Here is some interesting infomation on Halo. I just posted this at AF too. It is a short compilation of some studies and some quotes by Big Cat on the compound. These were taken from CEM.
J Dial. 1977;1(4):357-66. Related Articles, Links
Fluoxymesterone therapy in anemia of patients on maintenance hemodialysis: comparison between patients with kidneys and anephric patients.
Acchiardo SR, Black WD.
Nineteen patients with their kidneys and 11 anephric patients who were stable on maintenance hemodialysis received 20 mg a day of Fluoxymesterone. At the end of four months, there was a significant increase (p less than 0.005) in the mean hematocrit with a parallel increase in the hemoglobin level in both groups of patients. Concomitantly, we observed an increment of the red cell mass that was significant at the level of p less than 0.05. Blood transfusion requirements decreased significantly (p less than 0.1), independent of the presence or absence of kidneys. No changes in body weight, serum albumin, and serum cholesterol levels were observed. Secondary effects were hirsutism and hoarsening of the voice.
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Big Cat (CEM.com): "Fluoxymesterone isn't a strong androgen at all, its a rather weak androgen. All the characteristics it causes that some consider synonymous with androgenic effect, are in fact the result of glucocorticoid deprivation since fluoxymesterone is both a potent GR antagonist and 11bHSD blocker. Increases in agression, red blood cell count and appetite are all a result of this."
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Is there any other oral AAS that has all of the above characteristics?
Big Cat (CEM): "No, that's because in many ways you shouldn't classify it as an AAS its more specifically a glucocorticoid blocker. It will lean you out, increase oxidative (endurance) capacity, increase appetite and won't cause many androgenic side-effects. Some androgenic risk is still associated with use due to target tissue 5-alpha reduction. A fluoxymesterone with a 1,2 double bond would not suffer this problem, and have even higher affinity for the glucocorticoid receptor."
"I have experimented with an analog that has the 1,2 double bond and a 16-alpha-methyl. This possesses no androgenic effects at all anymore. But users stop after less than 2 weeks on 10 mg due to symptoms associated with glucocorticoid deprivation."
"Fluoxymesterone is a great steroid, its sad it has become so hard to find on the international market. For cutting a combination with high dose boldenone and moderate dose trenbolone will work wonders."
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Also, how would you decide how androgenic a certain steroid is without judging based "on levator ani against ventral prostate weight in rats"?
Big Cat (CEM): "Truth be told, you can't really. It would be hard to have a quantifiable model with regards to the tissues and issues we have with androgenic nature, such as development of acne and hair loss (hard to quantify, no in vitro or animal model to do it on) and prostate issues are even worse. Prostate seems to be regulated by so many different factors that you simply can't take any change in prostatic tissue, especially if it were malignant like most cell lines, and say that an event that will occur in under standardized circumstance will occur in a same degree in vivo for a diverse group of humans. In healthy young men acute side effects are rather exception than rule as well, making it even harder because we are basing our concept of androgenicity on threshold appearances. A lot of androgens block the GR directly, reducing the amount of activated GR. Not only is fluoxymesterone one of the most potent drugs in this regard, it also blocks the peripheral enzyme 11bHSD1 which turns cortisone to cortisol, resulting in lower plasma cortisol levels as well."
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"The effects of fluoxymesterone administration on testicular function."
Jones TM, Fang VS, Landau RL, Rosenfield RL.
Long term daily administration of fluoxymesterone (9alpha-fluoro-17alpha-methyl-11beta, 17beta-dihydroxyandrost-4-en-3-one) was associated with a modest suppression of sperm production and a profound suppression of testosterone levels in the absence of significant effects on plasma gonadotropin levels. Nine normal male volunteers took either 10, 20, or 30 mg of fluoxymesterone daily for twelve weeks. Plasma samples were obtained for testosterone, estrogen, LH and FSH levels at biweekly intervals before, during and for up to 12 weeks after fluoxymesterone treatment. Samples were obtained for dehydroepiandrosterone sulfate, testosterone binding globulin and free testosterone assays at representative times before, during and after treatment. Although lower sperm counts were observed at several points during both the treatment and follow up periods, significant consistent suppression of spermatogenesis could not be demonstrated. Reduced plasma testosterone levels were seen within 24 h after beginning fluoxymesterone, and further reductions were noted throughout the treatment period. Changes in plasma estrogen levels did not correlate with fluoxymesterone administration. Neither plasma LH nor plasma FSH levels were significantly altered by fluoxymesterone. A short term study utilizing a single dose of fluoxymesterone yielded similar findings. It is proposed that fluoxymesterone has a local effect on the Leydig cell which is not mediated by gonadotropins.
Question: "Would this suggest that HCG would be ineffective in counteracting fluoxymesterone induced ITT suppression?"
