Find round 1 here.

This time I'm going to try the androgen side of things, because stopping estrogen didn't fucking work.

Running:

Wks

1-3 Havoc @ 20 mg ED + Lipoderm Ultra (4 squirts BID on the chest) + low calorie keto-ish diet
4-8 (ish) Andractim @ 5 mg (2.5/side) ED + recomp/maintenance diet
9-18 (ish) clomid (100, 50 for a few days, then taper to 25 mg for the rest) + ATD @ 25 mg EOD (very low dose, but as a suicide inhibitor it should work fine)

I will possibly add in Bromo / caber for those last 10 weeks as well pending the results of a prolactin blood test I took yesterday (Steve carries them).


Overall idea: Gyno results from a imbalance between androgen and estrogen signaling (E signaling is amplified by Prl). So wks 1-3 I'm burning fat, which has lots of aromatase. Hopefully chest fat will be emphasized, lipo will free up the FA and the caloric deficit will eat them up while Havoc plays 2 roles: prevent muscle wasting and induce a little HPTA shutdown (maybe). Shutdown in this case is good because low endogenous aromatizable steroids means low estrogen, optimizing the next step: andractim. This should make my A:E ratio pretty fucking amazing in my chest for a while.

The final step (clomid + atd + maybe bromo) should "seal the deal," with 10 weeks of elevated test and low(er) E.

I'm also using forskolin + RK intermittently, as well as various other supps. Short on time, I'll go into it later. Maybe.


I'm currently on day 2. I like lipo -- the cool feeling is nice, like menthol.


Starting pics:

I am not sure that you have actual "gyno" it looks like it may just be skin, not breast tissue underneath. What about a skin tightening cream? Also, did you used to be a fat kid?

Thats gyno and I think the andractim will make some substantial improvements in the situation.

Dash, out of curiosity, what is the scar on your left side from?

He has the puffy nipples, but other than that it is hard to see any appearance breast tissue. I wonder if he has eradicated all breast tissue and now just has puffy nipples and some loose skin.

OT comment - your looking hyyyyuge Dash. Not sure what your putting in your lattes, but I want that cup'o'java.

DHEA may be useful during the first few weeks:

http://www.mindandmuscle.net/forum/index.php?showtopic=1771

DHEA has an estrogenic metabolite and an AI won't prevent the formation of it. Can't recall the name/structure.

It's 5-AD, an ER agonist.

PA weighs in : http://forum.bodybuilding.com/showthread.p...p;highlight=5AD

I hope dashforce wins this comp over gyno this time.

Man your love handle area is really deficient of fat. Is that fat distribution due to anything in particular?

Thanks,DHEA is out then.

Per an old post of Loki's,I've been looking into Lisuride Maleate.




This may very well be a viable alternative to bromo or caber.

isn't that the super bromo we had discussed earlier? Is it to be had in today's market?


EDIT: dopergin is it's pharm name apparently. It has been approved for the onset stages of Parkinson's

Nope, plenty of mammary tissue branching throughout the chest, some all the way to the armpits. Long strands.

Which reminds me -- I'm going to do caliper measurements so we can get something more concrete than "well my gyno might have shrunk a little..." (although it seems that my masses do shrink and grow noticeably... most notable is that they seem much, much smaller immediately post workout... not the nipples, but the actual hard cylinder of tissue feels like the diameter has shrunk).

Anyway, calipers (Accu-Measure 3000)--

Chest (fat), halfway between nipple and armpit -- 4-4.5 mm
Supriliac 6-6.5mm

Rt mass (the one directly under the nipple, as there are several) ~6 mm (hard to measure)
Lt mass ~4mm (feels much smaller than rt)




I used to BMX when I was a teenager. Just one of many wipeouts (and a relatively minor one, at that). Had the end of a handlebar come across my side, was actually very superficial, just left a big, wide, shallow scab.



The nipples are puffy because of glandular tissue underneath. Having gyno doesn't necessarily mean you'll have huge amounts of chest fat, just glands. And glands are not all that huge. Again, this is real live actual gynecomastia. I think there's a more detailed description (if you're interested) in the log that I linked to in my first post.



Ha. I knew I liked you for some reason, thanks. These are just gyno pics. Better pics of my lame-ass physique are here, taken at the same time as these.

I'm following a program Marc McD laid out for me in the IC (I'm sure you can dig up the thread). For back, it's got some cable rows, DLs, weighted pullups, lying incline back flyes/flies (whatever these are called... basically lat raises but leaning over at 45*, works rear delts and other back stuff) and cable pullovers.




Thanks for the well-wishes. I'm surprised -- I always felt like I carried disproportionately more fat in my love handles than other areas of my body. Nothing special -- short rest periods and lots of supersets, no cardio, keep carbs in check, and a job that keeps me constantly on my feet and moving (I'm a waiter). I bet that I would gain hella weight if I changed jobs -- it feels like I'm going a million miles an hour carrying 50 lb trays of food, and I do it for 5-11 hour shifts 4 or so days per week, plus walking b/t classes on campus. That's a lot of basically low intensity cardio, I suppose.



Colin, you make me laugh . You're always looking for a new way to skin a cat. Do you have something against actually using bromo or caber? I mean bromo has a track record of like 30 years, with some women having reported continuous use for up to 20 years... That's pretty damn good man. Caber's recently had a few issues, and I'm not sure I like the long-ass half life, but... damn man. It cracks me up how you're always looking for new angles to tackle this stuff.

I've got my reasons,will expound later.But to start,below is the tip of the iceberg as to why LM looks sweet.

And I'm too lazy ATM to explain relevance of these studies after digging them all up:




Independence of estrogen-induced pituitary proliferation on local IGF-I mRNA and EGF mRNA expression. Modifying effects of tamoxifen and terguride.
Hána V, Haluzík M, Schreiber V.

Third Department of Internal Medicine, First Faculty of Medicine, Charles University Prague, Czech Republic.

