DHT vs Estrogen or Why Do Some Get Sides While Others Don't?

[harold]

Maybe this should be in the sides forum but I thinnk this has a slightly braoader applicability and to be honest this forum gets a lot more views. I guess it can always be moved by the mods.

Anyway there is a line of thinking that the reason some people (the exact numbers being a highly contentious issue round here) experience sides on dutasteride/finasteride is because of the rise in estrogen/estradiol produced by the shutdown of pathways converting test to DHT and the subsequent rise in test. Or perhaps more importantly it is the shift in the androgen/estrogen ratio that is causing the sides. DHT has effectively antiestrogenic effects in many parts of the body such as the chest so when you are lowering DHT as well as raising estrogen its possible that you are doubling the odds against you.

On the other hand there is the possibility that DHT is necessary for errectile function, libido and general normal sexual functioning. Without it you are screwed more or less and any excess estrogen will only have an effect on things like gyno and perhaps extra fat deposition. After all DHT does seem to be necessary (at least at physiological levels - discounting the recent study where it managed to destroy even occipital scalp hair at high enough concentrations) for hairloss going by pseudohemaphrodites and the majority of users of finasteride/dutasteride who show at least maintenance. If this is true and even large increases in test do not produce worsening of balding in the absence of DHT then it may well be true that even large increases in testosterone won't make up for the loss of DHT in androgenic areas such as the brain and genitals .ie too llittle DHT = sexual sides.

On the other hand there are a lot of people who have close to normal to normal sexual function (some evn claim improvements) while inhibiting huge ammounts of DHT in the body. Should this be possible. Is it just that although 90% of serum DHT may be inhibited the 60-70% or so reduction in sexually related organs leaves just enough to keep them going? Does the question of whether you are going to respond well hairwise and/or not respond well sexually comee down to whether or not your scalp is more sensitive to small levels of DHT/testosterone than your penis?

Or do these people respond without sides because in the absence of huge ammounts of estrogen and its negative feedback upon the HPTA there is more than enough androgens to produce normal sexual response? Basically what it comes down to I guess is that if its primarily DHT that is responsible for sexual function then those who have intolerable sides on finasteride/dutasteride can't really hope to derive any benefit from these meds. If on the other hand it is primarily a redution in the androgen/estrogen ratio that screws up these folkss then there may be hope that with the use of arommatase inhibitors and SERMs that they can still derive some benefit from what are usually very effective meds. Unless of course one cannot achieve a balance between estrogenic and androgenic effects such that the scalp is protected and sexual function is also preserved. (ie by taking enough anti-estrogen to restore errections etc you will inevitably lose hair.)

I know these are questions that we probably dont have enough info to answer but there are some pretty knowledgeable folk here and perhaps more importantly some psople who have had experiences with combining dutasteride/finasteride with an anti-aromatase like arimidex/letro or a SERM like clomid/nolva. If anyone can list their experiences (did it help sexual sides, did you shed more) that would be a big help. Going through the archives there seem to be reports of people doing or at least planning such things but as so often happens there is no follow-up report of what happened.
The correct answer may well be that it is a bit of both and varies from individual to individual but if we can come up with something that means less people need to choose between having a head of hair and having sex that would be a great thing.

Below I will post some abstracts of studies and maybe some facts/observations that may shed light on the issue.
hh
And please lets not have a big flame war between those who never got sides and those who have. Such a thing helps nobody.

 

[harold]

Firstly I think it should be noted that many of the sides complained about by finasteride/dutasteride users are similar to those experienced by bodybuilders coming off a cycle of steroids. In this community it has become standard practice to begin a regimen of drugs and hormones designed to normalise endogenous test production, keep muscle gains and get rid of problems like low libido. Central to these regimens are typically a SERM and/or an arommatase inhibitor.

Now a study showing testosterone alone was insufficient to restore erectile function after castration in rate - DHT was necessary.

