In the SS4% (high sea salt) group, dehydroepiandrosterone, 5α-androstane-3α,17β-diol, 6-dehydroestradiol, and 6α-hydroxyestradiol decreased by 119, 52, 23, 5, 4, 4, 4, 3, 3, and 2 times, respectively, whereas most other urinary steroid hormones increased two to seven times. However, a different study reported that high-salt (8%)-fed rats showed increased testosterone levels. Although further investigation into the correlation between steroid hormones and physiological changes upon salt intake is needed, these results pertaining to the steroid hormones strongly suggest that salt-related physiological changes may differ with gender because female hormones, such as estrogens, are significantly more affected by sea salt intake than the male hormones.

Unlike the alteration of female sex hormones, testosterone, the primary sex hormone in males, was not altered by sea salt intake, except for minor changes in the levels of dihydrotestosterone and 17α-methyltestosterone. However, a different study reported that high-salt (8%)-fed rats showed increased testosterone levels. Although further investigation into the correlation between steroid hormones and physiological changes upon salt intake is needed, these results pertaining to the steroid hormones strongly suggest that salt-related physiological changes may differ with gender because female hormones, such as estrogens, are significantly more affected by sea salt intake than the male hormones.

One hundred and four postmenopausal women selected from 312 healthy volunteers on the basis of high serum testosterone levels were randomized to dietary intervention or control. The intervention included intensive dietary counseling and specially prepared group meals twice a week over 4.5 months. In the intervention group, sex hormone-binding globulin increased significantly (from 36.0 to 45.1 nmol/liter) compared with the control group (25% versus 4%; P < 0.0001) and serum testosterone decreased (from 0.41 to 0.33 ng/ml; −20% versus −7% in control group; P = 0.0038). A radical modification in diet designed to reduce insulin resistance and also involving increased phytoestrogen intake decreases the bioavailability of serum sex hormones in hyperandrogenic postmenopausal women.

Findings suggested that dietary sodium intake may be a critical modifying factor in the level of plasma insulin. However, it showed a limited effect on obesity and other inflammation markers and hormone levels. Among the examined variables using multivariate linear regression analyses, plasma insulin was the sole marker associated with sodium intake; plasma insulin was higher with higher sodium intake, and this association was independent of other dietary intake and overweight.

Another important finding from this study is that dietary sodium intake significantly affects sex differences in aldosterone concentrations. Interestingly, men had higher aldosterone concentrations than women under conditions of high sodium intake but not low sodium intake, whereas sex differences in blood pressure, extracellular volume, and adrenal response to angiotensin II persisted under both low and high sodium dietary intakes.

High sodium diet was associated with increased urinary cortisol and its metabolites. Also, high salt diet was associated with hypertension, insulin resistance, dyslipidaemia and hypoadiponectinaemia, even when adjusting by confounding variables. Further, we observed that high salt intake, insulin resistance and higher cortisol metabolites, alone or combined in a clinical simple model, accurately predicted metabolic syndrome status, suggesting an additive mechanism in obesity-related metabolic disorders.

This Korean Q&A on "the relationship between sodium intake and sex hormones" states: "There is a lack of definitive research results on the relationship between sodium intake and sex hormones. Clear evidence has not yet been found as to whether sodium intake has a direct and significant effect on sex hormone levels." It goes on to emphasize that excessive sodium causes cardiovascular problems, but does not identify increased androgen levels as an established effect.

Emerging novel evidence indicates that aldosterone production is sex-specifically heightened in salt-sensitive hypertensive women and female rodent models, which may be regulated by intra-adrenal renin-angiotensin system activation and sex hormone receptors. … Emerging clinical and experimental data indicate that dietary salt intake governs aldosterone production in a sex-specific manner favoring higher production in women, which may be a token mechanism contributing to the higher prevalence of salt-sensitive hypertension in women. … Recent emerging data provides evidence for a 2-pronged novel hypothesis that may explain the higher prevalence of salt sensitivity in women: females are more likely to maintain, or increase, aldosterone production in response to increased dietary sodium which leads to endothelial dysfunction, and consequently hypertension, via activation of endothelial MR expression.

In conclusion, we observed that high sodium intake is associated with increased urinary cortisol metabolites, insulin resistance, dyslipidaemia and lower adiponectin levels. Subjects with high, compared with adequate sodium intake (50–149 mEq/day) had higher urinary free cortisol, tetrahydrometabolites, HOMA-IR, and prevalence of hypertension. High sodium intake was associated with increased glucocorticoid production even when adjusting by confounding variables.