Pituitary hyperplasia as well as proliferation of the endometrium are typical responses to estrogen administration in rodents. Both insulin-like growth factor-I (IGF-I) and epidermal growth factor (EGF) have been implicated as paracrine mediators and amplifiers of estrogen action in the rodent uterus. The auto/paracrine role of IGF-I, EGF, their receptors and IGF binding proteins in pituitary proliferation has not yet been solved. Here we have used a semi-quantitative reverse transcription polymerase chain reaction (RT PCR) assay to demonstrate the changes in IGF-I mRNA and EGF mRNA abundance in the proliferating male rat pituitary in response to estradiol benzoate (EB; 1 mg/kg b.w. twice weekly i.m. for 3 weeks) and modifying effect of drugs antagonizing the pituitary enlargement - antiestrogen tamoxifen (TAM, 5 mg/kg b.w. daily) and also the dopaminergic agonist terguride (TER, 0.66 mg/kg b.w. daily, routinely used for the treatment of prolactinomas). In three separate experiments, EB induced a 2.2-2.5 fold increase in pituitary weight. The abundance of IGF-I and EGF mRNAs in pituitaries of EB-treated animals did not differ from the controls in two experiments and in the third series with the most marked pituitary hyperplasia mRNAs of both growth factors were even significantly decreased. Antiestrogen TAM administered with EB partially blocked the EB-induced proliferation and significantly stimulated IGF-I mRNA (p=0.003) and EGF mRNA (p=0.023) expression, while EB or TAM alone did not stimulate mRNAs of the studied growth factors. Significant antiproliferative effect of dopaminergic agonist TER on EB-induced pituitary proliferation (p=0.006) was accompanied with decreased IGF-I mRNA (p=0.025), but not EGF mRNA abundance. Our results suggest that the estrogen-induced pituitary proliferation is independent of the local expression of IGF-I and EGF mRNAs.

PMID: 9706996 [PubMed - indexed for MEDLINE]


Effects of bromocriptine and terguride on cell proliferation and apoptosis in the estrogen-stimulated anterior pituitary gland of the rat.
Yonezawa K, Tamaki N, Kokunai T.

Department of Neurosurgery, Kobe University School of Medicine.

The effects of bromocriptine and terguride on the estrogen-stimulated anterior pituitary gland of the female Wistar rat were investigated. Pituitary weight and serum prolactin (PRL) levels were reduced by treatment with bromocriptine or terguride. Immunohistological staining for proliferating cell nuclear antigen (PCNA) revealed that the PCNA labeling index of PRL-producing cells was significantly decreased by treatment with bromocriptine or terguride compared with untreated cells. The number of apoptotic cells analyzed by the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate-biotin nick end labeling method was significantly increased in rats treated with bromocriptine or terguride. Suppression of cell proliferation and induction of apoptosis are important effects of bromocriptine and terguride in the treatment of prolactinomas and other hyperprolactinemias.

PMID: 9465588 [PubMed - indexed for MEDLINE]



Lisuride, a dopamine receptor agonist with 5-HT2B receptor antagonist properties: absence of cardiac valvulopathy adverse drug reaction reports supports the concept of a crucial role for 5-HT2B receptor agonism in cardiac valvular fibrosis.
Hofmann C, Penner U, Dorow R, Pertz HH, Jähnichen S, Horowski R, Latté KP, Palla D, Schurad B.

Global Medical Safety, Schering AG, Berlin, Germany. christoph.hofmann@schering.de

OBJECTIVES: The high incidence of fibrotic cardiac valvulopathies reported in association with the 8beta-ergoline dopamine (DA) agonist, pergolide, and also case reports for cabergoline and bromocriptine have made it necessary to review the theoretical basis and actual findings in the case of another DA agonist, the 8alpha-ergoline lisuride (used since the 1970s for migraine prophylaxis as well as since the 1980s for its prolactin-lowering and anti-Parkinson activity). METHODS: We have reviewed the pharmacology of lisuride in relation to other DA agonists, and we have performed a throughout literature search as well as a search of our own and other adverse drug reaction databases for a possible relationship of lisuride with cardiac valvulopathy or for any reports of fibrosis in other locations. RESULTS: Our review of the pharmacology and the literature strongly suggests that drug-induced cardiac valvulopathies are always related to a stimulatory drug effect on trophic 5-HT(2B) receptors. As lisuride is devoid of such an effect, but on the contrary is an extremely potent 5-HT(2B) antagonist, an association of lisuride therapy with cardiac valvulopathies seems to be highly unlikely. In agreement with this hypothesis, not a single report of a cardiac valvulopathy associated with lisuride therapy has been identified in any database so far.Furthermore, against a background of an estimated 360,000 patient years, we have found only a very small number of cases of any other form of fibrosis (1x retroperitoneal, 2x pleural, 2x pulmonary, 1x interstitial pulmonary changes), in part combined with other risk factors and confounding variables. This closely matches 4 reports available from WHO (1x retroperitoneal, 3x pleural fibrosis). In addition, only 5 other possibly related conditions (3x pleural effusion, 1x pleuritis, 1x pericarditis) were identified in the lisuride adverse drug reaction database of Schering, Berlin. CONCLUSIONS: No link has been found between lisuride use and fibrotic cardiac valvulopathy, in agreement with the 5-HT(2B) receptor antagonist effect of this drug. The very low incidence of spontaneous reports of any other fibrosis could be even compatible with an association by chance in the population exposed to lisuride. Although close monitoring for this kind of side effects is still to be recommended in the therapy with lisuride, our data do not support the concept of a class effect suggesting that all ergot-derived drugs and especially DA receptor agonists with some chemical similarity to the ergot structure will cause or facilitate cardiac valvulopathies as observed with pergolide.

PMID: 16614540 [PubMed - indexed for MEDLINE]


Effects of LSD, ritanserin, 8-OH-DPAT, and lisuride on classical conditioning in the rabbit.
Welsh SE, Kachelries WJ, Romano AG, Simansky KJ, Harvey JA.

Department of Pharmacology, Allegheny University of the Health Sciences, Philadelphia, PA 19129, USA.

d-Lysergic acid diethylamide (LSD), an agonist at the 5-HT(2A/2C) and 5-HT1A receptors, has previously been demonstrated to enhance associative learning as measured by accelerated acquisition of the rabbit's classically conditioned nictitating membrane (NM) response. The present study examined further the role of these receptors in the action of LSD. LSD (30 nmol/kg, I.V.) significantly enhanced conditioned response (CR) acquisition to both tone and light conditioned stimuli (CSs), while the 5-HT1A receptor agonists 8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT; 50 and 200 nmol/kg) and lisuride (0.3-30 nmol/kg) had no effect. Ritanserin (6.7-6700 nmol/kg, S.C.), a selective 5-HT(2A/2C) receptor antagonist, retarded acquisition of CRs to both tone and light CSs in a dose-dependent manner. Ritanserin (6.7-670 nmol/kg, S.C.) also dose dependently antagonized the enhancement of CR conditioning produced by LSD (30 nmol/kg, I.V.) to both tone and light CSs. We conclude that the enhancement of CR acquisition by LSD was due to an action at the 5-HT(2A/2C) receptor. These results suggest that the 5-HT(2A/2C) receptor plays an important role in learning.

