Wait. First things first - 130 pounds? I hate you!
Now that that is finished, HRT does reduce body hair. On my chest I'd say it was about 95 to 98%. Between that and epilation, the hair gets finer over time so even if the number of hairs does not decrease, the overall mass of hair does get less. Dr. McGinn once recommended I wait until I'd been on HRT for at least 3 months before beginning hair removal. I'd say wait a year, speaking strictly about the effects on body hair and disregarding the fact that you'll have boobs within a few months.
HRT also makes for better hair growth on one's head. Spiro pretty much filled in a bald spot for me...
I think HRT also makes your skin thinner and better looking, too. That may also be one of the reasons why waiting a few months for HRT to take effect before starting hair removal, simply because it probably makes it easier removing hair from those places you don't want hair.
High doses of oestrogen inhibits T production as does spiro. I am on 6mg of oestrogen & 100mg spiro & I have not had any measurable T for the past 3 yrs, but we are all different & therefore doses will vary between individuals.
With T effectively blocked then the effects of T on hair will be reversed. Male pattern baldness will diminish, body hair will thin & regrowth will be slower. Pubic hair will thin a little. Beard growth will slow a little. As mentioned earlier there are skin changes as well, softer thinner & more sensitive for a start. There is also a reduction in sebum production so your body odour will change & another consequence of reduced sebum is that you may not need to wash your hair as frequently.
So my young friend yes it will all happen to you, but just be a little more patient & get your doctor to monitor your blood levels of both oestrogen & T so that you are sure that you are on the correct dose of HRT for you.
50 of SPIRO ?????? to see any difference you need to be on a minimal of 100 mg ! With a dose of 50 it is basicly just at the highest level of a blood thinner and will do nothing as a t blocker.
Danica - I am sorry but you have misread Emily's post. Assuming Emily is talking about her Spiro dose in mg's then "50 of the spiro bid" means 50mg twice a day. bid is a medical abbreviation used to mean twice a day.
Also Spiro is not a blood thinner. It is a potassium sparing diuretic & as such would possibly thicken the blood rather than the reverse by causing the kidneys to produce more urine.
Spiro is an anti-androgen drug - working on cell receptors for testosterone. So while it does not reduce testosterone directly, it definitely keeps cells from using T. That is why it reduces hair loss on your head, promotes hair growth, especially when applied as creme, reduces sex drive, aids in breast enlargment in men, drops overall blood pressure typically because of reduced heart rates, reduces acne, and has a load more other side effects.
As mentioned below being potassium sparing is a huge one. If you are on large doses and don't want real trouble, you have to end eating things high in potassium like bananas.
Normal doses, btw, can be as low as 25 mg and as much as 400 mg / day when treating other medical conditions such as high blood pressure, kidney diseases, congestive heart failure, and others. Because SPIRO affects so many parts of the body and how it all works together, one should work with their doctor to determine levels rather than put yourself at risk.
Lastly, Aspirin REDUCES the effects of Spiro so you may wish to use another pain reliever if you believe that you need a full dose of spiro. You may also note that many an endo suggest that baby aspirin be used daily while on HRT. Of course, over time HRT will reduce your need for Spiro as your testes will shrink. Based upon blood work and physical condition / symptoms, your physician may suggest a reduction or increase in the amount you take.
Remember that one size pantyhose doesn't fit all... and neither does doses for drugs with complex interactions and a multitude of side effects like this one.
Lisa --> where on Emily's page does it say 50 mg x 2 times a day ? All I see is spiro 50, And Do some more research , my dr even told me Spiro use to be perscribed in lower doses as blood thinners ranging in strength s of 5 - 50 until they discovered it was better used this way . EVEN my paperwork from the pharmacy says it is used as a blood thinner in alot of cases.
I have taken the step of providing the product information about Spiro as there seems to be a lot of misinformation about what it does & how it does it. This information is provided by Pfizer, the products manufacturer. Please read it carefully as there is a lot of information in there that maybe difficult to interpret without medical training. If anyone wants more info or help with this info you can send me an email via PE.
