Halotestin (Fluoxymesterone): Androgenic Profile, CNS Mechanism, and Bloodwork Guide
HALOTESTIN (FLUOXYMESTERONE): 7 PROVEN FACTS, SIDE EFFECTS
Halotestin is fluoxymesterone, a 17-alpha-alkylated oral androgen with a fluorine at carbon 9 and a hydroxyl at carbon 11, the same two features that make cortisol-like drugs potent. That structure is the key to halotestin. In human cells it is a potent inhibitor of the enzyme that inactivates cortisol in the kidney, a mechanism the authors linked to electrolyte disturbance and hypertension (PMID 22273746); in the muscle androgen receptor its binding was too weak to rank (PMID 6539197); and in the largest randomised trial it was chosen as the reference androgen for aplastic anemia because it was the most effective of four (PMID 2872720).
This profile answers what is halotestin in the papers rather than the forums: a drug with forty years of trials in anemia, breast cancer, short boys and dialysis patients, no trial in a healthy man, a liver record that includes fatal peliosis (PMID 577673), and a strength reputation that has never been measured. It lists halotestin side effects by the evidence behind each and sets out the bloodwork that tests them. No dose or protocol is given; the compound is a prescription drug whose effects follow the oral alkylated class it belongs to.
Halotestin in brief
Three numbers frame halotestin: how strongly it hits the enzyme that protects the kidney from cortisol, how weakly it binds the receptor that builds muscle, and what the oral alkylated class does to cholesterol.
Against recombinant human 11-beta-HSD2, fluoxymesterone was a potent inhibitor with a half-maximal concentration of 60 to 100 nanomolar, while oxymetholone, danazol and testosterone were only medium; the authors proposed cortisol-driven mineralocorticoid activation, electrolyte disturbance and hypertension as the consequence (PMID 22273746).
In rat and rabbit skeletal muscle, fluoxymesterone was among the steroids whose binding to the androgen receptor was too low to rank, below stanozolol and methandienone, in the same assay where testosterone, nandrolone and methenolone bound strongly (PMID 6539197).
In the class comparison, oral stanozolol lowered HDL cholesterol 33 percent against 9 percent on injected testosterone in healthy men (PMID 2915439). No lipid trial exists for halotestin; the class result is the one it has to be tested against.
Every figure is taken from the abstracts of the twenty-one papers at the end. Halotestin and fluoxymesterone are named because the papers name them; no dose, schedule or cycle is given here.
What this halotestin profile covers
What is halotestin: fluoxymesterone, the fluorine and hydroxyl that make it cortisol-shaped, and what its binding numbers actually say.
What has actually been measured in randomised trials of anemia, breast cancer and cancer cachexia, in short boys and dialysis patients, and in the cell and animal work.
Halotestin side effects by the evidence behind each: blood pressure and electrolytes, liver, thyroid, the axis, virilisation, and the strength and aggression claims.
The bloodwork that tests the cortisol and liver mechanisms in one person, and the five mistakes the reputation leads to.
Not coveredDoses, cycle lengths, stacks or a protocol. The trials dosed patients for anemia and cancer; nothing here is an instruction.
The other oral alkylated steroids. Anadrol, Anavar and Winstrol have their own pages; Anadrol shares the peliosis record on this one.
Buying, sourcing or legality. Not on this site.
What is halotestin? Fluoxymesterone, a cortisol-shaped androgen
What is halotestin, chemically: fluoxymesterone, 9-alpha-fluoro-11-beta-hydroxy-17-alpha-methyltestosterone, an oral androgen first marketed in the late 1950s and still listed as a prohibited substance in sport (PMID 41721113). The 17-alpha-methyl group is what lets it survive the liver on the way in and what makes the liver the main casualty of halotestin; the 9-fluoro and 11-hydroxy groups are borrowed from the chemistry of synthetic glucocorticoids, and they turn out to matter more than the forums know.
The binding study everyone quotes for the androgenic index says the opposite of what it is quoted for. When halotestin and other anabolic steroids were tested as competitors for the androgen receptor in rat and rabbit skeletal muscle and prostate, fluoxymesterone was among the compounds with relative binding affinities below 0.05, alongside stanozolol and methandienone, while testosterone, nandrolone and methenolone bound strongly (PMID 6539197). Whatever halotestin does in a person, it does not do it by sitting hard on the muscle androgen receptor.