PMID: 9476997 [PubMed - indexed for MEDLINE]




8R-lisuride is a potent stereospecific histamine H1-receptor partial agonist.
Bakker RA, Weiner DM, ter Laak T, Beuming T, Zuiderveld OP, Edelbroek M, Hacksell U, Timmerman H, Brann MR, Leurs R.

Leiden/Amsterdam Center for Drug Research, Department of Medicinal Chemistry, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. ra.bakker@few.vu.nl

The human histamine H1 receptor (H1R) is an important, well characterized target for the development of antagonists to treat allergic conditions. Many neuropsychiatric drugs are known to potently antagonize the H1R, thereby producing some of their side effects. In contrast, the tolerability and potential therapeutic utility of H1R agonism is currently unclear. We have used a cell-based functional assay to evaluate known therapeutics and reference drugs for H1R agonist activity. Our initial functional screen identified three ergot-based compounds possessing heretofore-unknown H1R agonist activity. 8R-lisuride demonstrated potent agonist activity in various assays including receptor selection and amplification technology, inositol phosphate accumulation, and activation of nuclear factor-kappaB with pEC50 values of 8.1, 7.9, and 7.9, respectively, and with varying degrees of efficacy. Based on these assays, 8R-lisuride is the most potent stereospecific partial agonist for the human H1R yet reported. Investigation of the residues involved in histamine and lisuride binding, using H1R mutants and molecular modeling, have revealed that although these ligands are structurally different, the lisuride-binding pocket in the H1R closely corresponds to the histamine-binding pocket. The discovery of a potent stereospecific partial H1R agonist provides a valuable tool to further characterize this important therapeutic target in vitro.

PMID: 14978232 [PubMed - indexed for MEDLINE]



Muscle GLUT-4 and insulin binding to erythrocytes and to adipose, liver and muscle tissue in genetically hypertensive obese rats and in their lean siblings: effect of long lasting terguride treatment.
Golda V, Hilgertová J, Zórad S.

Institute of Experimental Neurosurgery, Charles University, Faculty of Medicine and Teaching Hospital, Hradec Králové.

Experiments were performed in the genetically hypertensive obese rats of Koletsky type (SHR/N-cp) and in their lean siblings of both sexes. Insulin binding to erythrocytes and to adipose tissue, lever tissue and muscle tissue was monitored in the control animals and in the animals under the long lasting terguride treatment. In control animals insulin binding shows substrain and tissue dependence being elevated in lean rats except insulin binding to erythrocytes where inverse is true. Terguride increases percentage of specific insulin binding to erythrocytes in all groups except obese females, terguride increases percentage of specific binding to adipose tissue except lean females, the mentioned drug remained without effect in muscle tissue in all group except lean females where drug induced elevation was detected. The effect of terguride in liver tissue was monitored only in males of both substrains, elevation was found only in lean. GLUT-4 was analyzed only in muscle tissue. The effect of terguride was found in obese females, i.e., in the group which shows reduced GLUT-4 relative to lean females.

PMID: 9919714 [PubMed - indexed for MEDLINE]



Five-year follow-up of early lisuride and levodopa combination therapy versus levodopa monotherapy in de novo Parkinson's disease. The French Lisuride Study Group.
Allain H, Destée A, Petit H, Patay M, Schück S, Bentué-Ferrer D, Le Cavorzin P.

Laboratoire de Pharmacologie Expérimentale et Clinique et Service de Neurologie, Faculté de Médecine, Université de Rennes I, Rennes, France.Herve.Allain@univ-rennes.fr

The value of an early initial coadministration of levodopa (L-dopa) and lisuride in Parkinson's disease was the main goal of the present study. Eighty-two patients with recently diagnosed idiopathic Parkinson's disease were randomized into two groups for treatment with L-dopa alone or L-dopa + lisuride. The trial was double-blinded for the first year and open for the following 4 years. Selegiline (10 mg/day b.i.d.) was added in both groups at the end of the first year. Outcome measures were evolution of L-dopa dosage and Unified Parkinson's Disease Rating Scale scores and subscores, and incidence of motor complications. The dropout rate was higher in the L-dopa group (63.4%) than in the combination group. Motor improvement was better (p < 0.01) in the L-dopa + lisuride group. Expected motor complications were rare, moderate and equivalent in the two groups despite a difference in L-dopa dosage (446.7 vs. 387.5 mg/day). Long-term follow-up demonstrated the L-dopa-sparing effect of lisuride (average 1 mg/day), the beneficial effect of early combination therapy on motor status and the paucity of motor complications in both groups. Copyright 2000 S. Karger AG, Basel

PMID: 10894991 [PubMed - indexed for MEDLINE]



Hyperprolactinemia in obese as well as in lean females of Koletsky rats: effect of long lasting terguride treatment.
Golda V, Jurcovicová J.

Institute of Experimental Neurosurgery, Charles University, Faculty of Medicine and Teaching Hospital, Hradec Králove.

Plasma prolactin was measured in genetically hypertensive obese Koletsky rats, in their lean siblings and in normotensive rats of Wistar strain. Lean as well as obese females show hyperprolactinemia. The males of Wistar strain as well as obese rats and their siblings show comparable prolactinemia except lean males which show higher level than Wistar males. Sex dependence of prolactinemia is missing in the rats of Wistar strain. Long lasting terguride treatment decreases prolactinemia in obese as well as lean rats of both sexes. The drug showed decreased prolactinemia in the males of Wistar strain. When the group of rats are considered in correlation computation positive correlation can be documented between total plasma cholesterol and plasma prolactin. In obese females positive correlation was found between plasma insulin and plasma prolactin.

PMID: 9951046 [PubMed - indexed for MEDLINE]




Muscle GLUT-4 and insulin binding to erythrocytes and to adipose, liver and muscle tissue in genetically hypertensive obese rats and in their lean siblings: effect of long lasting terguride treatment.
Golda V, Hilgertová J, Zórad S.

Institute of Experimental Neurosurgery, Charles University, Faculty of Medicine and Teaching Hospital, Hradec Králové.

Experiments were performed in the genetically hypertensive obese rats of Koletsky type (SHR/N-cp) and in their lean siblings of both sexes. Insulin binding to erythrocytes and to adipose tissue, lever tissue and muscle tissue was monitored in the control animals and in the animals under the long lasting terguride treatment. In control animals insulin binding shows substrain and tissue dependence being elevated in lean rats except insulin binding to erythrocytes where inverse is true. Terguride increases percentage of specific insulin binding to erythrocytes in all groups except obese females, terguride increases percentage of specific binding to adipose tissue except lean females, the mentioned drug remained without effect in muscle tissue in all group except lean females where drug induced elevation was detected. The effect of terguride in liver tissue was monitored only in males of both substrains, elevation was found only in lean. GLUT-4 was analyzed only in muscle tissue. The effect of terguride was found in obese females, i.e., in the group which shows reduced GLUT-4 relative to lean females.