Cardiovascular System - Diuretics
MIMS revision date:
01 Oct 2010
Actions Pharmacology. Aldactone (spironolactone) is a specific pharmacological antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone dependent sodium potassium exchange site in the distal convoluted renal tubule. Aldactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Aldactone acts both as a diuretic and as an antihypertensive agent. It may be given alone or with other diuretic agents which act more proximally in the renal tubule.
Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Oedematous states in which secondary aldosteronism is usually involved include congestive cardiac failure, hepatic cirrhosis, and the nephrotic syndrome. By competing with aldosterone for receptor sites, Aldactone provides effective therapy for the oedema and ascites in those conditions.
Aldactone is effective in lowering the systolic and diastolic blood pressure in patients with primary hyperaldosteronism. It is also effective in most cases of essential hypertension despite the fact that aldosterone secretion may be within normal limits in benign essential hypertension.
Through its action in antagonising the effect of aldosterone, Aldactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
Aldactone has not been demonstrated to elevate serum uric acid, to precipitate gout or to alter carbohydrate metabolism. Aldactone has moderate antiandrogenic activity in humans by inhibition of the interaction between dihydrotestosterone and the intracellular androgen receptor. It also inhibits several steps in ovarian steroidogenesis resulting in lowered plasma levels of testosterone and some other weak androgenic steroids. Through this activity Aldactone is effective in the treatment of female hirsutism.
In the human, the bioavailability of spironolactone from orally administered Aldactone tablets exceeds 90% when compared with an optimally absorbed solution (spironolactone in polyethylene glycol 400). Spironolactone is rapidly and extensively metabolised.
Approximately 25 to 30% of the dose administered is converted to canrenone. Sulfur containing products are the predominant metabolites and together with spironolactone are thought to be primarily responsible for the therapeutic effects of the drug. Canrenone attains peak serum levels at two to four hours following single oral administration. Canrenone plasma concentrations decline in two distinct phases, being rapid in the first 12 hours and slower from 12 to 96 hours. The log linear phase half-life of canrenone, following multiple doses of Aldactone, is between 13 and 24 hours. Both spironolactone and canrenone are more than 90% bound to plasma proteins. The metabolites of spironolactone are excreted primarily in urine, but also in bile. Food may increase the bioavailability of spironolactone; the clinical relevance of this effect is uncertain.
Indications Essential hypertension.
Oedematous disorders, e.g. oedema and ascites of congestive cardiac failure, cirrhosis of the liver and nephrotic syndrome.
Diagnosis and treatment of primary hyperaldosteronism.
As adjunctive therapy in malignant hypertension.
In diuretic induced hypokalaemia when other measures are considered inappropriate or inadequate.
Prophylaxis of hypokalaemia in patients taking digitalis when other measures are considered inadequate or inappropriate.
Essential hypertension. Aldactone, when used alone, is effective in lowering both systolic and diastolic blood pressure. Aldactone improves the hypotensive action of thiazide diuretics, while at the same time reducing or preventing potassium loss due to the thiazide. Aldactone enhances the effectiveness of other antihypertensive agents, e.g. beta-blockers and vasodilators.
Congestive cardiac failure. Aldactone, when used alone, is effective in the management of oedema and sodium retention associated with congestive cardiac failure. Aldactone may be used in combination with a thiazide or other conventional diuretics for achieving diuresis in patients whose oedema is resistant to a thiazide or other conventional diuretics. Unlike conventional diuretics, Aldactone does not produce hypokalaemia. When administered with a thiazide or other conventional diuretics, Aldactone offsets hypokalaemia induced by these diuretics. The prevention of potassium loss is particularly important in the treatment of digitalised patients, since digitalis intoxication may be precipitated if hypokalaemia is induced by conventional diuretic therapy.
Hepatic cirrhosis with ascites and oedema. Aldactone, when used alone, is frequently adequate for the relief of ascites and oedema associated with hepatic cirrhosis. Aldactone provides a mild and even diuresis and prevents excessive potassium excretion caused by thiazide diuretics, thus avoiding possible precipitation of hepatic coma.