The cortisol connection is the measured mechanism of halotestin. In recombinant human 11-beta-HSD2 and in two human cell lines, fluoxymesterone inhibited cortisol inactivation with half-maximal concentrations of 60 to 100 nanomolar in lysates and 160 to 530 nanomolar in intact cells; structural modelling showed it binding the enzyme the way cortisol does; it did not act on the mineralocorticoid receptor directly; and the effect was much weaker in rat and mouse enzyme, so animal studies cannot see it (PMID 22273746). The authors proposed that the resulting cortisol excess at the receptor leads to electrolyte disturbance and contributes to hypertension. What that means for a blood pressure cuff is on do steroids raise blood pressure.
What is measured on fluoxymesterone, and in whom
Halotestin has a long clinical record, almost all of it in people who were ill and none of it in lifters. The table sorts what exists on halotestin by design, and the weight column is the one to read.
| Finding | Design | Weight |
|---|---|---|
| Fluoxymesterone the most effective of four androgens in moderately severe aplastic anemia, stanozolol the least; high dose improved survival (PMID 2872720) | 110 randomised plus 125 compared | Randomised |
| Breast cancer response 53 percent on tamoxifen plus fluoxymesterone vs 42 percent on tamoxifen; time to progression 350 vs 199 days; more androgenic toxicity; no survival gain (PMID 3284975) | 238 women, randomised | Randomised |
| Adjuvant fluoxymesterone added to tamoxifen: no difference in relapse or survival at 11.4 years; more virilisation (PMID 16538529) | 541 women, randomised | Randomised |
| Cancer anorexia: fluoxymesterone gave significantly less appetite gain than megestrol or dexamethasone and did not have a favourable toxicity profile (PMID 10506633) | Randomised, three arms | Randomised |
| Short boys: growth velocity 1.7 to 2.5 times baseline on a low daily dose, final height above prediction, no adverse androgenic effects (PMID 8464656) | 82 boys, prospective | Uncontrolled |
| Dialysis anemia: hematocrit, hemoglobin and red cell mass rose in four months; hirsutism and voice deepening; cholesterol unchanged (PMID 608858) | 30 patients | Uncontrolled |
| Myelodysplasia: platelets rose in 55 percent on fluoxymesterone or danazol, bleeding stopped in 6 of 6; side effects moderate (PMID 7947249) | 20 patients | Uncontrolled |
| Subfertile men: sperm motility and normal morphology improved over 12 months, benefit in some, not others (PMID 3435196) | 69 men, uncontrolled | Uncontrolled |
| Primary testicular failure: fluoxymesterone lowered thyroid-binding globulin, testosterone, gonadotropins and the LH response to LHRH; mesterolone did none of this (PMID 6437958) | 27 men | Uncontrolled |
| Total T4 and binding globulin fell in four weeks; women on thyroid replacement became hyperthyroid and needed 25 to 50 percent less levothyroxine (PMID 7518657) | 11 women | Uncontrolled |
| Peliosis hepatis in 12 patients on high-dose oxymetholone or fluoxymesterone; liver failure the cause of death in three (PMID 577673) | Case series | Cases |
| Persistent gynecomastia after childhood fluoxymesterone for aplastic anemia, hormones normal (PMID 25948845) | Case report | Case |
| Potent inhibition of human 11-beta-HSD2, cortisol-like binding, hypertension proposed (PMID 22273746) | Human cells | Cell |
| Androgen receptor binding in muscle too low to rank, below stanozolol (PMID 6539197) | Rat and rabbit tissue | Tissue |
| Mitochondrial and sarcotubular enzymes changed in soleus, not in fast muscle; effect muscle-type specific (PMID 1827788) | Trained and sedentary rats | Animal |
| Oral stanozolol lowered HDL 33 percent vs 9 percent on injected testosterone (PMID 2915439); long-term users HDL 0.69 vs 1.25 mmol/l, coronary disease 17 percent (PMID 35460300) | Class | Class |
Read the weight column first. The randomised trials show a real androgen: it grew red cells and platelets, it moved breast cancer, it lengthened boys. They also show the cost, virilisation in every trial that reported it and toxicity that made it the losing arm in cachexia. Nothing in the table measures strength, aggression or muscle in a healthy adult. That is the whole evidence base, and the rest of this page stays inside it.