PMID: 9919714 [PubMed - indexed for MEDLINE]



Agonist activity of LSD and lisuride at cloned 5HT2A and 5HT2C receptors.
Egan CT, Herrick-Davis K, Miller K, Glennon RA, Teitler M.

Department of Pharmacology and Neuroscience, Albany Medical College, NY 12208, USA.

Evidence from studies with phenylisopropylamine hallucinogens indicates that the 5HT2A receptor is the likely target for the initiation of events leading to hallucinogenic activity associated with LSD and related drugs. Recently, lisuride (a purported non-hallucinogenic congener of LSD) was reported to be a potent antagonist at the 5HT2C receptor and an agonist at the 5HT2A receptor. LSD exhibited agonist activity at both receptors. These data were interpreted as indicating that the 5HT2C receptor might be the initiating site of action for hallucinogens. To test this hypothesis, recombinant cells expressing 5HT2A and 5HT2C receptors were used to determine the actions of LSD and lisuride. LSD and lisuride were potent partial agonists at 5HT2A receptors with EC50 values of 7.2 nM and 17 nM, respectively. Also, LSD and lisuride were partial agonists at 5HT2C receptors with EC50 values of 27 nM and 94 nM, respectively. We conclude that lisuride and LSD have similar actions at 5HT2A and 5HT2C receptors in recombinant cells. As agonist activity at brain 5HT2A receptors has been associated with hallucinogenic activity, these results indicate that lisuride may possess hallucinogenic activity, although the psychopharmacological effects of lisuride appear to be different from the hallucinogenic effects of LSD.

PMID: 9600588 [PubMed - indexed for MEDLINE]


Lisuride prevents learning and memory impairment and attenuates the increase in extracellular dopamine induced by transient global cerebral ischemia in rats.
Caldwell MA, Reymann JM, Allain H, Leonard BE, Bentué-Ferrer D.

Department of Pharmacology, University College Galway, Ireland.

In this experiment, we tested the efficacy of neuroprotection with lisuride, a dopamine agonist, using the 4-vessel occlusion rat model. Functional improvement was evaluated with two behavior tests exploring learning and memorization capacity in the rat, the Morris water maze and the 14-unit T-maze, 18 days after ischemia. Extracellular dopamine levels during ischemia were determined in search of a possible neuroprotection mechanism. Dopamine and its metabolites, DOPAC and HVA, as well as the serotonin metabolite, 5-HIAA, were assayed with HPLC-EC, in striatal extracellular fluid obtained by in vivo microdialysis in the awake rat. Lisuride was administered at a total dose of 10 ng by continuous intrastriatal infusion or at the dose of 0.5 mg/kg by i.p. infusion, 160 minutes before onset of ischemia for the neurochemical study and at the dose of 0.5 mg/kg via i.p. infusion, 1 hour before occlusion of the carotid arteries, for the behavior tests. Behavioral testing showed significantly better recovery in both sets of behavioral tests, with more pronounced positive results with the 14-unit T-maze, in comparison with the saline-treated animals. Microdialysis confirmed a significant attenuation of the ischemia-induced dopamine surge, whatever the mode of administration, compared with saline-treated animals. These results show that lisuride offers significant neuroprotection from the effect of experimental transient global forebrain cerebral ischemia in the rat; the mechanism would imply, at least in part, reduced levels of extracellular dopamine.

PMID: 9401751 [PubMed - indexed for MEDLINE]

is this pubescent gyno?

That was a lot of abstracts, but I'm not sure how most of them are relevant.

My point was, why use a new drug when an old drug does just as well? Might look at the full text to see if there was a difference in the magnitude of results, but this one seems to suggest that bromo works just as well.

Effects of bromocriptine and terguride on cell proliferation and apoptosis in the estrogen-stimulated anterior pituitary gland of the rat.
Yonezawa K, Tamaki N, Kokunai T.

Department of Neurosurgery, Kobe University School of Medicine.

The effects of bromocriptine and terguride on the estrogen-stimulated anterior pituitary gland of the female Wistar rat were investigated. Pituitary weight and serum prolactin (PRL) levels were reduced by treatment with bromocriptine or terguride. Immunohistological staining for proliferating cell nuclear antigen (PCNA) revealed that the PCNA labeling index of PRL-producing cells was significantly decreased by treatment with bromocriptine or terguride compared with untreated cells. The number of apoptotic cells analyzed by the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate-biotin nick end labeling method was significantly increased in rats treated with bromocriptine or terguride. Suppression of cell proliferation and induction of apoptosis are important effects of bromocriptine and terguride in the treatment of prolactinomas and other hyperprolactinemias.

PMID: 9465588 [PubMed - indexed for MEDLINE]

Half or more of the studies have no relevance to gyno but indicate that there are numerous other benefits to be had with terg (body comp via GLUT-4 binding and so on) over the long term with the same safety profile getting two thumbs up.

It may even have some hallucigenic properties (recreational purposes) at higher dosages as terg is comparable to LSD in several respects.

Bromo may work just as well WRT prolactin but the last time I used bromo it made me feel like complete shit.However the bulk of the lethargy/nausea was probably due to concurrent use of Rimonabant.Even if proves to be the case,terg looks like the better choice between the two,given tergs' other positive benefits.

for the record Dash I meant Latte' as in the drink, but your lats are the cat's ass as well. Good work.

Damn I'm fuckin retarded. Esp because my latts are pretty poor - that's one of the things Marc's program was specifically designed to work on lol.

Ha. Haha.

Dat be nice lattes dere dashforce. I can tell you are holding a coffee just outside the picture frame.

what dose of bromo are you thinking here Dash?

Couple thoughts:

It seems that bezafibrate could be a replacement for high dose CLA,or both could be used if not opposed to the expense.Beza is pretty cheap though,in comparison to 20 grams or so of CLA ED.

OTOH,I did read a case report of beza inducing gyno so it would be better if gemfibrozil (no reports of inducing gyno) relpicated the effects on PPARbeta as seen in the study below with beza.I haven't looked into gem's effect on PPARbeta yet but I'm guessing it would be weaker as gem is the weaker fibrate of the two by far.Still,if CLA + gem were used,some synergy has to take place.