Endocrinology. 1995 Apr;136(4):1495-501.Click here to read Links
Dihydrotestosterone is the active androgen in the maintenance of nitric oxide-mediated penile erection in the rat.

* Lugg JA,
* Rajfer J,
* Gonzalez-Cadavid NF.

Department of Surgery, University of California at Los Angeles (UCLA) School of Medicine, Harbor-UCLA Medical Center, Torrance 90509.

Androgens are essential for the expression of normal libido in the male, but their role in the maintenance of the erectile response in humans is controversial. It has been shown previously in the rat that castration induces 1) loss of penile reflexes; and 2) considerable reduction in the erectile response to electric field stimulation (EFS) of the cavernosal nerve. Both of these effects can be reversed by testosterone replacement. The current study was performed to determine whether these testosterone effects are mediated via its conversion to dihydrotestosterone (DHT), and to what extent the synthesis of the mediator of penile erection, nitric oxide, is affected by castration and androgen replacement. Five-month-old rats were either castrated or left intact. The orchiectomized rats were implanted with SILASTIC brand silicon tubing (Dow Corning) containing testosterone or DHT with or without daily injections of the 5 alpha-reductase inhibitor finasteride. After 7 days, rats were submitted to EFS and the intracavernosal pressure was recorded. Castration reduced the EFS-induced erectile response by 50% in comparison with intact rats and testosterone restored this decrease to normal. When finasteride was given to these testosterone-treated castrate rats, erectile response was not restored. DHT was as effective as testosterone in restoring response to EFS in castrates and this effect was not decreased by finasteride. Nitric oxide synthase activity in the penile cytosol was measured by the arginine-citrulline conversion and was found to correlate with the EFS determinations. These results show that DHT is the active androgen in the prevention of erectile failure seen in castrated rats, and suggest that this effect may be mediated, at least partially, by changes in nitric oxide synthase levels in the penis.

Another on DHT vs testosterone in penile NO synthase

BJU Int. 1999 Feb;83(3):327-33.Click here to read Links
Effects of androgens on the expression of nitric oxide synthase mRNAs in rat corpus cavernosum.

* Park KH,
* Kim SW,
* Kim KD,
* Paick JS.

Sung Kyun Kwan University and Seoul National University, College of Medicine, Seoul, Korea.

OBJECTIVE: To examine the effects of androgens on erectile response and the expression of nitric oxide synthase (NOS) isoform mRNAs in the penile corpus cavernosum of castrated rats. MATERIALS AND METHODS: The study comprised 50 adult male Sprague-Dawley rats in five groups: sham controls; castrated; castrated and receiving testosterone; castrated and receiving dihydrotestosterone (DHT); castrated and receiving testosterone and 5alpha-reductase inhibitor (finasteride). Androgen replacements were administered via implants of silicone tubing. After 7 days, some animals underwent electrical stimulation of the cavernosal nerves and the remainder were used for further analysis. NOS activity was measured in the soluble fraction of the corpus cavernosum, using the Griess reaction. Total RNA was isolated and nNOS and eNOS mRNA expression examined using semiquantitative reverse-transcriptase polymerase chain reaction. RESULTS: Castration caused a marked decrease in erectile response and the ratio of maximal intracavernosal pressure (ICPmax) to systemic blood pressure (SBP), although both testosterone and DHT effectively restored the response to normal. NOS activity and the amount of nNOS mRNA were reduced in castrated rats but restored by androgen replacement. Although there was no significant difference in NOS activity between the androgens, nNOS mRNA expression was higher in rats treated with DHT. There were no effects of androgen in rats treated with finasteride, as the ICPmax/SBP ratio, NOS activity and amount of nNOS mRNA decreased. eNOS mRNA expression was independent of androgen. CONCLUSIONS: Androgens enhance nNOS gene expression in the penile corpus cavernosum of rats, suggesting that they play an important role in maintaining NOS activity. Of the two androgens, DHT was more potent.