The medical record: anemia, breast cancer, short boys
Halotestin was a marrow drug and an oncology drug long before it was a powerlifting rumour. In the French cooperative programme, 110 patients with aplastic anemia were randomised to fluoxymesterone or norethandrolone at high or low dose and 125 more were compared across four androgens; high-dose androgens improved survival and blood counts in the less severe cases, and fluoxymesterone was the most effective of the four with stanozolol the least, so the authors named it the reference drug for future trials (PMID 2872720). In 20 patients with low-risk myelodysplasia, androgen therapy raised platelets in 55 percent and stopped bleeding in all six who bled, with moderate side effects (PMID 7947249).
Breast cancer is where the randomised numbers on halotestin are largest. In 238 postmenopausal women with metastatic disease, adding fluoxymesterone to tamoxifen raised the objective response rate from 42 to 53 percent and the median time to progression from 199 to 350 days, at the cost of more androgenic side effects and with no survival advantage; 40 percent of women who failed tamoxifen then responded to fluoxymesterone (PMID 3284975). The adjuvant trial that followed, 541 women followed for a median of 11.4 years, found no difference in relapse or death, a hazard ratio of 0.84 with a confidence interval crossing one, and as expected more virilisation (PMID 16538529).
The rest of the record is smaller and consistent. In 30 dialysis patients, four months of halotestin raised hematocrit, hemoglobin and red cell mass and cut transfusions, with hirsutism and a deepened voice as the recorded cost and no change in cholesterol (PMID 608858). In 82 short boys treated for up to five years, growth velocity rose 1.7 to 2.5-fold, final height exceeded prediction, and no adverse androgenic effects were seen (PMID 8464656). In the one trial where it competed as a weight-gain drug, cancer cachexia, it lost: significantly less appetite gain than megestrol or dexamethasone and a toxicity profile the authors called unfavourable (PMID 10506633).
Cortisol, blood pressure and thyroid: the two binding globulins
Two findings separate halotestin from every other steroid in this series, and both come from its cortisol-like structure. The first is the enzyme result already described: potent, competitive inhibition of human 11-beta-HSD2, the enzyme that keeps cortisol away from the mineralocorticoid receptor in the kidney, with the authors proposing electrolyte disturbance and hypertension as the clinical result and noting that rodent enzyme is far less sensitive, so the effect is invisible in animal studies (PMID 22273746). No human trial has measured blood pressure on halotestin. The class data are the stand-in: fluid retention in 56 percent of 100 men on cycles (PMID 33038020).
What halotestin did to thyroid measures in women treated for breast cancer, within four weeks (PMID 7518657).
All four women on replacement became clinically hyperthyroid within four weeks of starting the androgen; values returned to baseline six to twelve weeks after it was stopped.
The second halotestin finding is thyroid. In 11 women receiving fluoxymesterone for breast cancer, total thyroxine and thyroxine-binding globulin fell within four weeks while free hormone stayed normal in the seven without thyroid disease; the four on long-term levothyroxine became clinically hyperthyroid, free T4 rose, TSH fell, and their replacement dose had to be cut by 25 to 50 percent (PMID 7518657). The older endocrine study found the same fall in thyroid-binding globulin, with T3 down and resin uptake up and thyroid function unchanged (PMID 6437958). A man on thyroid medication who adds halotestin has a measured interaction, not a theoretical one.
Halotestin and the liver: the alkylated record
Halotestin is 17-alpha-alkylated, which is the modification behind the liver toxicity of oral steroids as a class, and its own record is one of the worst in the literature. In a pathology series of 12 patients treated with high-dose oxymetholone or fluoxymesterone, all had peliosis hepatis, blood-filled cavities in the liver; in three, liver failure was the primary cause of death; in eight the lesion was an incidental finding at autopsy; in one it was diagnosed on biopsy, the drug was stopped, and the lesion was gone two years later (PMID 577673). That last case is the reason to test and stop early.
The class comparison gives the lipid side. Six weeks of oral stanozolol, another alkylated androgen, lowered HDL cholesterol by 33 percent against 9 percent on injected testosterone in healthy men (PMID 2915439). No lipid trial on halotestin exists; the dialysis series recorded unchanged cholesterol in anemic patients (PMID 608858), which is a total cholesterol in the wrong population and not a lipoprotein panel. In long-term users of the class, HDL was 0.69 against 1.25 mmol/l in clean athletes and coronary artery disease was present in 17 percent (PMID 35460300); in Turkish gym users, transaminases were higher than in non-users (PMID 42312743).