Incidentally I happened across an interesting study on NO and its effects on mammory gland tissue and estrogen,which sucks as this means that I will have to quit smoking if I want my gyno cessation cycle to actually work.Motherfucker ....that study is directly following the first.The upside is that NO can be cheaply and drastically bumped through citriline (eh,sp) malate supplementation,as effectively as consuming A-AGK by the hour so we have a another weapon in our "no more moobs" onslaught.


Peroxisome proliferator-activated receptor beta expression in human breast epithelial cell lines of tumorigenic and non-tumorigenic origin.
Suchanek KM, May FJ, Lee WJ, Holman NA, Roberts-Thomson SJ.

School of Pharmacy, The University of Queensland, St. Lucia, QLD 4072, Australia.

Peroxisome proliferator-activated receptor beta (PPARbeta) is a member of the nuclear hormone receptor superfamily and is a ligand activated transcription factor, although the precise genes that it regulates and its physiological and pathophysiological role remain unclear. In view of the association of PPARbeta with colon cancer and increased mRNA levels of PPARbeta in colon tumours we sought in this study to examine the expression of PPARbeta in human breast epithelial cells of tumorigenic (MCF-7 and MDA-MB-231) and non-tumorigenic origin (MCF-10A). Using quantitative RT-PCR we measured PPARbeta mRNA levels in MCF-7, MDA-MB-231 and MCF-10A cells at various stages in culture. After serum-deprivation, MDA-MB-231 and MCF-10A cells had a 4.2- and 3.8-fold statistically greater expression of PPARbeta compared with MCF-7 cells. The tumorigenic cell lines also exhibited a significantly greater level of PPARbeta mRNA after serum deprivation compared with subconfluence whereas such an effect was not observed in non-tumorigenic MCF-10A cells. The expression of PPARbeta was inducible upon exposure to the PPARbeta ligand bezafibrate. Our results suggest that unlike colon cancer, PPARbeta overexpression is not an inherent property of breast cancer cell lines. However, the dynamic changes in PPARbeta mRNA expression and the ability of PPARbeta in the MCF-7 cells to respond to ligand indicates that PPARbeta may play a role in mammary gland carcinogenesis through activation of downstream genes via endogenous fatty acid ligands or exogenous agonists.

PMID: 12009300 [PubMed - indexed for MEDLINE]



No more Lucky Strikes for Colin:


Nitric oxide produced by inducible nitric oxide synthase is associated with mammary tumorigenesis in irradiated rats.
Inano H, Onoda M.

Redox Regulation Research Group, Research Center for Radiation Safety, National Institute of Radiological Sciences, 9-1 Anagawa-4-chome, Inage-ku, Chiba 263-8555, Japan. inano@nirs.go.jp

This study evaluated whether nitric oxide (NO) derived from nitric oxide synthase (NOS) induced by radiation is associated with tumorigenesis in the mammary glands. When rats were exposed to whole-body irradiation with gamma-rays (1.5 Gy) immediately after weaning and then treated with diethylstilbestrol, as an irradiated control, the tumor incidence (85%) was increased 7.6-fold in comparison with that (11.1%) of the non-irradiated control. The tumor incidence declined to 28.6% in the rats injected intraperitoneally with phenyl-N-tert-butylnitrone (PBN, 160 mg/kg), an inhibitor of inducible NOS (iNOS) expression and also a spin trapping agent, 30 min before irradiation. Also, the tumor incidence (25%) in rats orally administered with N-(3-(aminomethyl)-benzyl)-acetamide (1400W, 2.3+/-0.1 mg/day), a highly selective inhibitor of iNOS, dissolved in drinking water for 3 days after the irradiation was less than one-third of that in the irradiated control. On treatment with PBN or 1400W, no adenocarcinoma developed. Many of the mammary tumors that developed in the irradiated rats were positive for the estrogen receptor (ER). In contrast, ER was not detected in the tumors yielded from irradiated rats administered with PBN or 1400W. These results indicate that iNOS-derived NO may participate in the formation of estrogen-dependent mammary adenocarcinomas following radiation.

PMID: 15631943 [PubMed - indexed for MEDLINE]

Updates?

Philosophical musings?

Only been a week. No real changes in fat or tissue mass. Bromo and clomid ordered (Prl test came back within physiological norms for an adult male, but at the very top of the range). Pics / caliper measurements will come with each stage.

You've no interest in adding fibrates,given the studies posted above?

I'm on the fence WRT beza as it *can* induce gyno (you actually pointed that abstract out to me) but it looks pretty damn money otherwise.And it's pretty damn cheap.

bromo will inhibit prl production. No need to worry about beza inducing gyno... or anything else for that matter. Remember - prl + estro are required for gyno formation.

I'm not sure that Prl is necessary, but it certainly can amplify the effects of E2.

Bromo will inhibit pituitary Prl secretion, but I don't think it will do anything about production in other parts of the body (isn't there some cool latin phrase that means this? In sitio?). B-adrenergic stimulation, for example, produces Prl in sitio IIRC. Not sure how significant the amounts produced are, though.

Further, agonists of the Prl receptor will not be affected by bromo, just to mention it.

Colin -- I have yet to see tangible results among the tons and tons of M&M testers WRT fibrates. They look great on paper, but many many that once praised them have eventually admitted (in other threads) that they're not really sure that they saw anything. With that in mind, they're not worth my money at this moment, especially when diet and exercise can effectively do what they have been hypothesized to do.

As another note, I believe the beza-induced gyno was due to liver malfunction, which has been implicated in multiple kinds of gyno (alcoholic, starvation-induced). Can't remember the mechanism, though... perhaps reduced E2 breakdown or something...

I've used beza a LOT in the past and always noticed a substantial rise in body temp if a large dose was taken before a large (2000+ kcal) binge,to the point of profusive sweating immediately after and sometimes during the meal.

So while they are overplayed as some sort of drug lore,I will attest to a profound thermogenic effect.

I've eaten the same type of foods,same amount of kcals sans fibrates and never had a subttantial rise in body temperature.Not even remotely close to dropping sweat in beads from my nose after eatinga large bowl of ice cream.....

Good to hear that the gyno from beza was due to liver function BTW,I'll dig up that study.

Can you confirm the temperature rise with a thermometer? Because increases in prolactin cause sweating, and prolactin increases with food consumption.

I can be sweating my ass off with a body temp of only 96.5 or so -- just from prolactin.

I also sweat during/after large binges (without fibrates) just fine. Just curious if you're sure the sweating is indicative of true thermogenesis, because there's a perfectly plausible (though unpleasant) alternate explanation.