Nephrotic syndrome. Although glucocorticoids, whose anti-inflammatory activity appears to benefit the primary pathological process in the renal glomerulus, should probably be employed first, Aldactone either alone or in combination with a conventional diuretic is useful for inducing diuresis.
Primary hyperaldosteronism. Aldactone may be used to establish the diagnosis of primary hyperaldosteronism by therapeutic trial. Spironolactone may also be used for the short-term preoperative treatment of patients with primary hyperaldosteronism, long-term maintenance therapy for patients with discrete aldosterone producing adrenal adenomas who are judged to be poor operative risks (or who decline surgery), and long-term maintenance therapy for patients with bilateral micronodular or macronodular adrenal hyperplasia (idiopathic hyperaldosteronism).
Hirsutism in females. Aldactone is effective in the treatment of females with hirsutism, an androgen related increase in facial and body hair. A reduction in hair growth, hair shaft diameter and hair pigmentation is seen.
Use of Aldactone should be considered only after all other alternatives of nondrug therapy have been explored. For women of childbearing age, see Contraindications and Precautions, Use in pregnancy.
Contraindications Acute renal insufficiency, significant impairment of renal function, anuria, Addison's disease, hyperkalaemia, pregnancy (see Precautions), hypersensitivity to spironolactone or with concomitant use of eplerenone.
Precautions Concomitant use of spironolactone with angiotensin converting enzyme (ACE) inhibitors, angiotensin II antagonists, aldosterone blockers, heparin, low molecular weight heparin, or potassium supplements, a diet rich in potassium, including salt substitutes, or of other potassium sparing agents is not recommended as it may lead to severe hyperkalaemia.
Hyperkalemia may be fatal in patients with severe heart failure (NYHA class III-IV). Potassium and creatinine levels should be closely monitored one week after initiation or monthly for the first 3 months, then quarterly for a year, and then every 6 months when increasing the dose of spironolactone. Concomitant use of spironolactone and other potassium sparing diuretics in patients with severe heart failure should be avoided. If serum potassium > 3.5 mEq/L, oral potassium supplements should be avoided. Treatment with spironolactone should be discontinued or interrupted in patients with serum potassium > 5 mEq/L or for serum creatinine > 4 mg/dL.
Periodic estimation of serum electrolytes is desirable due to the possibility of hyperkalaemia, hyponatraemia and possible transient blood urea nitrogen (BUN) elevation especially in the elderly and/or patients with pre-existing impaired renal or hepatic function, in whom the risk/ benefit ratio should always be weighed.
Somnolence and dizziness have been reported to occur in some patients. Caution is advised when driving or operating machinery until the response to initial treatment has been determined.
Reversible hyperchloraemic metabolic acidosis, usually in association with hyperkalaemia, has been reported to occur in some patients with decompensated hepatic cirrhosis, even in the presence of normal renal function.
The safety of Aldactone for the treatment of hirsutism in women of childbearing age has not been established by specific long-term clinical trials. Epidemiological studies are also inadequate to establish the safety of long-term use in this population.
Use in pregnancy (Category B3)
Experimentally, passive transfer of potassium sparing diuretics across the human placenta has been demonstrated. Maternal treatment during pregnancy may result in electrolyte disturbances in the fetus. Spironolactone should not be used in pregnancy (see Contraindications). Women of childbearing potential should employ adequate contraception, i.e. oral contraceptives or intrauterine devices (IUDs), during administration of spironolactone, and the drug should be stopped if pregnancy occurs or is suspected.
In animal studies, spironolactone was devoid of teratogenic effects in mice and rabbits at oral doses up to 20 mg/kg/day, and in rats at dietary doses up to 50 mg/kg/day. However, increased resorption rate was seen at 20 mg/kg/day in rabbits, and the incidence of stillbirths was increased in rats dosed at 50 mg/kg/day. Subcutaneous administration of spironolactone (approximately 50 to 100 mg/kg/day) to rats during late pregnancy caused endocrine dysfunction in both sexes of offspring 70 to 80 days after birth (hypoprolactinaemia and decreased ventral prostate and seminal vesical weights in males; increased luteinising hormone secretion and ovarian and uterine weights in females). Feminisation of the external genitalia of male fetuses was reported in another study in rats at oral doses of approximately 200 mg/kg/day. Subcutaneous administration of spironolactone to neonatal female mice caused histological changes in the cervicovaginal epithelium that were similar to those caused by diethylstilboestrol (a drug which causes vaginal neoplasia in adulthood following
The risk of demasculinisation of the male fetus will only occur from about six weeks postconception onwards, hence if inadvertent spironolactone administration is stopped at an early stage, the risk to the male fetus is small.
