of this study indicate that hCG is a weak thyroid stimulator in man.

PMID: 122416 [PubMed - indexed for MEDLINE] Actually, no. You're 100% incorrect. I advised her to use it to fix her thyroid, not as PCT. Can you even read?

Do you like being wrong so often?

The thing that cracks me up about you is that you never post any references or anything other than "I'm a doctor, and I declare you wrong"

You even said the scientists' conclusions in one of my studies was wrong in another thread, and claimed that I posted "only animal studies" when one was also in human men!

Ha ha...

Also....have you noticed that none of the people you suggested to remove me from their payroll have? Thats what they think of you...they disregarded you totally. Pathetic.

[SWALE]

Yes, "Bill Roberts" is the one who provided the articles there and here. This "Roberts" is not the same guy. I can see where the illusion arises; yet no one who knows anything about this stuff would credit "Anthony Roberts" blatherings with "Bill Roberts" extensive knowledge and experience.

I am glad to clear up this matter.

I have never met Bill Roberts face-to-face. But he and I emailed back and forth years ago, and he gave me a lot of help.