Two measured details temper the picture without changing it. In the rat, fluoxymesterone changed mitochondrial and sarcotubular enzymes in slow soleus muscle but not in fast muscle, a muscle-type-specific effect rather than a general one (PMID 1827788), and in cultured heart cells it was less directly injurious than testosterone cypionate at the same concentrations (PMID 1549009). Neither is a liver finding, and neither is a person. The markers that catch cholestasis before jaundice are on liver markers: AST, ALT, GGT.
Hormones on halotestin: the axis, fertility and the breast
Halotestin does not aromatise, and it suppresses. In 27 men with primary testicular failure, six weeks of fluoxymesterone reduced testosterone, gonadotropins and the LH response to releasing hormone, while mesterolone in the same protocol changed none of them (PMID 6437958). That is the direct measurement of what a non-aromatising oral androgen does to the axis: the absence of estrogen does not spare the pituitary. In the class, gym users identified by gonadotropin suppression had a median LH of 0.12 IU/l (PMID 42312743).
The fertility and breast findings on halotestin are the surprises. In 69 subfertile men treated for up to a year, sperm motility and normal morphology improved, benefiting some men and not others, in an uncontrolled series (PMID 3435196); the mesterolone trials that later tested androgens for infertility against placebo found nothing, a record set out on the proviron page. And a compound that cannot aromatise has a published case of gynecomastia: a man treated with fluoxymesterone for aplastic anemia in childhood developed persistent breast tissue at puberty with a normal hormonal work-up, leaving the drug as the cause (PMID 25948845). In 100 men on mixed cycles, gynecomastia occurred in 19 percent (PMID 33038020).
What is not measured is the list that sells halotestin: strength, aggression, competition-day performance. A search of PubMed on 30 September 2026 for fluoxymesterone with strength, aggression or athletes returns metabolite studies, rat muscle enzymes and no human trial. The androgen receptor data point the other way (PMID 6539197). The claim is a reputation, and the bloodwork below is how one person tests what the literature has not. Recovery of the axis afterwards is on when to start PCT and the baseline on estradiol before steroids.
Halotestin side effects by the evidence
Halotestin side effects are described on the forums as liver strain and aggression, one of which is measured. The table gives each effect with the strongest source that exists and says which kind of source it is.
| Effect | Strongest evidence | Read as |
|---|---|---|
| Liver: peliosis, cholestasis | Peliosis hepatis in 12 patients on high-dose oral androgens, three fatal (PMID 577673); transaminases higher in class users (PMID 42312743) | Human, serious |
| Blood pressure, sodium, potassium | Potent 11-beta-HSD2 inhibition, cortisol-driven mineralocorticoid activation proposed (PMID 22273746); fluid retention 56 percent on cycles (PMID 33038020) | Cell, plus class |
| Virilisation, hirsutism, voice | Reported in every trial in women: breast cancer (PMID 3284975, PMID 16538529), dialysis (PMID 608858) | Human, certain |
| Axis suppression | Testosterone, gonadotropins and LH response fell in six weeks (PMID 6437958); class median LH 0.12 IU/l (PMID 42312743) | Human |
| Thyroid interaction | T4 and binding globulin fell; women on levothyroxine became hyperthyroid, dose cut 25 to 50 percent (PMID 7518657) | Human, measured |
| HDL fall | Not measured on fluoxymesterone; oral alkylated class minus 33 percent (PMID 2915439); users 0.69 vs 1.25 mmol/l (PMID 35460300) | Class |
| Red cells and platelets | The licensed effect: hematocrit and red cell mass rose in dialysis patients (PMID 608858); platelets in 55 percent of MDS (PMID 7947249) | Human, certain |
| Appetite and weight | Inferior to megestrol and dexamethasone in cancer cachexia, unfavourable toxicity (PMID 10506633) | Randomised, negative |
| Gynecomastia | One case after childhood treatment, hormones normal (PMID 25948845); 19 percent on mixed cycles (PMID 33038020) | Case, plus class |
| Heart muscle | Less directly injurious than testosterone cypionate in cultured heart cells (PMID 1549009); class users ejection fraction 50 vs 54 percent (PMID 35460300) | Cell, plus class |
| Aggression, strength | No human measurement; androgen receptor binding in muscle too low to rank (PMID 6539197) | Not measured |
The honest summary of halotestin side effects is that the drug does what every oral alkylated androgen does to the liver, with a fatal case series of its own; that it has a cortisol mechanism no other steroid on this site shares, pointing at blood pressure and electrolytes; that it suppresses the axis and interacts with thyroid medication in measured ways; and that its famous effect on strength has never been measured at all.