I can't do so ATM as I have no beza on hand but I'm placing an order within a day and will post up what I find w/a thermometer.

Given that beza is the strongest of the fibrates by far I don't think it is far fetched that high dosing (800mg at once) it can act asa switch to burn (to some degree) a simultaneous large influx of calories.

FWIW,the rise in body temp(perceived due to flushing and ridiculous sweating) would not be remotely comparable if fibrates were not taken along with the ingestion of food.IME if I eat a bunch of spicy food (shit ton of taco bell) I get a bit flushed/borderline sweaty but the perceived heat and sweatiness would be multiplied tenfold if I were to eat nothing but ice cream with 800mg beza.

I'm IF'ing ATM so I can take thermometer readings on several occasions.My nightime meal will be considered the "binge" for this purpose with 800mg of beza dosed.

What would be your unpleasant alternative?

I'm not going so far to say that beza can magically burn off a gallon of ice cream in a caloric surplus but I think there is something pretty damn profound at hand.

What I'm saying is that it's quite possible that the effects you're feeling are in large part due to the postprandial prolactin response -- with or without fibrates.

Sorry for the redundancy,I thought you were alluding to somehing that wasn't plain.

You may be right but how can such profusive sweating be explained?

By profusive I mean sweating as heavily as you would running a couple miles wrapped in plastic trash bags in August,damn near immeiately after beza + large amount of food is ingested.

I'll test this out when I receive beza.

Do some pubmed searches on prolactin, bromocriptine, exercise, sweating, face cooling... You'll be surprised.

Okay, ended Havoc yesterday, did first round of andractim today. That stuff seems to absorb a shitload better than the lipoderm did.

Toward the end of my lipo + Havoc cycle, my nips felt a little sore -- but not the tissue, only the skin. Felt like skin irritation, so my guess is that the nips just got sensitive from 2 weeks of lipoderm BID.

Weight up 5.6 from 176.6 to 182.2, did a carb-up/refeed yesterday so this doesn't reflect loss of water weight from my keto-ish diet.

Calipers (old) new--

Left nip (4) 5 mm (this doesn't feel like it has changed -- maybe just differences in measuring technique)
Right nip (6) 6 mm

Chest fat (4-4.5) 5 (surprised that this went up with a deficit and lipoderm -- maybe I'm holding water?)
Supriliac (6-6.5) 5 (somewhat confirms a calorie deficit at least).

Thinking that skinfold loss at supriliac with a gain at the chest (site of lipo application) means that I'm holding water from the lipo (my first day off).

OKay, the fight's on -- more later guys.

Oh, on my next to last day of havoc, I set a new PR for deads -- 435, @ ~181 lbs, up from 415 @ ~ 185 lbs.. Not too bad. Wasn't real pretty, though.

C'mon, andractim... please work...

EDIT: Comparing pics, def looks like I'm holding a little water... or maybe it's just that last pics were taken immediately PWO, these were taken "cold" ~11:30 am, after a sushi night. Not sure.

As mentioned, my 2 week havoc cycle is over. I did 2 ED the first week, then 4 for the first 5 days of the second week, and 5 for the last 2 days.

Nipples are tender, but as I mentioned it feels like topical soreness.

Unfortunately, it's been a few days and they are still sore; either the andractim is causing the same skin problem the lipoderm was, or it wasn't just a superficial irritation to begin with.

My libido is ridiculously low; I honestly expected the andractim to make it extra high (it is being suggested for andropause therapy... why wouldn't it?) But it's not. I can't hardly get an erection for the life of me ATM, and keeping one is next to impossible.

The gyno is not looking good.

Theories --
Progesterone activity (a la trenbolone -- which was found in Epistane)
Way low estrogen (although I thought this only impeded ejaculation, and not mounting frequency in rats)
Prolactin issues again (I though I saw something the other day about exogenous androgens increasing prolactin)

Granted this is a special case, and DHT isn't aromatizable, but I wonder...

The novel use of very high doses of cabergoline and a combination of testosterone and an aromatase inhibitor in the treatment of a giant prolactinoma.Gillam MP, Middler S, Freed DJ, Molitch ME.
Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University, The Feinberg Medical School, Chicago, Illinois 60611, USA.

Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia. A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 micro g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 micro g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 micro g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.

PMID: 12364416 [PubMed - indexed for MEDLINE]

My nipples often has boughts of tenderness. Actually then get hard a lot as well. Often times I'll all the sudden become "aware" of their presence. While normally I forget they exist.

Bromo + AI + andrictim??? Bromo will bring your libido back (in theory)... Any chance of androgens messing with dopamine at all? Just a thought... One I need to research before I go opening my friggin mouth.. but I figured you'd forgive me if I spoke first looked later considering your a helluva citizen.

On a side note to you personally - I did a bunch of research on bez after out PM discussion and then when you told me PPAR activation doesn't occur in humans I trashed it. At least that's what I thought you said. I found studies later on displaying that alpha stimulation of PPAR doesn't happen in humans from said compound but gamma does. Which is probably where we're getting the preceived raise in temp.

Look at this Dash, some of it reinforces what you and I have talked about WRT estrogen upregulating receptors of Prl...

Endocrinology. 2007 Dec 27 [Epub ahead of print] Links
Hypothalamic prolactin receptor mRNA levels, prolactin signaling and hyperprolactinaemic inhibition of pulsatile LH secretion are dependent on estradiol.Anderson GM, Kieser DC, Steyn FJ, Grattan DR.
Centre for Neuroendocrinology and Dept of Anatomy and Structural Biology, University of Otago School of Medical Sciences, PO Box 913, Dunedin 9054, New Zealand.

Hyperprolactinaemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinaemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinaemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovarectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of long form prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1, -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride only induced SOCS-1 in the in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus PRL-R, SOCS-3 and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3 and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinaemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

PMID: 18162529 [PubMed - as supplied by publisher]


The part that concerns me is it seems that with exogenous androgens we can expect an increase in test => estrogen... but using a harsh steroidal AI will kill estrogen which in turns unregulates Prl secretion, but if we leave estrogen high then we're running into Prl-R upregulation and in males I'm sure this equates to puffy nipples.

Jake, aren't you a little old to be playing with Magic cards?

Can you see what it says?? I've never owned any in my whole life, but I thought it that one was funny.

I can't.




Copied from the epi + DHT thread...



This is one of my theories as well. My shoulder was hurting last night, as it often does with either low carb or low estrogen (AI/havoc).
In addition to libido, my mood and energy sucks today. Bad. And I have a headache. According to this little article, low estrogen may well be the issue.