Use during lactation Canrenone, an active metabolite of spironolactone, appears in breast milk. If the use of the drug is deemed essential, an alternative method of infant feeding should be instituted.
Carcinogenic and mutagenic potential Spironolactone has been shown to be tumorigenic in chronic toxicity studies performed in rats. It should be used only for approved indications. Unnecessary use of this drug should be avoided.
In chronic toxicity studies of spironolactone in rats, changes were observed in the endocrine organs and the liver. In one study using 50, 150 and 500 mg/kg/day there was a statistically significant dose related increase in benign adenomas of thyroid follicular cells and testicular interstitial cells. In female rats, there was a statistically significant increase in malignant mammary tumours at the mid dose only. In male rats, there was a dose related increase in proliferative changes in the liver which included hyperplastic nodules and hepatocellular carcinomas at the mid and high doses.
In a two year oral carcinogenicity study in which rats were administered spironolactone 10, 30, 100 and 150 mg/kg/day, the range of proliferative effects observed was consistent with earlier studies. There were statistically significant increases at the higher doses in hepatocellular adenomas and testicular interstitial cell tumours in males, and in thyroid follicular cell adenomas and carcinomas in both sexes. There was also a statistically significant increase in benign uterine endometrial polyps in females. There was an increase in hepatocellular carcinomas in males at 150 mg/kg but this was not statistically significant. There was no significant increase in the incidence of mammary tumours.
The significance of these findings with respect to clinical use is not known.
Spironolactone was not mutagenic in the Ames test using five strains of Salmonella typhimurium with or without metabolic activation.
A dose related (above 20 mg/kg/day) incidence of myelocytic leukaemia was observed in rats fed daily doses of potassium canrenoate for a period of one year. Canrenone and canrenoic acid are the major metabolites of potassium canrenoate. Spironolactone is metabolised to canrenone. In long-term (two year) oral carcinogenicity studies of potassium canrenoate in the rat, myelocytic leukaemia and hepatic, thyroid, testicular and mammary tumours were observed. Potassium canrenoate did not produce a mutagenic effect in tests using bacteria or yeast. It did produce a positive mutagenic effect in several in vitro tests in mammalian cells following metabolic activation. In an in vivo mammalian system, potassium canrenoate was not mutagenic. An increased incidence of leukaemia was not observed in chronic rat toxicity or carcinogenicity studies conducted with spironolactone at doses up to 500 mg/kg/day. The recommended human dose of spironolactone is 1.4 to 5.7 mg/kg/day.
Interactions Hyperkalaemia has been associated with the use of indomethacin or ACE inhibitors in combination with potassium sparing diuretics.
Spironolactone reduces the vascular responsiveness to noradrenaline. Therefore caution should be exercised in the management of patients subjected to regional or general anaesthesia while they are being treated with Aldactone.
NSAIDs may attenuate the natriuretic efficacy of diuretics due to inhibition of intrarenal synthesis of prostaglandins.
As carbenoxolone may cause sodium retention and thus decrease the effectiveness of spironolactone, concurrent use of the two agents should be avoided.
Spironolactone has been shown to increase the half-life of digoxin. This may result in increased serum digoxin levels and subsequent digitalis toxicity. It may be necessary to reduce the digoxin dose when spironolactone is administered, and the patient should be carefully monitored to avoid overdigitalisation or underdigitalisation.
Spironolactone may have an additive effect when given concomitantly with other diuretics and antihypertensive agents. The dose of such drugs may need to be reduced when spironolactone is added to the treatment regimen.
Aspirin, indomethacin and mefenamic acid have been shown to attenuate the diuretic effect of spironolactone.