This is a great paper that tries to explain why different hormonal conditions can still produce sexually normal behaviour, why oestrogen is necessary for male sexual response and many other seemingly contradictory findings by stressing the importance of the ratio of androgens to estrogens.

Int J Androl. 2005 Apr;28(2):78-87.Click here to read Links
The physiological basis of human sexual arousal: neuroendocrine sexual asymmetry.

* Motofei IG,
* Rowland DL.

St Pantelimon Hospital, Carol Davila University of Medicine and Pharmacy, Dionisie Lupu Street, No. 37, Sect. 1, Bucharest, Romania. igmotofei@yahoo.com

Normal sexual arousal and response suppose an integrated process involving both physiological and psychological processes. However, the current understanding of sexual arousal does not provide a coherent model that accounts for the integration of multiple physiological systems that subsequently generate a coordinated sexual response at both the spinal peripheral and cerebral central levels. Herein we suggest a model that involves both sympathetic and parasympathetic activation during sexual arousal via the two classes of gonadal hormones, androgens and oestrogens. We discuss the manner in which gonadal hormones may activate such a system, transforming pre-pubertal (non-erotic) genital stimulation to post-pubertal erogenization of stimulation and subsequent sexual arousal. Finally, we indicate that the different balance of androgens and oestrogens in men and women may generate asymmetric effects on each of the components of the autonomic nervous system, thereby explaining some of the differences in patterns of sexual arousal and the responses cycle across the sexes.

 

[harold]

Now a whole bunch of studies that are less relevant or informative perhaps but may still be suggestive.
hh

Fertil Steril. 2003 Jan;79(1):203-5.Click here to read Links
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

* Tan RS,
* Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. robert.s.tan@uth.tmc.edu

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

PMID: 12524089 [PubMed - indexed for MEDLINE]


1: Alcohol Alcohol. 1987;22(1):7-15.Click here to read Links
Androgen-oestrogen imbalance in men with chronic alcoholism and fatty liver.

* Myking O,
* Aakvaag A,
* Digranes O.

The plasma concentrations of oestrone (E1), oestradiol (E2), oestrone sulphate (E1S), testosterone (T), sex hormone binding globulin (SHBG) and apparent free testosterone (AFTC) were measured in 20 normal-weight men with chronic alcoholism and fatty liver. Twenty normal-weight male blood donors matched for age acted as controls. In the alcoholic subjects (patients) the plasma levels of E1, E2 and SHBG were significantly elevated, whereas the concentrations of E1S and AFTC were significantly decreased. No difference in plasma T was seen between the two groups. Both patients and controls showed a significant correlation between SHBG and E2, whereas a significant correlation between SHBG and T, and between E2 and T, was only found in the controls. Eight of the patients showed signs and/or symptoms of hypogonadism or feminization. Only patients with hypogonadism and/or feminization showed significantly higher plasma levels for E2 and decreased T/E2 ratio than matched controls. The ratio E1S/E1 was in every case lower than in the control and tended to be even lower in the patients with hypogonadism and/or feminization.

1: Arch Androl. 1992 May-Jun;28(3):171-6. Links
Role of testosterone and dihydrotestosterone in spontaneous gynecomastia of adolescents.

* Villalpando S,
* Mondragon L,
* Barron C,
* Perez-Pasten E,
* Castaneda G,
* Alonso-Uriarte R,
* Cortes-Gallegos V.

Unidad de Investigacion Clinica en Nutricion y, Instituto Mexicano del Seguro Social, Mexico, DF.

To test a possible hormonal mechanism of gynecomastia at puberty, a group of pubertal spontaneous gynecomastia (PSG) and healthy young volunteers (HYV), Tanner's stage II-V, were studied. Peripheral blood samples were obtained for measuring follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), testosterone (T), dihydrotestosterone (DHT), estradiol (E-2) and estrone (E-1). No difference was established in steroids in pituitary hormonal concentration when both groups were compared on a sexual stage-matched control basis, except for T 2 SD in 5/9 subjects of PSG and DHT 2 SD in all of PSG. The THT ratio varied from 5.0 to 15.4 in PSG and from 0.42 to 2.224 in HYV. Whether spontaneous gynecomastia might exist in an enzimatic blockade of 5 alpha-reductase and whether a decrease in the THT ratio might favor the estrogen action for the progression of breast enlargement deserve further analysis.