Big Cat (CEM reply): "The authors explained the discrepancy by calling on a short loop theory. Meaning it supressed testosterone at the local level (downstream of the leydig cells) since it did not significantly supress spermatogenesis, LH or FSH. One weird thing I did notice was that there was a supression of spermatogenesis, and to a lesser extent gonadotrophins, after cessation of fluoxymesterone. They took it for 12 weeks, 10,20 or 30 mg a day, and end of study was at 16 weeks. Also, across the board for all doses and the full length of the study sperm motility was severely decreased. The authors concluded that F was a strong supressor of testosterone, but not the HPTA. All things taken together, these findings are in support of a beneficial effect of the anti-gluco effect of F, given that the positive effect would be situated at the hypothalamary and hypophysiary level, but not downstream in the HPTA, where the androgen would continue to be supressive. The shortlived dip when stopping treatment seems to confirm that since at that point the beneficial effect is removed as well."
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Tell me. In your opinion for a strength athlete (sprinter cycling or running) is halo a good compound to use? If so for how long?
Would cycles of 3 weeks in length 20mg a day with a decent pct be good?
I honestly always thought halo was one drug I would never take, but I wonder from all that I've read, if in decent dosage and length of time, it is not quite a good drug, especially for strength athletes?
Perhaps stack it with prop 125mg eod?
Big Cat: (CEM reply): "For strength athletes it has the added benefit of agression, but the downside that it is rather pro-inflammatory, so perhaps not the ideal drug. It has some merit for long distance athletes though. It stimulates appetite and endurance. I'd say 5-6 weeks at 20-40 mg is the normal range of use."
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Big Cat (CEM): "Although both the 17a-methyl and the 11b-substituent cause a slight shift toward PR, there is nothing to point in the direction of halo being remotely antagonistic toward the PR. For the 11b by the way, its usually rule of thumb that the bulkier the substituent, the more PR binding you get, and an OH group isn't really that bulky. (Ojasoo and Raynaud, 1978 and 1995). THe typical effects of too much gluco blocking are increased agression, painful joints, bouts of feeling faint due to blood sugar problems etc. That's usually a sign that you need to stop or lower dosages."
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Big Cat (CEM): "You can do 40 of halo for 6 weeks without too much trouble, if you take a long break from orals afterwards. With halo its hard to define poor results, at 20 or 40 mg, regardless, you won't see any real weight increases. Strength, agression, appetite, and appearance if you are lean are more the type of thing you'll look to get out of halo. But I'd say 30 is the standard dose. 100 of test just to keep test levels in the normal range. If you want to keep from gaining real weight, you don't use too much test, just the bare necessities. Halo, 40 is really the max I would ever do. With var, you can go up to 80 or 100 easily, you'll find that is actually the range where you will be most pleased with var. At 40 its usually nothing but a dissapointment unless you respond really well. But at 80 var is a very good drug."
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Pharmacol Toxicol. 1995 Oct;77(4):264-9. Related Articles, Links
[3H]dexamethasone binding activity in liver microsomes is modulated differently by 17 alpha-alkylated androgens and testosterone in vivo.
Fernandez L, Boada LD, Luzardo OP, Zumbado M, Lopez A, Diaz-Chico BN, Chirino R.
Department of Clinical Sciences, Faculty of Health Sciences, University of Las Palmas de G.C., Spain.
Rat liver microsomes contain a single class of steroid binding sites, capable of binding various glucocorticoids and progesterone. In a previous article, we have described the in vitro interaction of several androgens with this binding site. Unlike natural androgens, the 17 alpha-alkyl derivatives stanozolol and danazol were capable of interacting with this binding site through a negative allosteric pattern. Now, the effects these steroids exert on the microsomal [3H]dexamethasone binding site have been studied in vivo. The administration of a single dose of stanozolol to rats provoked a significant reduction in the microsomal [3H]dexamethasone binding capacity. This effect was maximal two hr after stanozolol administration and persisted for six hr. The restoration of the [3H]dexamethasone binding level after stanozolol administration was dependent on protein synthesis, since it was blocked by the concomitant administration of cycloheximide. None of the other androgens tested (danazol, methyltestosterone, fluoxymesterone, and testosterone propionate) was capable of provoking a similar effect when administered 2 or 24 hr prior to sacrifice. In rats treated for seven days with a daily dose of diverse androgens and sacrificed 24 hr after the last treatment, none of the 17 alpha-alkyl androgens assayed provoked significant changes in the microsomal [3H]dexamethasone binding level, although stanozolol, danazol, and methyltestosterone provoked a significant increase in glucocorticoid receptor concentration. In contrast, the administration of testosterone propionate provoked a 50% reduction in the [3H]dexamethasone binding level without causing changes in the glucocorticoid receptor concentration. These results provide new evidence on the existence of different effects on the liver of 17 alpha-alkyl androgens, compared to the effects produced by natural androgens.
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Big Cat (CEM): "This all taken together suggest the need for glucocorticoid control in the PCT if we want to achieve maximal recovery. In the first place we can do this by avoiding the use of 17AA steroids near the end of a cycle. It has been shown that several 17AA steroids including stanozolol, danazol and methyltestosterone, but not fluoxymesterone or metribolone, can upregulate GR expression (6). Potent short-acting androgens however may be the best way to finish a cycle. Short-acting, to avoid lingering supression from androgens that won't clear the body fast enough, and potent because it has been demonstrated that AR activation in the adrenocortical cells inhibits their growth and steroidogenisis."
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BMJ
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