Salt-sensitive women, emerging clinical and experimental evidence indicates that females do not suppress the renin–angiotensin–aldosterone system as efficiently as males, thereby resulting in a sex-specific balance favoring higher RAAS activation despite high sodium intake. Combined, these data show that salt-sensitive premenopausal females have higher aldosterone sensitivity than males and are therefore more likely to have higher activation of endothelial mineralocorticoid receptors leading to vascular dysfunction and giving rise to salt sensitivity of blood pressure. This review discusses sex differences in salt sensitivity of blood pressure but does not report that excess dietary salt increases androgen levels in women.

High salt intake activates the hypothalamic–pituitary–adrenal (HPA) axis, but the consequences are poorly understood. We find evidence of accumulated glucocorticoid excess with sustained high salt intake in male C57BL/6 mice. Given that human salt intake is habitually high, our results are relevant to human health. HPA axis induction by high salt intake may serve a critical role in preserving fluid balance but the long-term consequences of this are likely detrimental: glucocorticoid excess typically promotes sodium retention and salt-sensitive blood pressure abnormalities. HPA activation may also contribute to poor metabolic and cognitive health when salt intake is high.

These results suggest that female sex confers a greater ability to maintain Na+ homeostasis during acclimation to dietary Na+ challenges and indicate that the intrarenal endothelin‐1 natriuretic pathway is enhanced in women. Of note, women excreted significantly more endothelin‐1 than men. We postulate that sex steroids, possibly ovarian hormones, facilitate high‐salt‐induced natriuresis; however, this study did not measure or report changes in androgen levels in women in response to high salt intake.

Overall, research has revealed mixed results regarding the impact of dietary sodium intake on various hormones. Although several studies have demonstrated that high sodium intake elevates aldosterone levels, others have found that aldosterone decreases in response to increased sodium intake. Furthermore, high sodium intake has been associated with increased cortisol levels and alterations in sex hormones in some studies, but not in others, indicating that the hormonal response to sodium intake is complex and may depend on individual factors such as sex, age, and health status.

Reduction in the free androgen index (FAI) in overweight women was achieved through an intervention based on a low-glycemic index diet with anti-inflammatory elements and slight energy deficit. The intervention decreased total testosterone levels, increased sex hormone-binding globulin levels, and decreased FAI. Dietary sodium intake was not manipulated in this trial, and the study focuses on other dietary factors affecting androgens in women.

This Korean-language medical education article on sodium explains multiple adverse effects of high sodium intake (cardiovascular disease risk, kidney damage, increased proteinuria, renal artery sclerosis, kidney stones). It does not mention any effect of salt or sodium intake on sex hormones or androgen levels in women, suggesting that such a link is not part of standard clinical teaching about sodium-related risks.

Testosterone supplementation increased renal sodium reabsorption and blood pressure and worsened renal pathology in female spontaneously hypertensive rats on a high sodium diet. In conclusion, testosterone accelerated the development of hypertension similar to the blood pressure pattern observed in males; the presence of ovaries attenuated the testosterone-induced increase in blood pressure. This study examines how androgens affect sodium handling and blood pressure in females on a high-salt diet, rather than whether salt intake increases androgen levels.

Altogether, our results demonstrate that endogenous as well as exogenous female sex hormones strongly affect the renal hemodynamic response to salt in young normotensive women, although these hormones do not affect the blood pressure response to sodium. The study focuses on how estradiol and progesterone modulate renal responses to salt loading; it does not report that salt intake increases androgen hormone levels in women.

In patients with primary aldosteronism placed on a low sodium diet, sex-dependent modulation of T and NK cells and gut microbiome was observed. We additionally observed inverse correlations of Bacteroides uniformis abundance and testosterone (r = -0.2702, p = 0.0088), dihydrotestosterone (r = -0.2295, p = 0.0269) and 17-hydroxyprogesterone (r = -0.2699, p = 0.0089). This study assesses immunologic and microbiome changes under low sodium intake and correlates them with sex hormones but does not claim that excess dietary salt increases androgen levels in women.

There were no significant associations between sex hormone gene variants and salt sensitivity in women, with genotype–gender interactions noted for the ESR1 markers that achieved significance in men. The minor alleles of ESR1 rs9397453 and rs9383951, plus additional markers rs9340844, rs9371562, and rs9397459, were shown to significantly decrease blood pressure responses to sodium in men but not women. This genetic analysis links estrogen receptor polymorphisms to salt sensitivity but does not show that salt intake alters androgen levels in women.