Halotestin bloodwork: eight markers
The two halotestin mechanisms with the best evidence, cortisol at the kidney and cholestasis at the liver, are both caught by ordinary blood tests before they are caught by symptoms. The eight markers follow the findings on this page.
| Marker | What the data show | Priority |
|---|---|---|
| ALT, AST, GGT, bilirubin, alkaline phosphatase | Peliosis and liver failure on high-dose oral androgens (PMID 577673); transaminases higher in users (PMID 42312743). Guide: liver markers | First |
| Blood pressure | 11-beta-HSD2 inhibition, hypertension proposed (PMID 22273746). Guide: blood pressure | First |
| Sodium and potassium | The same cortisol mechanism, read as electrolytes: retained sodium, lost potassium (PMID 22273746) | First |
| HDL and LDL cholesterol | Class: stanozolol minus 33 percent HDL (PMID 2915439); users 0.69 vs 1.25 mmol/l (PMID 35460300). Guide: lipid panel | First |
| Hematocrit and hemoglobin | Rose in four months in dialysis patients (PMID 608858); users 0.50 vs 0.44 (PMID 35460300). Guide: high hematocrit | Second |
| LH, FSH, testosterone | Fell in six weeks (PMID 6437958). Guide: estradiol before steroids | Second |
| TSH and free T4 | Binding globulin and total T4 fall; anyone on levothyroxine can become hyperthyroid within four weeks (PMID 7518657) | If on thyroid medication |
| Estradiol | Not measured on fluoxymesterone; it does not aromatise, yet a gynecomastia case exists (PMID 25948845). Guide: high estrogen symptoms | Standard |
Timing follows the data: thyroid and binding globulins had moved within four weeks (PMID 7518657) and the axis within six (PMID 6437958), and peliosis was found at autopsy in patients who had no warning (PMID 577673), so a baseline and a first-month panel are the minimum. The baseline set is on blood tests before steroids.
Five mistakes people make with halotestin
Each of these comes from treating the halotestin index number as a measurement.
1. Reading the androgenic index as receptor power. In the binding assay, fluoxymesterone was among the steroids too weak to rank on the muscle androgen receptor (PMID 6539197). Whatever it does, the receptor number is not why.
2. Watching only the liver. The liver deserves it (PMID 577673), but the mechanism unique to this drug is cortisol at the kidney (PMID 22273746). Blood pressure and electrolytes belong on the same panel as ALT.
3. Assuming no estrogen means no suppression and no gyno. Testosterone and gonadotropins fell in six weeks (PMID 6437958), and a gynecomastia case exists on this drug (PMID 25948845).
4. Combining it with thyroid medication unchecked. Four of four women on levothyroxine became hyperthyroid within four weeks and needed 25 to 50 percent less (PMID 7518657).
5. Expecting body mass. In the one randomised trial where halotestin was meant to add weight, it was the inferior arm (PMID 10506633). The rat data are muscle-type specific, not general (PMID 1827788). Strength in a person has not been measured.
Verdict: a cortisol-shaped oral androgen with a measured liver record and an unmeasured reputation
Halotestin, after the papers rather than the forums, is fluoxymesterone: a 17-alpha-alkylated androgen that was the most effective of four in aplastic anemia (PMID 2872720), that added 11 points of response and five months to progression in metastatic breast cancer at the cost of virilisation and with no survival gain (PMID 3284975), that lengthened short boys without harm (PMID 8464656), and that lost the only trial in which it was asked to add body mass (PMID 10506633). Its liver record includes fatal peliosis (PMID 577673); its cortisol mechanism is potent, human-specific and points at blood pressure (PMID 22273746); its receptor binding in muscle is too weak to rank (PMID 6539197).
The halotestin side effects that matter are the ones a panel catches in the first month: liver enzymes and bilirubin, blood pressure with sodium and potassium, lipids, the axis, and thyroid for anyone on replacement. Everything upstream of that panel is on the PED side effects hub and on blood tests before steroids; the oral alkylated steroid that shares its peliosis record and has the trials it lacks is anadrol.
Halotestin: frequently asked questions
What is halotestin?
