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Spironolactone and Claims About Increased Visceral Fat in Transfeminine People

By Aly | First published October 25, 2020 | Last modified December 18, 2025

A claim has been originated by some in the online transgender community that the antiandrogen spironolactone increases visceral fat in transfeminine people and that this effect is irreversible. Visceral fat is a type of adipose tissue located in the intra-abdominal region which surrounds the internal organs (viscera) in that area. In excess, visceral fat causes the abdomen to look bloated and unattractive. The supposed phenomenon of visceral fat accumulation with spironolactone has sometimes been referred to by people in the transgender community as “spiro belly”. The claim is based on theory—specifically that spironolactone has been found to increase levels of the corticosteroid hormone cortisol due to its antimineralocorticoid activity and cortisol is known to increase visceral fat, which together imply that spironolactone might likewise be able to increase visceral fat. It is also based on claimed anecdotal observations of transfeminine people taking spironolactone, which are said to corroborate the hypothesis. Despite these claims however, there is no actual direct scientific or medical literature to support the idea that spironolactone increases visceral fat, and there is considerable evidence contradicting it.

The influence of spironolactone on cortisol levels in clinical studies is variable and the magnitude of effect is limited. Hence, the clinical significance of increased cortisol levels with spironolactone is uncertain. Moreover, cortisol is an agonist of the glucocorticoid receptor (thereby producing glucocorticoid effects) and of the mineralocorticoid receptor (thereby producing mineralocorticoid effects). As already touched on, spironolactone has potent antimineralocorticoid activity (that is, mineralocorticoid receptor antagonism). Hence, even if spironolactone did increase cortisol levels enough to potentially increase visceral fat, its antimineralocorticoid activity could modify the capacity of cortisol to produce this effect. In relation to this, there is accumulating research to suggest that spironolactone may actually decrease visceral fat via its antimineralocorticoid activity. Antimineralocorticoids like spironolactone show antiadipogenic (anti-fat-accumulation) effects in vitro (Caprio et al., 2007; Caprio et al., 2011) and have been shown to decrease visceral fat in animals (Karakurt, 2008; Armani et al., 2014; Mammi et al., 2016; Olatunji et al., 2018). It is possible that they may also be able to do so in humans. Here are some notable literature excerpts relevant to this topic (Infante et al., 2019; Giordano, Frontini, & Cinti, 2016):

A possible explanation for [MR antagonists reducing cardiovascular morbidity and mortality more in patients with abdominal obesity] may be that patients with heart failure and abdominal obesity have higher aldosterone concentrations due to excessive secretion of specific aldosterone-releasing factors from [visceral adipose tissue]. […] Several studies on murine models of genetic and diet-induced obesity have widely reported beneficial effects of MR antagonism in terms of metabolic outcomes, such as body weight, fat mass, adipose tissue inflammation, insulin sensitivity, and lipid metabolism (Armani, Cinti, et al., 2014; Armani, Marzolla, et al., 2014; Garg & Adler, 2012; Guo et al., 2008; Hirata et al., 2009). Nevertheless, data on the outcomes of MR pharmacological blockade for prevention and treatment of obesity and metabolic syndrome are still scarce in humans (Tirosh et al., 2010). Of note, Tanko et al. demonstrated that the powerful MR antagonist drospirenone, in combination with estradiol, leads to a significant reduction of central fat mass and central fat mass/peripheral fat mass ratio in healthy post-menopausal women (Tankó & Christiansen, 2005). Moreover, another study has reported that MR antagonists significantly reduce body mass index and visceral fat area in patients with primary aldosteronism after a 1-year treatment period (Karashima et al., 2016). […] In light of these data, MR antagonism may be a useful therapeutic tool for prevention and treatment of cardiometabolic derangements observed in metabolic syndrome, even though additional studies are deemed necessary to confirm its impact on larger clinical settings.

An anti-obesity drug whose primary mode of action is to induce browning should act predominantly on visceral fat, thereby directly counteracting the major cause of obesity-associated metabolic disorders. Accumulation of abdominal visceral fat is, to some extent, linked to increased local levels and/or activity of androgen and glucocorticoid steroid hormones145,146. These hormones are also ligands of the mineralocorticoid receptors, which are found on white and brown adipocytes and could have a role in abdominal visceral fat accumulation and BAT to WAT conversion147–151.** […] **In this context, mineralocorticoid receptor antagonism has been shown to protect mice from the adverse obesogenic and metabolic effects of a high-fat diet via conversion of a substantial amount of visceral and subcutaneous WAT into BAT153. Given that mineralocorticoid receptor antagonists are widely prescribed diuretics, used to manage chronic heart failure, hyperaldosteronism and female hirsutism154, patients receiving such drugs should also be assessed for weight loss and metabolic parameters to establish whether these compounds have anti-obesity properties.

A number of studies have assessed the influence of antimineralocorticoids like spironolactone and eplerenone (another antimineralocorticoid) on visceral fat in humans. Spironolactone (12.5–100 mg/day) and eplerenone (25–100 mg/day) decreased visceral fat in people with pathologically high levels of aldosterone (a major endogenous mineralocorticoid hormone) (Karashima et al., 2016). A study of cisgender girls with polycystic ovary syndrome (PCOS) found that a combination of spironolactone (50 mg/day), pioglitazone, and metformin decreased visceral fat (Diaz et al., 2018). However, this study was of course confounded by the other medications. In addition to the preceding studies, many other clinical studies (at least 10) have assessed and similarly found no indication of increased visceral or abdominal fat with spironolactone (25–200 mg/day) (as measured by visceral fat directly or by indirect related measures like waist circumference or waist–hip ratio) (Wild et al., 1991; Lovejoy et al., 1996; Ganie et al., 2004; Meyer, McGrath, & Teede, 2007; Karakurt et al., 2008; Vieira et al., 2012; Ganie et al., 2013; Harmanci et al., 2013; Leelaphiwat et al., 2015; Alpañés et al., 2017). I was not able to identify any studies assessing visceral fat with higher doses of spironolactone (>200 mg/day). Additional studies are also underway to assess the possibility that spironolactone could decrease visceral fat.