PMID: 1530365 [PubMed - indexed for MEDLINE]


1: Int J Impot Res. 2003 Feb;15(1):38-43.Click here to read Links
Oestrogen-mediated hormonal imbalance precipitates erectile dysfunction.

* Adaikan PG,
* Srilatha B.

Department of Obstetrics & Gynaecology, National University Hospital, National University of Singapore, Singapore. obgadaik@nus.edu.sg

Declining testosterone (T) in an aging male offsets the equilibrium between androgen and oestrogen (oestradiol, E(2)) with a resultant increase in E(2)-T ratio. Similar functional hormone imbalance is existent in clinical states of hypogonadism and is likely to arise from exposure of males to environmental oestrogens. The pathophysiological significance of this derangement on erectile function, hitherto unknown, was estimated in sexually mature male rats following acute and chronic treatment with oestrogen. A total of 60 male Sprague-Dawley rats (200-250 g) were divided into control and two treatment groups, administered 0.01 and 0.1 mg of oestradiol through oral gavage daily for 1 week (n=30, acute study) and 12 weeks (n=30, long-term study), respectively. Sexual activity in the presence of hormonally primed female rats and intracavernous pressure (ICP) response to electrical stimulation estimated treatment-induced changes, which were correlated with hormone levels and penile morphology at 12 weeks. Following two to five-fold elevation in serum E(2) levels (and simultaneous reduction in testosterone), there was a significant prolongation of mount, intromission, ejaculation latencies and some decrease in frequencies. The ICP response to nerve stimulation was also impaired in all the treated groups. Histologically, trichrome staining highlighted the cavernosal connective tissue hyperplasia in the long-term study groups. Results of this investigation indicate that oestradiol causes pathophysiological changes in erectile function. These observations provide an indirect evidence for the possible sexual health hazards in man upon inadvertent exposure to environmental oestrogens, ageing and derangement of E(2)-T ratio.

PMID: 12605239 [PubMed - indexed for MEDLINE]


1: Asian J Androl. 2003 Dec;5(4):307-13. Links
Oestrogen-androgen crosstalk in the pathophysiology of erectile dysfunction.

* Srilatha B,
* Adaikan PG.

Department of Obstetrics Gynaecology, National University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074.

Ageing in man is associated with a decline in testosterone following changes in the hypothalamo-pituitary-testicular axis. This may offset the physiologic equilibrium between oestrogen and androgen and at some point when the ratio of free testosterone to oestradiol reaches a critical level, the oestrogenic gonadotropin suppressive effect predominates with decreased release of FSH and LH. Adding to this endocrinal complexity is the continued peripheral conversion to oestradiol through aromatisation. Although the androgen deficiency is not the sole cause for impotence in the elderly, there is a gradual decrease in nocturnal penile tumescence (NPT) and spontaneous morning erections with ageing. Despite the age related increase in oestrogen levels, the information on the pathophysiological role of the "female hormone" in erectile dysfunction has been scanty. Together with our identification of oestrogen receptors within the penile cavernosum, we have delineated dysfunctional changes on male erection mediated by oestradiol. These findings parallel the recent concerns over environmental oestrogens on fertility declines in young men. Oestrogenic activity is also present in plants and thereby in human diet. These phytoestrogens are structurally and functionally similar to oestradiol and more potent than the environmental oestrogenic chemicals such as organochlorine and phenolic compounds. Thus in the light of growing concerns of possible compromising effects on sexuality by endogenous and environmental oestrogens, we are faced with the scientific need to delineate their role on the mechanism of male erectile pathway in health and disease for clinical correlates and prognostics.




