Medications and Candida

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    I’m a transgender woman and I believe I acquired candida last summer after starting estrogen therapy (though there were two catalysts, I believe, as my symptoms really became apparent after an intense round of antibiotics a month and a half later).

    However, my question is not in regards to either of those medications. I’m not currently taking estrogen, as I want to beat this candida. But I have been taking a low dose of the other med trans girls usually take, spironolactone–a potassium sparing diuretic which also acts as an androgen blocker.

    Does anyone know if the spironolactone could be hindering my candida fight?

    I’m also currently taking Topamax (for migraines) and I’m wondering if this could effect the candida (though because it doesn’t effect hormones, I’m less concerned about this one).




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    Hey Sasha!

    I am also transgender (FTM) and have wondered if going on testosterone did bad things for my candida :p I haven’t stopped it during my treatment, however, and I am getting better, slowly but surely (today is day 75 and I think I’m on track…still having some issues, but much improved from 75 days ago, where I was pretty sure I was either going to die from this directly or through killing myself because I couldn’t take it another day).

    I’m not a doctor or anything, so I don’t know how those meds would affect the candida…I just wanted to say hi, mostly. Hi 🙂


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    Hi alexalgebra. I’m so sorry. I didn’t mean to be rude. Hi! I’m glad you’re situation is getting better.


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    I thought I’d try this again. This is what daily med has to say about spirolactone. Can anyone tell me if this would feed my candida problem somehow?

    From dailymed:

    spironolactone (Spironolactone) tablet, film coated
    [Mylan Pharmaceuticals Inc.]
    Rx only


    Spironolactone has been shown to be a tumorigen in chronic toxicity studies in rats (see PRECAUTIONS). Spironolactone should be used only in those conditions described under INDICATIONS AND USAGE. Unnecessary use of this drug should be avoided.


    Spironolactone oral tablets contain 25 mg, 50 mg or 100 mg of the aldosterone antagonist spironolactone, 17-hydroxy-7α-mercapto-3-oxo-17α-pregn-4-ene-21-carboxylic acid γ-lactone acetate, which has the following structural formula, molecular formula, and molecular weight:


    Spironolactone is practically insoluble in water, soluble in alcohol, and freely soluble in benzene and in chloroform.

    Each tablet for oral administration contains 25 mg, 50 mg or 100 mg of spironolactone and the following inactive ingredients: calcium sulfate dihydrate, colloidal silicon dioxide, croscarmellose sodium, crospovidone, hypromellose, lactose monohydrate, magnesium stearate, peppermint flavor, polydextrose, polyethethylene glycol, povidone, pregelatinized (corn) starch, sodium lauryl sulfate, titanium dioxide and triacetin.


    Mechanism of Action

    Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule.

    Aldosterone Antagonist Activity

    Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Edematous states in which secondary aldosteronism is usually involved include congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. By competing with aldosterone for receptor sites, spironolactone provides effective therapy for the edema and ascites in those conditions. Spironolactone counteracts secondary aldosteronism induced by the volume depletion and associated sodium loss caused by active diuretic therapy.

    Spironolactone 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 antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

    Spironolactone has not been demonstrated to elevate serum uric acid, to precipitate gout, or to alter carbohydrate metabolism.


    Spironolactone is rapidly and extensively metabolized. Sulfur-containing products are the predominant metabolites and are thought to be primarily responsible, together with spironolactone, for the therapeutic effects of the drug. The following pharmacokinetic data were obtained from 12 healthy volunteers following the administration of 100 mg of spironolactone (as tablets) daily for 15 days. On the 15th day, spironolactone was given immediately after a low-fat breakfast and blood was drawn thereafter.

    Accumulation Factor:
    AUC (0–24 hr, day 15)/AUC (0–24 hr, day 1) Mean Peak Serum Concentration Mean (SD) Post-Steady State Half-Life
    7-α-(thiomethyl) spirolactone (TMS) 1.25 391 ng/mL at 3.2 hr 13.8 hr (6.4) (terminal)
    6-β-hydroxy-7-α-(thiomethyl) spirolactone (HTMS) 1.50 125 ng/mL at 5.1 hr 15.0 hr (4.0) (terminal)
    Canrenone (C)
    1.41 181 ng/mL at 4.3 hr 16.5 hr (6.3) (terminal)
    Spironolactone 1.30 80 ng/mL at 2.6 hr Approximately 1.4 hr (0.5) (β half-life)
    The pharmacological activity of spironolactone metabolites in man is not known. However, in the adrenalectomized rat the antimineralocorticoid activities of the metabolites C, TMS, and HTMS relative to spironolactone, were 1.1, 1.28, and 0.32, respectively. Relative to spironolactone, their binding affinities to the aldosterone receptors in rat kidney slices were 0.19, 0.86, and 0.06, respectively.

    In humans the potencies of TMS and 7-α-thiospirolactone in reversing the effects of the synthetic mineralocorticoid, fludrocortisone, on urinary electrolyte composition were 0.33 and 0.26, respectively, relative to spironolactone. However, since the serum concentrations of these steroids were not determined, their incomplete absorption and/or first-pass metabolism could not be ruled out as a reason for their reduced in vivo activities.

    Spironolactone and its metabolites are more than 90% bound to plasma proteins. The metabolites are excreted primarily in the urine and secondarily in bile.

    The effect of food on spironolactone absorption (two 100 mg spironolactone tablets) was assessed in a single dose study of 9 healthy, drug-free volunteers. Food increased the bioavailability of unmetabolized spironolactone by almost 100%. The clinical importance of this finding is not known.

    Name (Active Moiety) Type Strength
    Spironolactone (Spironolactone) Active 50 MILLIGRAM In 1 TABLET
    calcium sulfate dihydrate Inactive
    colloidal silicon dioxide Inactive
    croscarmellose sodium Inactive
    crospovidone Inactive
    hypromellose Inactive
    lactose monohydrate Inactive
    magnesium stearate Inactive
    peppermint flavor Inactive
    polydextrose Inactive
    polyethethylene glycol Inactive
    povidone Inactive
    pregelatinized (corn) starch Inactive
    sodium lauryl sulfate Inactive
    titanium dioxide Inactive
    triacetin Inactive

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