This review focuses on the involvement of genetic, hormonal, and epigenetic factors in the relationship between sodium intake, sodium excretion, and cardiovascular risk. Hormonal factors discussed include the renin-angiotensin-aldosterone system, natriuretic peptides, and sex hormones, which can modulate the effects of sodium on blood pressure and cardiovascular outcomes. Evidence suggests that sex hormones and their receptors may interact with sodium handling and blood pressure regulation, contributing to sex differences in cardiovascular risk associated with sodium intake, although direct effects on androgen levels in women are not clearly defined.

This page on hyperandrogenism from Apollo Hospitals notes: "Lifestyle choices and eating habits can affect hormone levels. For example, obesity is a significant risk factor for hyperandrogenism, especially in women. Excess body fat can increase estrogen production, which may raise androgen levels. Diets high in refined carbohydrates and sugars can cause insulin resistance, worsening hormone imbalance." The discussion focuses on obesity and high-sugar/refined carbohydrate diets, not salt or sodium intake, as contributors to elevated androgen levels.

The Thai-language version of Apollo Hospitals’ hyperandrogenism article similarly states (translated): "Lifestyle choices and eating habits can affect hormone levels. For example, obesity is an important risk factor for high androgen levels, especially in women. Excess body fat may lead to increased estrogen production, which can raise androgen levels. Eating a diet high in refined carbohydrates and sugar can lead to insulin resistance, resulting in more severe hormone imbalance." No mention is made of dietary salt or sodium as a factor in increasing androgen levels.

High salt intake alters the expression of COX-2 in endothelial renal cells, leading to reduced production of prostaglandins such as PGE2 and PGI2, which are critical for vasodilation. Some groups, such as Black people and postmenopausal women, are at high risk. The increased ADMA, an endogenous inhibitor of eNOS, enhances the reduction in NO bioavailability, thus compromising vasodilation and the ability of the vessels to regulate blood pressure in response to high salt intake. In premenopausal women, estrogen has a protective role through the enhancement of NO production as well as the suppression of angiotensin II in the renin–angiotensin–aldosterone system, but this review focuses on vascular and metabolic effects rather than changes in androgen hormone levels.

This study showed no change in the serum testosterone in salt-loaded male rats compared with control. In summary, dietary salt loading while precipitating hypertension also activated increased production of white blood cells and CD4 cells without any change in the serum testosterone level. The experiment was conducted in male rats, not women, but it provides animal evidence that high dietary salt does not necessarily increase circulating testosterone.

This Korean medical information page on hyperandrogenism in women advises lifestyle and diet changes but focuses on glycemic load rather than salt: "Eat a balanced, healthy diet and do not excessively consume high glycemic index carbohydrates." It links hyperandrogenism with conditions like polycystic ovary syndrome, insulin resistance, and obesity, but does not describe excess salt intake as a known cause of increased androgen levels.

These findings suggest a biological relationship between salt intake and benign prostatic hyperplasia (BPH) development. Dietary salt worsened the pathology of testosterone-induced BPH but not in a dose-dependent pattern. This study demonstrated that rat diets containing low, standard and high quantity of dietary salt promoted inflammation/oxidative stress, and also inhibited apoptosis and angiogenesis in prostatic tissues. However, the rats were given exogenous testosterone; the study does not show that salt intake itself increases endogenous testosterone production.

Spearmint tea – 2 cups per day has been researched to reduce total and free testosterone levels in those with polycystic ovary syndrome (PCOS), and within 30 days the participants found a significant reduction in hair growth. Improving blood glucose levels and insulin resistance management, omega-3 intake, nuts (especially walnuts to boost SHBG), and vitamin D are suggested as strategies to lower androgens in women with PCOS. The article does not mention dietary sodium or salt intake as a factor increasing androgen levels in women.

Behavior change interventions resulted in significant improvements in salt consumption behavior, leading to reductions in sodium intake as measured by urinary sodium in 32 trials and dietary sodium in 19 trials, equivalent to a reduction of more than 1 g of salt intake daily. The systematic review and meta-analysis focus on blood pressure and cardiovascular outcomes; sex hormone changes, including androgens, were not assessed as outcomes of salt reduction.

This Korean article on high androgen levels in women ("고안드로겐 치료제") stresses overall lifestyle: "Meals should be taken according to caloric needs, and exercise therapy, lifestyle correction, and drug treatment should be combined." It discusses hyperandrogenism related to PCOS and metabolic syndrome but does not implicate salt or sodium intake specifically as a factor that raises androgen hormone levels.