Halotestin is the brand name of fluoxymesterone, an oral 17-alpha-alkylated androgen with a fluorine at carbon 9 and a hydroxyl at carbon 11, first used in the 1950s for anemia, breast cancer and delayed growth. In human cells it potently inhibits 11-beta-HSD2, the enzyme that inactivates cortisol in the kidney (PMID 22273746), and in muscle tissue its androgen receptor binding was too weak to rank (PMID 6539197).
What are the halotestin side effects?
The measured ones are liver injury, including peliosis hepatis with three deaths in a 12-patient series on high-dose oral androgens (PMID 577673); suppression of testosterone and gonadotropins within six weeks (PMID 6437958); virilisation in every trial in women (PMID 3284975); and a thyroid interaction that made women on levothyroxine hyperthyroid (PMID 7518657). The cell data flag blood pressure and electrolytes through cortisol (PMID 22273746). Lipids follow the oral alkylated class (PMID 2915439).
Does halotestin raise blood pressure?
No human trial has measured it, but the mechanism is the best documented of any steroid on this site. Fluoxymesterone potently inhibits human 11-beta-HSD2 at nanomolar concentrations, letting cortisol act on the mineralocorticoid receptor, which the authors proposed leads to sodium retention, potassium loss and hypertension (PMID 22273746). On cycles of the class, fluid retention affected 56 percent of men (PMID 33038020).
Is halotestin bad for the liver?
It is 17-alpha-alkylated, the modification behind oral steroid liver injury, and its record includes a pathology series of 12 patients with peliosis hepatis on high-dose oxymetholone or fluoxymesterone, three of whom died of liver failure, and one whose lesion resolved two years after stopping (PMID 577673). Transaminases were higher in users of the class (PMID 42312743).
Does halotestin increase strength or aggression?
Neither has been measured in a person. A PubMed search on 30 September 2026 finds no controlled trial of fluoxymesterone on strength, muscle or aggression in healthy adults. Its binding to the muscle androgen receptor was too low to rank (PMID 6539197), rat muscle enzyme changes were confined to slow muscle (PMID 1827788), and in the cancer cachexia trial it was the inferior arm for appetite and weight (PMID 10506633).
Does halotestin suppress testosterone?
Yes: halotestin suppressed the axis in the one direct measurement. In 27 men with primary testicular failure, six weeks of fluoxymesterone lowered testosterone, gonadotropins and the LH response to releasing hormone, while mesterolone in the same study changed none of them (PMID 6437958). Not aromatising does not spare the pituitary; class users had a median LH of 0.12 IU/l (PMID 42312743).
Does halotestin cause gyno?
It cannot aromatise, and yet a documented case exists: persistent gynecomastia at puberty in a man treated with fluoxymesterone for aplastic anemia in childhood, with a normal hormonal work-up that left the drug as the cause (PMID 25948845). On mixed cycles of the class, gynecomastia occurred in 19 percent of 100 men (PMID 33038020).
What bloodwork should be checked on halotestin?
Liver enzymes with bilirubin and alkaline phosphatase first, because of the peliosis record (PMID 577673); blood pressure with sodium and potassium, because of the cortisol mechanism (PMID 22273746); a lipid panel, because the oral alkylated class lowers HDL by a third (PMID 2915439); hematocrit; LH, FSH and testosterone for the axis (PMID 6437958); and TSH with free T4 for anyone on thyroid medication (PMID 7518657).
Sources and further reading
Every figure on this page comes from one of the twenty-one papers below, each checked against its PubMed abstract on 30 September 2026. Animal and cell studies are cited as such and never as human results. Reference links are dofollow to support open science.
Keep reading
Four pages around halotestin: the liver markers that catch cholestasis early, the blood pressure question its cortisol mechanism raises, the oral alkylated steroid with the trials, and the class data on injectables against orals.
Final Educational Note
This article is educational and is not medical advice. It reports what randomised trials, case series, cohorts, animal and cell studies measured about fluoxymesterone, a prescription androgen with serious hepatic, cardiovascular and endocrine risks. It gives no dose, schedule, cycle or protocol, does not recommend the drug, and is not an encouragement to use anabolic steroids, which carry serious health and legal risks. More guides sit on the PED side effects hub.
Jaundice, dark urine, right upper abdominal pain, a rising blood pressure, swelling, palpitations or symptoms of an overactive thyroid during or after androgen exposure are clinical findings that a physician should assess at once. Read more about how this site works on the about page and in the full disclaimer.