Maybe I'll down a quart of soy milk and see if that helps; at least that will identify the problem.

The question is why my nipples are looking bigger, not smaller, if my E is low and DHT is high...



There is... normally. I looked up a study the other day on its pharmacokinetics (on a few young boys 1-8 with microphallus) and was really surprised -- in one or two, DHT SPIKED at 1 hr, another one or two at 2-3 hrs, and several had no plasma increase at all. Weird.



Not just andractim -- remember, I purposely did a havoc cycle first to induce this type of effect (if that's really what we're seeing).

Sorry, I'll move this convo back to my thread (AAMOF, I think I'll copy this post there, too).

Wow -- now there's something interesting. Let's take a look at LIF -- pellets, even.

Leukemia inhibitory factor induces apoptosis of the mammary epithelial cells and participates in mouse mammary gland involution.
Schere-Levy C, Buggiano V, Quaglino A, Gattelli A, Cirio MC, Piazzon I, Vanzulli S, Kordon EC.

ILEX-CONICET División de Medicina Experimental, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina.

Leukemia inhibitory factor (LIF) is a multifunctional glycoprotein that displays multiple biological activities in different cell types, but to date there has been no report on its expression in the normal mammary gland. In this study we found that LIF is expressed at low but detectable levels in postpubertal, adult virgin, and pregnant mouse mammary glands. However, LIF expression drops after parturition to become almost undetectable in lactating glands. Interestingly, LIF expression shows a steep increase shortly after weaning that is maintained for the following 3 days. During this period, known as the first stage of mammary gland involution, the lack of suckling induces local factors that cause extensive epithelial cell death. It has been shown that Stat3 is the main factor in signaling the initiation of apoptosis, but the mechanism of its activation remains unclear. Herein, we show that LIF expression in the gland is induced by milk stasis and not by the decrease of circulating lactogenic hormones after weaning. Implantation of LIF containing pellets in lactating glands results in a significant increase in epithelium apoptosis. In addition, this treatment also induces Stat3 phosphorylation. We conclude that LIF regulated expression in the mouse mammary gland may play a relevant role during the first stage of mammary gland involution. Our results also show that LIF-induced mammary epithelium apoptosis could be mediated, at least partially, by Stat3 activation.

PMID: 12490192 [PubMed - indexed for MEDLINE]

Not that I want to use dexamethasone, but... topical? Local?

The 24p3 gene is induced during involution of the mammary gland and induces apoptosis of mammary epithelial cells.
Bong JJ, Seol MB, Kim HH, Han O, Back K, Baik M.

Department of Applied Bioscience and Biotechnology, Biotechnology Research Institute, Institute of Agricultural Science and Technology, Chonnam National University, Gwangju 500-757, Korea.

To understand the molecular mechanism of mammary gland involution we identified involution-induced clones by differential screening of a mouse mammary gland cDNA library. Characterization of clones by sequencing and Northern analysis showed that expression of 24p3 was induced during involution of the mammary gland. RNA in situ hybridization showed that it was mainly expressed in the secretory epithelial cells surrounding the lumen of the mammary gland alveoli. Induction of 24p3 was also observed in apoptotic HC11 mammary epithelial cells under serum starvation. In these cells, dexamethasone increased 24p3 gene expression four-fold. Transient expression of 24p3 increased the percentage of apoptotic cells 3- to 4-fold over a period of 3 days after transfection. This study provides evidence that overexpression of 24p3 gene can induce apoptosis of mammary epithelial cells.

PMID: 15055523 [PubMed - indexed for MEDLINE]

Any chance your andractim is bunk?

I really doubt it. Sealed, looks new, and I got it from someone reputable. Actually, the person I got it from has a little gyno problem; I really doubt they'd be cruel enough to screw a fellow man-boob guy.


Looks like I'll definitely need that post-andractim PCT (contrary to the label claims). I'm using 5g of 2.5% gel, so that's 125 mg ED, right? That doesn't sound right... but anyway (and noting that this is in old dudes)


Comparative pharmacokinetics of three doses of percutaneous dihydrotestosterone gel in healthy elderly men--a clinical research center study.
Wang C, Iranmanesh A, Berman N, McDonald V, Steiner B, Ziel F, Faulkner SM, Dudley RE, Veldhuis JD, Swerdloff RS.

Department of Medicine, Harbor-UCLA Medical Center, Torrance, California 90509-2910, USA. wang@harbor6.humc.edu

Twenty-five men, 60-80 yr old, participated in a pharmacokinetic study to compare three doses (16, 32, and 64 mg/day, n = 8 or 9 in each group) of 5alpha-dihydrotestosterone (DHT) gel (0.7% hydroalcoholic gel with 2.3 g gel delivering 16 mg DHT) applied daily over one upper arm (16 mg); both arms and shoulders (32 mg); and bilateral arms, shoulders, and upper abdomen (64 mg), respectively. Multiple blood samples for the pharmacokinetic profile for DHT and testosterone (T) were drawn over a 24-h period before application, after first application, and after 14 days of daily application of DHT gel. Additional blood samples for DHT, T, and estradiol were obtained 24 h after application on days 3, 5, 7, and 11 and after discontinuation of DHT gel for 3, 5, 7, and 14 days (days 17, 19, 21, and 28 after first instituting treatment). No skin irritation was observed in any of the subjects. Before treatment, mean serum DHT and T levels were not different among the three dose groups. The serum DHT levels increased gradually after gel application on the first day, reaching a plateau between 12-18 h. During the 14 days of daily application of DHT gel, the mean baseline DHT levels reached steady state by day 2 or 3 and were elevated considerably above baseline. Mean serum DHT levels varied between 8-11, 12-17, and 14-24 nmol/L in the 16-, 32-, and 64-mg groups, respectively. The area under curve (AUC) of serum DHT levels over 24 h on day 14 were 6.0-, 6.9-, and 16.1-fold above pretreatment levels for the three doses. Concomitant with the increase in serum DHT levels, the AUC produced by endogenous serum T levels decreased to 75, 56, and 36% of baseline after 14 days of 16, 32, and 64 mg/day DHT gel. Similar patterns of decreases in AUC of serum estradiol levels were found. The calculated mean total androgen levels (T + DHT) rose with DHT gel application in all groups (P < 0.0001) on both days 1 and 14. We conclude that the three doses of DHT gel tested might provide adequate androgen replacement in hypogonadal men at the low, middle, and high physiological androgen (T + DHT) range.