With regard to the anecdotal claims of spironolactone increasing visceral fat in transfeminine people, it’s important to note that anecdotes are unreliable and are considered to be the lowest form of evidence in medicine. This is for well-founded reasons—succinctly, anecdotes very often don’t hold up when rigorous studies are conducted. It’s probable that excess abdominal fat—a problem which afflicts many—has been misattributed to spironolactone rather than to the real causes in transfeminine people. It’s notable in this regard that androgens are known to increase visceral fat and that men have twice as much visceral fat as women on average (Blouin, Boivin, & Tchernof, 2008; Zerradi et al., 2014). It’s possible that many transfeminine people may have excess visceral fat due to prior androgen exposure and that this visceral fat may not fully reverse with hormone therapy. As we know, hormone therapy unfortunately isn’t able to reverse all established bodily sexual dimorphism.

Besides increased visceral fat, many other serious adverse effects with spironolactone have been claimed. However, these claimed adverse effects are likewise based on anecdotes and theory, and there is a lack of direct clinical evidence to support such side effects. In actuality, spironolactone even at high doses appears to be well-tolerated per studies and systematic reviews. The claimed side effects of spironolactone may actually largely be due to phenomena like nocebo and misattribution—which can be controlled for in systematic studies but not in the case of anecdotal observations.

To summarize, no research, animal or clinical, has found increased visceral fat with spironolactone, and there is accumulating evidence that spironolactone may cause the very opposite effect. More studies are needed to further characterize this possible benefit of spironolactone in humans however.

Update: Talathi et al. (2025)

The following clinical study of hormone therapy in transfeminine people was published by Talathi and colleagues in December 2025:

  • Talathi, R., Juhasz, V., Delgado, M., Quinaglia, T., Ghamari, A., Wang, M., Alhallak, I., Stinebaugh, S., Campbell, S., Stockman, S. L., Ozturk, M. A., Ahmadi, S. M., Looby, S. E., Lee, H., Poteat, T. C., Szczepaniak, L. S., Zanni, M. V., Neilan, T. G., & Toribio, M. (2025). Visceral adipose tissue and liver fat on 17-beta estradiol-dominant gender-affirming hormone therapy: A US-based cohort. The Journal of Clinical Endocrinology and Metabolism, online ahead of print. [DOI:10.1210/clinem/dgaf665]

It was a 12-month prospective observational study of hormone therapy with estradiol and an antiandrogen in 26 transfeminine people in the United States. The primary aim of the study was to assess the effects of feminizing hormone therapy on visceral and liver fat in transfeminine people. The individuals in the study were either newly or very recently initiating hormone therapy. The antiandrogen used was spironolactone in 24 of 26 (92%) individuals. Of the 26 people, 14 (56%) were also on a progestogen, which was bioidentical progesterone in all but one case. The spironolactone dose used was median 100 mg/day (IQR 50 to 100 mg/day) at the start of the study and was median 125 mg/day (IQR 100 to 200 mg/day) at the end of the study. As the dosage spread statistic was interquartile range (IQR), a subset of people in the study appear to have been on spironolactone doses in excess of 200 mg/day. Estradiol levels were 188 pg/mL (690 pmol/L) and testosterone levels were 16 ng/dL (0.55 nmol/L) at the end of the study and were both within the normal and acceptable female range.

Visceral fat was assessed via dual-energy X-ray absorptiometry (DEXA) and liver fat was assessed via magnetic resonance spectroscopy (MRS). After 12 months, visceral adipose tissue mass non-significantly decreased from 308 g to 250 g (–18.8%; p = 0.25) and visceral adipose tissue volume non-significantly decreased from 332 cm3 to 271 cm3 (–18.4%; p = 0.25). In addition, intrahepatic triglyceride content (i.e., liver fat) decreased significantly from 0.9% to 0.8% (–11%; p = 0.03). In contrast to the case of visceral and liver fat, total body fat mass and percentage both significantly increased (+2.8 kg (+6.2 lbs) and +2.8%, respectively). Body weight, body mass index (BMI), waist circumference, and waist–hip ratio (WHR) all did not significantly or importantly change. Other metabolic parameters were also reported.

There are some limitations of this study, such as it not having control or comparison groups, the sample size being small, the median spironolactone dose being on the lower side of the clinical range used in transfeminine people, and the spironolactone dose being variable and increased over the course of the study rather than fixed. In any case, the results of this study do not support the notion that spironolactone increases visceral fat in transfeminine people. Instead, there is a clear trend for visceral fat decreasing with hormone therapy including spironolactone in transfeminine people. This was even though total body fat (i.e., subcutaneous and visceral together) showed the opposite pattern and increased, which is notably an expected effect in line with feminization of fat distribution that occurs in conjunction with decreased muscle mass. Moreover, it was the case even though about 25% of the people in the study on spironolactone were treated with doses of 200 mg/day or more. The observed trends towards decreased visceral fat are in line with other studies of hormone therapy in transfeminine people that did not employ spironolactone, in which visceral fat was significantly decreased, and suggest that spironolactone-containing regimens may not differ in this regard from other regimens. Based on the findings of this study, transfeminine people can feel reassured about claims that spironolactone causes visceral fat accumulation and may instead more plausibly expect the opposite with such regimens.

References

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