Hyperkalaemic metabolic acidosis has been reported in patients given spironolactone concurrently with ammonium chloride or cholestyramine.
Effect on laboratory tests Spironolactone can interfere with assays for plasma digoxin concentrations.
Adverse Reactions Gynaecomastia may develop in association with the use of spironolactone, and doctors should be alert to its possible onset. The development of gynaecomastia appears to be related to both dosage level and duration of therapy and is normally reversible when Aldactone is discontinued. In rare instances some breast enlargement may persist.
Other adverse reactions that have been reported in association with Aldactone are gastrointestinal symptoms, including cramping, diarrhoea, nausea, vomiting, gastric bleeding, ulceration and gastritis; drowsiness, lethargy, headache, maculopapular or erythematous cutaneous eruptions, urticaria, mental confusion, drug fever, ataxia, inability to achieve or maintain erection, irregular menses or amenorrhoea, postmenopausal bleeding, malaise, benign breast neoplasm, breast pain, leucopenia (including agranulocytosis), thrombocytopenia, abnormal hepatic function, electrolyte disturbances, hyperkalaemia, leg cramps, dizziness, changes in libido, alopecia, hypertrichosis, pruritus, rash and acute renal failure.
Carcinoma of the breast has been reported in patients taking spironolactone, but a cause and effect relationship has not been established.
Dosage and Administration Adults. Essential hypertension. 50 to 100 mg/day which may be given either in divided doses or as a single daily dose.
Dosage should be adjusted according to response, but it should be noted that maximum effect of Aldactone therapy may not occur for up to two weeks after starting treatment.
Aldactone may potentiate the action of diuretics or other antihypertensive drugs, and their dosage should first be reduced by at least 50% when Aldactone is added to the regimen, and then adjusted as necessary.
Oedematous disorders. The daily dose may be given either in divided doses or as a single daily dose.
Congestive cardiac failure. The initial dose is 100 mg/day. In difficult or severe cases the dosage may be gradually increased up to 200 mg/day. When oedema is controlled, the usual maintenance level is 25 to 200 mg/day.
Cirrhosis. If the urinary sodium:potassium ratio is greater than one, the recommended dose is 100 mg/day. If the ratio is less than one, the recommended dose is 200 to 400 mg/day. Maintenance dosage should be individually determined.
Nephrotic syndrome. Usually 100 to 200 mg/day. Spironolactone is not anti-inflammatory and has not been shown to affect the basic pathological process; its use is only advised when treatment of the underlying disease, restriction of fluid and sodium intake, and the use of other diuretics do not provide an adequate response.
Diagnosis and treatment of primary aldosteronism. Aldactone may be employed as an initial diagnostic measure to provide presumptive evidence of primary hyperaldosteronism while patients are on normal diets.
Long test. Aldactone is administered at a daily dosage of 400 mg for three to four weeks. Correction of hypokalaemia and of hypertension provides presumptive evidence for the diagnosis of primary hyperaldosteronism.
Short test. Aldactone is administered at a daily dosage of 400 mg for four days. If serum potassium increases during administration but drops when Aldactone is discontinued, a presumptive diagnosis of primary hyperaldosteronism should be considered.
After the diagnosis of hyperaldosteronism has been established by more definitive testing procedures, Aldactone may be administered in doses of 100 to 400 mg daily in preparation for surgery. For patients who are considered unsuitable for surgery, Aldactone may be employed for long-term maintenance therapy at the lowest effective dosage determined for the individual patient.
Malignant hypertension. Aldactone should be used as adjunctive therapy only, where there is an excessive secretion of aldosterone, hypokalaemia and metabolic alkalosis. The initial dosage is 100 mg/day, increased as necessary at intervals of two weeks to 400 mg/day. Initial therapy should include a combination of other antihypertensive drugs and spironolactone. Do not automatically reduce the dose of other treatments as is recommended for essential hypertension.
Hypokalaemia. Aldactone may be useful in treating diuretic induced hypokalaemia when oral potassium supplements are considered inappropriate. In treating hypokalaemia, the lowest dose should be used and titrated upwards. A daily dose exceeding 100 mg is not recommended.