This Korean blog post on foods promoting polycystic ovary syndrome explains a mechanism linking certain diets to increased androgens: "When these high-calorie foods suddenly enter the body, the sensitivity of GLP-1 hormone receptors decreases and false appetite appears, leading to carbohydrate addiction. Repeated blood sugar spikes cause the pancreas to secrete much more insulin than usual, and male hormone androgen is excessively synthesized." It specifically identifies high-sugar and refined carbohydrate foods, not salt, as dietary drivers of increased androgen levels and menstrual disruption.

Vitamin D supplementation has been shown to lower total testosterone in women with PCOS. Strength training significantly changes body composition, which lowers high levels of androgens in females. Spearmint tea twice a day for 30 days has been shown to have anti-androgen effects in PCOS; no discussion is made of increased androgen levels due to high salt or sodium intake in women.

This Korean Q&A on excess steroid/androgen hormones in women describes clinical manifestations of high androgen levels: "When steroid hormones are excessively secreted in women, various symptoms may appear. This condition is called hyperandrogenism. Major symptoms include increased acne, weight gain and abdominal obesity, facial flushing or swelling, increased muscle mass, menstrual irregularities or amenorrhea, hirsutism, deepening of the voice, and hair loss." The article outlines symptoms and related conditions like PCOS but does not mention dietary salt or sodium intake as a cause of elevated androgens.

Androgens are often thought of as "male" hormones, but women also produce androgens, primarily testosterone, androstenedione, and dehydroepiandrosterone (DHEA). Excess androgen levels in women can lead to symptoms such as hirsutism, acne, and irregular periods, and are commonly associated with conditions like polycystic ovary syndrome (PCOS). Lifestyle factors including weight, diet quality, and insulin resistance are known to influence androgen levels, but high sodium intake is not listed among established direct causes of androgen excess in women in this general health resource.

This Korean health news article on hormone imbalance in women notes that during menopause: "Estrogen and progesterone both decrease. This can induce an increase in androgens." It explains that relative androgen excess in menopausal women is primarily driven by changes in ovarian hormone production and balance, not by dietary salt or sodium intake.

This YouTube lecture on diet for polycystic ovary syndrome emphasizes sugar, refined carbohydrates, and trans fats as dietary factors that worsen insulin resistance and estrogen excess: "Sugar, refined carbohydrates, trans fats, and foods with many environmental hormones cause insulin resistance and estrogen excess and therefore should be avoided." It lists high-sugar drinks, desserts, and refined carbs as foods that rapidly raise blood glucose and worsen PCOS-related hormone issues, but does not associate dietary salt with increased androgen levels.

Existing human and animal studies on dietary sodium more consistently report effects on blood pressure, aldosterone, insulin, and glucocorticoid production rather than direct increases in androgen hormone levels in women. Some rodent studies have observed increased testosterone with very high salt diets, but these findings are not clearly demonstrated in women, and at least one rat study found no change in testosterone with high sea salt intake while estrogens were reduced. Overall, high salt intake is linked to sex-specific hormonal changes, especially in estrogens and aldosterone, but robust evidence that excess dietary salt increases androgen levels in women is lacking.

Excess androgen levels are a hallmark of polycystic ovary syndrome (PCOS) and can cause irregular menstrual cycles, acne, and unwanted hair growth. Dietary strategies to lower androgens in women with PCOS focus on improving insulin sensitivity and reducing inflammation, such as low-glycemic diets and weight loss; specific recommendations on restricting salt are generally related to blood pressure and cardiovascular risk rather than directly to androgen hormone levels. This clinical overview describes multiple modifiable factors affecting androgens but does not identify excess dietary salt as a known driver of androgen increase in women.

This Korean news feature on salty foods and women’s health explains: "Dr. Chantmel advises, 'After menopause, women have higher salt sensitivity, so it is wise to pay a little more attention to salt intake.'" The article frames salt mainly as a cardiovascular and blood pressure risk that is greater for women after menopause; it does not mention any evidence that salt intake increases androgen hormone levels in women.

This Korean nutrition/health article lists diseases caused by excessive salt intake, such as hypertension, stroke, heart disease, kidney disease, osteoporosis, and stomach cancer, and then offers practical tips: "Do not pick up the salt shaker. Change a tongue accustomed to salty taste to sour or spices. Help sodium excretion by eating vegetables and fruits. Even when eating out, check sodium content and ask for ‘less salty’. Eat natural foods rather than processed foods." No mention is made of any effect of salt intake on androgen hormone levels in women.