1: Epilepsy Behav. 2004 Apr;5(2):260-3.Click here to read Links
Aromatase inhibition, testosterone, and seizures.

* Harden C,
* MacLusky NJ.

Department of Neurology and Neuroscience, Comprehensive Epilepsy Center, Weill Medical College of Cornell University, New York, NY, USA. clharden@med.cornell.edu

The effect of testosterone on brain excitability is unclear. The excitatory aspect of testosterone's action in the brain may be due to its conversion to estrogen via aromatase. We report herein a 61-year-old man with temporal lobe epilepsy and sexual dysfunction due to low testosterone levels. Use of an aromatase inhibitor, letrozole, normalized his testosterone level and improved his sexual functioning. Letrozole, in addition to standard antiseizure medication, was also associated with improved seizure control. This was sustained and, further, was associated with seizure exacerbation after withdrawing letrozole, and subsequent seizure improvement after restarting it. During the course of treatment, his serum testosterone level increased, sex hormone-binding globulin decreased (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels increased, while serum estradiol levels remained undetectable. Letrozole may, therefore, have produced a central alteration in the testosterone/estrogen ratio, thereby impairing estrogen-mediated feedback control of the pituitary, resulting in the observed increase in circulating LH and FSH levels. This experience suggests that aromatase inhibitors should be further investigated as a beneficial treatment modality for male patients with epilepsy.


1: J Sex Med. 2005 Sep;2(5):716-21.Click here to read Links
Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism.

* Shabsigh A,
* Kang Y,
* Shabsign R,
* Gonzalez M,
* Liberson G,
* Fisch H,
* Goluboff E.

Department of Urology, NY Presbyterian Medical Center, New York, NY, USA.

AIM: Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio. METHODS: Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed. RESULTS: The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 +/- 39.8 ng/dL and 32.3 +/- 10.9, respectively. By the first follow-up visit (4-6 weeks), the mean testosterone level rose to 610.0 +/- 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P <0> 27.5 kg/m2) subjects (17.8 +/- 10.1 vs. 13.5 +/- 6.8, P < 0.05). A net increase in IIEF-5 scores was observed at the endpoint (13.7 +/- 5.9 vs. 25.7 +/- 2.9, P < 0.0001). CONCLUSIONS: Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil might have a role in the regulation of erectile function.

PMID: 16839328 [PubMed - indexed for M



1: Annu Rev Med. 1976;27:357-70.Click here to read Links
Estrogens and the human male.

* Marcus R,
* Korenman SG.

PIP: Literature on the role of estrogens in men is reviewed. The primary active estrogens in males and females are estradiol-17beta (E2), estrone (E1), and estriol (E3). The active constituents of serum E2 and testosterone (T) are those which are not bound by testosterone-estrogen binding globulin (TEBG). The concentration of TEBG is stimulated by estrogen and suppressed by androgens. Both E1 and E2 appear to be derived from the peripheral metabolism of T and androstenedione. The metabolism and physiological roles of estrogens in men are briefly discussed. The association of gynecomastia with puberty, cirrhosis of the liver, hyperthyroidism, chronic renal failure, refeeding gynecomastia, administration of digitalis and diuretics, neoplasms, and hypergonadotropic hypogonadism is reviewed. In older men, the ratio of free E2:T is increased. The relationship of andorgens, estrogens, and male sex behavior is briefly reviewed. Areas for future research include the mechanisms by which estrogens and androgens exert antagonistic effects on similar tissues, variations in the fractional conversionr ate of androgens to estrogens, the etiology of pubertal gynecomastia, the role of the free E2:T ratio in male social and sexual behavior, and the interrelation between behavior, nutrition, hormone secretion, and degenerative changes such as benign prostatic hyperplasia.



1: Kongressbd Dtsch Ges Chir Kongr. 2002;119:743-7. Links
[Disordered hormone regulation in gynecomastia]
[Article in German]

* Pfeilschifter J.