Female hirsutism. 100 to 200 mg daily in divided doses is usual, however 50 mg daily has also been shown to be effective.
Clinical improvement is usually shown within three to six months and an initial course of treatment should continue for 12 months.
Aldactone may be administered continuously or as a cyclical dosage for approximately three weeks out of every four. Dosing from day 5 to 21 of the menstrual cycle, with a drug free interval during menstruation, has been effective.
Cyclical dosing may reduce menstrual irregularities in women with previously regular cycles.
Combined use with oestrogen/ progestogen oral contraceptives may also be considered to provide both regular menstrual cycles and adequate contraception (see Precautions, Use in pregnancy).
Children. Oedema.The initial daily dosage should provide spironolactone approximately 3.3 mg/kg bodyweight. For small children, Aldactone tablets may be pulverised and administered as a suspension in cherry syrup. When refrigerated, such a suspension is stable for one month.
Overdosage The minimum toxic or lethal dose is not well established in the literature.
Overdosage may be manifested by nausea and vomiting, dizziness and (more rarely) by drowsiness, mental confusion, maculopapular or erythematous rash or diarrhoea. Electrolyte imbalances and dehydration may occur. Hyperkalaemia may be produced; symptoms include paraesthesia, weakness, flaccid paralysis and tetany. The earliest signs are characteristic electrocardiographic abnormalities including tall 'tent shaped' T waves, decreased amplitude of the P waves and widening of the QRS complex. Delayed onset of hyperkalaemia has been reported after acute ingestion of spironolactone (peak levels at 24 and 32 hours).
Symptomatic and supportive measures should be employed. There is no specific antidote. Support respiratory and cardiac functions. Treat fluid depletion, electrolyte imbalances and hypotension by established procedures.
Severity of intoxication should be based on clinical findings and serial determination of serum potassium levels. Monitoring plasma levels of spironolactone is not clinically useful.
Hyperkalaemia can be treated promptly by the rapid intravenous administration of glucose (20 to 50%) and regular insulin (0.25 to 0.5 units/g of glucose). Potassium excreting diuretics and ion exchange resins may also be administered, and repeated as required.
Aldactone should be discontinued and potassium intake (including dietary potassium) restricted.
Contact the Poisons Information Centre for advice on the management of an overdose.
Presentation Tablets (round, biconvex, buff coloured, peppermint flavoured, film coated, unmarked on one side), 25 mg (8.7 mm diameter, marked SEARLE over 39 on reverse), 100 mg (11.2 mm diameter, marked SEARLE over 134 on reverse): 100's.
Aldactone® has been around forever. I prescribed it as a potassium sparing diuretic for years, first stage for water retention and early congestive heart failure. It's side effect is to block DHEA, the operational component of testosterone, so it is ideal for use as an anti androgen. Because it blocks the excretion of K at the tubules, K levels can rise dramatically in some individuals, and cause serious cardiac side effects. Combined with Proscar® the two, block DHEA and DHT nicely.
Sorry if I am too detailed, but pharmaceutical inserts, have to cover everything, and side effects tend to war about seeing green chickens on the moon as well, or rather anything that tends to be reported.
After 1.75 yrs of spiro & estradiol, I have practically no body hair except pubes. My head hair does seem to have regrown very slightly in the front. However, I never had much body hair to start with, and very happy to see it gone!
It is not spiro, but the decrease of testosterone or rather DHT, the working hormone for hair loss, that decreases body hair over 1 - 2 years, in some, not all. Every time you think the hair has disappeared, it pop ups again. Actually it is the level of DHEA and DHT that has to drop significantly for these effects to occur. Some have taken progesterone as part of HRT, but part of progesterone is converted back to testosterone which tends to have masculinizing effects. Also the level of estrogen or rather the working hormone estradiol is what is important and should be up there at ovulatory levels.
DHT is the working product of testosterone responsible for male pattern baldness, thus blocking it with Proscar® can improve scalp hair, or at least prevent further loss.
I would be curious to know your serum levels of Estradiol and DHEA, but since you have just started I would expect your physician to soon be raising the dose.
ANd why is this blog not sorting from newest to oldest??