PMID: 9709942 [PubMed - indexed for MEDLINE]

Well, my kidney function is (hopefully) okay, but...
Who knows, my BUN was elevated (21) when I tested a year-ish ago. Maybe a few years of consistent high PRO...

Yeah whatever. BTW -- parlodel = bromocriptine

Here's more on STAT and another reason,IMO,for beza and troglatizone usage.


Simultaneous, bidirectional inhibitory crosstalk between PPAR and STAT5b.
Shipley JM, Waxman DJ.

Division of Cell and Molecular Biology, Department of Biology, Boston University, MA 02215, USA.

The transcription factors peroxisome proliferator-activated receptor (PPAR) and signal transducer and activator of transcription 5 (STAT5) activate genes involved in fatty acid metabolism (PPARalpha) and adipogenesis (PPARgamma) and mediate hormonal responses important for body growth, liver gene expression, and mammary gland development (STAT5a and STAT5b). These seemingly disparate pathways are subject to mutually inhibitory crosstalk, with growth hormone (GH)-activated STAT5 able to inhibit PPAR-regulated gene transcription by approximately 80%, and conversely, ligand-activated PPAR able to inhibit STAT5-regulated transcription to a similar degree. Given the co-expression of PPAR and STAT5 in multiple tissues, we investigated whether one of the factors dominates the inhibitory crosstalk. A PPAR-responsive Renilla luciferase reporter was constructed and used to monitor PPAR transcriptional activity in COS-1 cells co-transfected with a STAT5 firefly luciferase reporter. In cells co-stimulated with GH and a PPAR agonist, STAT5b inhibited expression of the PPAR-regulated Renilla luciferase reporter, whereas PPARalpha and PPARgamma inhibited transcription of the STAT5b-regulated firefly luciferase reporter. The extent of the inhibitory crosstalk was dependent on the relative levels of expression of each transcription factor and on the relative concentrations of GH and PPAR agonist. Dose-response studies revealed that STAT5b was inhibited at an approximately 7-fold lower concentration of the PPARgamma ligand troglitazone than was required for activation of PPARgamma, indicating that only a portion of cellular PPARgamma is needed for STAT5b inhibition. Similarly, mono-(2-ethylhexyl)phthalate (MEHP), a reproductive toxicant and primary metabolite of the environmental chemical di-(2-ethylhexyl)phthalate (DEHP), inhibited STAT5b transcriptional activity with an EC50 value of 1.1 microM, corresponding to an approximately 10-fold lower concentration than required for activation of PPARgamma-dependent transcription. We conclude that the cross-inhibition between PPAR and STAT5 proceeds in a simultaneous, bidirectional manner. Exposure to phthalates and other environmental chemical activators of PPARs may thus lead to alteration of hormone-induced, STAT5-regulated gene expression in tissues such as liver, fat and breast, where both transcription factors are expressed. Conversely, STAT5-activating hormones and cytokines may modulate the responsiveness of PPARs to their foreign chemical ligands.

PMID: 15364543 [PubMed - indexed for MEDLINE]

Have you thought about Letrozole?

Hey, nice to see you 'round these parts.

No, I haven't considered Letro, as it is a nonsteroidal AIs, and the nonsteroidals have been linked to aromatase upregulation.

I never really researched it personally, although I've read on a couple boards that it has been effective against gyno.

You may want to inquire about it from Tripdog at AM. I've seen a couple of his posts where he has said

Thanks -- I will do some browsing of his posts.

Cochrane Database Syst Rev. 2007 Jul 18;(4):CD000152. Links

Update of:
Cochrane Database Syst Rev. 2000;(2):CD000152.
WITHDRAWN: Bromocriptine for idiopathic oligo/asthenospermia.Vandekerckhove P, Lilford R, Vail A, Hughes E.
St Mary's Hospital, IOW Healthcare NHS Trust, Parkhurst Road, Newport, Isle of Wight, UK PO30 5TG. Patrick.Vandekerckhove@iow.nhs.uk

BACKGROUND: Oligo-astheno-teratospermia (sperm of low concentration, reduced motility and increased abnormal morphology)of unknown cause is common and the need for treatment is felt by patients and doctors alike. As a result, a variety of empirical, non-specific treatments have been used in an attempt to improve semen characteristics and fertility.Whilst bromocriptine treatment for reducing prolactin levels in hyperprolactinaemic males (as in females), and, in the treatment of hypogonadotropic hypogonadism with hyperprolactinaemia, is beneficial, it has also been used for oligospermic men in the absence of any endocrinopathy. Prolactin may play a direct role in spermatogenesis and hormone production. It has also been claimed that in oligospermic men with normal gonadotrophins mean prolactin levels are higher and that hyperprolactinaemia is more common compared to fertile men. It has been proposed that the administration of bromocriptine under these circumstances might counteract a prolactin-induced block on the action of gonadotrophins on the testicles and, subsequently, that the reduction in prolactin levels might lead to an improvement in semen parameters and fertility. Although it is not licensed for use in male infertility, bromocriptine has been used for normogonadotrophic individuals with oligospermia and normal or slightly elevated prolactin levels. This review considers the available evidence of the effect of bromocriptine therapy for normoprolactinaemic males with idiopathic oligo and/or asthenospermia. OBJECTIVES: The objective of this review was to assess the effects of bromocriptine on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia. SEARCH STRATEGY: The Cochrane Subfertility Review Group specialised register of controlled trials was searched". SELECTION CRITERIA: Randomised trials of oral bromocriptine versus placebo or no treatment for couples with subfertility attributed to male factor. DATA COLLECTION AND ANALYSIS: Data were extracted by one reviewer and any disagreements were resolved by discussion with other reviewers. MAIN RESULTS: Four studies were included. The method of randomisation was not specified in any of the trials, which were all of crossover design. Compared with placebo, bromocriptine was associated with a significant reduction in serum prolactin levels (weighted mean difference -195.3 micro international units per litre, 95% confidence interval -276.5 to -114). No effects on sperm parameters were seen. There was also no effect on pregnancy rates observed between bromocriptine and placebo (0.70 odds ratio, 95% confidence interval 0.15 to 3.24). AUTHORS' CONCLUSIONS: Bromocriptine appears to reduce prolactin levels in subfertile men with normal gonadotrophic function. There is not enough evidence to show that bromocriptine is helpful in improving fertility.[This abstract was prepared centrally.].

PMID: 17636605 [PubMed - indexed for MEDLINE]


I know you had mentioned to me personally about playing with the dosing regimen. I might refer you to the full text which I assume you can get before doing so as it doesn't state what it is in the abstract.