Berufsgenossenschaftliche Kliniken Bergmannsheil, Universitatsklinik, Medizinische Klinik und Poliklinik, Burkle-de-la-Camp-Platz 1, 44789 Bochum. Johannes.Pfeilschifter@ruhr-uni-bochum.de

Gynecomastia develops when there is an increase in the ratio of estrogen to androgens. Whereas mild forms of gynecomastia are frequently encountered in the male population, any breast enlargement that is prominent, painful, progressive or of recent onset always requires a careful evaluation, as it may be an important clue to disease elsewhere. Underlying causes are plenty and include drugs, congenital and acquired disorders of androgen and estrogen production, various tumors, renal failure, cirrhosis of the liver, and thyrotoxicosis. Evaluation includes a careful patient's history, physical examination of sexual characteristics and the breast tissue, and measurements of serum LH, FSH, testosterone, estradiol, hCG-beta, TSH and tests of liver and kidney function.

 

[harold]

The infamous dog finasteride plus arimidex study:
The only real study to my knowledge that looked at the effect of the use of both a 5-alpha reductase inhibitor and a aromatase inhibitor at the same time. Bryan has talked about this a lot in the past.

: Prostate. 1998 Oct 1;37(2):70-6.Click here to read Links
Effect of dual inhibition of 5-alpha-reductase and aromatase on spontaneously developed canine prostatic hypertrophy.

* Suzuki K,
* Okazaki H,
* Ono Y,
* Kurokawa K,
* Suzuki T,
* Onuma E,
* Takanashi H,
* Mamiya Y,
* Yamanaka H.

Department of Urology, Gunma University School of Medicine, Maebashi, Japan. kazu@news.sb.gunma-u.ac.jp

BACKGROUND: Our aim was to assess the effect of dual inhibition of 5-alpha-reductase and aromatase on prostate glands. METHODS: We investigated the morphological changes in the prostate gland and the changes in the hormonal environment after administration of finasteride and arimidex to intact canine specimens. The study consisted of four groups: a 5-alpha-reductase only group (5RI only, n = 5); a 5RI plus aromatase-inhibitor combination group (5RI + ARI combination, n = 5); a BPH control group (n = 3); and a castration control group (n = 3). Finasteride (1 mg/kg/day) and the same dose of arimidex were orally administered for 80 days. RESULTS: In the 5RI group, a significant decrease in the serum dihydrotestosterone (DHT) level was found, and prostatic volume was significantly decreased. However, significant increases in serum testosterone (T) and DHT levels were observed, with a concomitant increase in prostatic volume in the 5RI + ARI combination group. Morphometric analysis showed that histopathological findings in the 5RI + ARI combination group were similar to those in the BPH control group. CONCLUSIONS: Dual inhibition of 5-alpha-reductase and aromatase resulted in a significant increase in prostate volume, accompanied by a 3-10-fold increase in serum testosterone levels and a significant increase in testicular volume.


Looking at the full study there are a couple off extra points and results:

Despite huge rises in testosterone and a rise in DHT level the prostatic growth in the arimidex/finas group was relatively modest at about 120%

The fall in E2 levels in the arimidex/inasteride group was modest but the huge increase in Test may reflect the extreme sensitivity of the canine HPTA to estrogenic feedback.

Finasteride was not able to keep DHT levels in check during arimidex administration.

The authors note the possibility of getting a dosage of both drugs that abbrogates the rise in serum DHT:
"Furthermore, DHT might be reduced by finasteride administration in combination with arimidex, under conditions of various dose settings."

finasteride/Arimidex led to an increase in testicle size and a decrease in adrenal gland size. finasteride led to a decrease in testicle size.

The increase in Test levels could not be explained in the authors opinion merely by a freeing up of excess testosterone with the blockade of conversion to estrogen. Though they were unabvle to test for LH levels they seem confident that Test levels went so high because of the loss of negative feedback to the extremely sensitive HPTA. The increase in testicle size seems to put this beyond doubt.
hh

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