In women, fructose intake from sugar-sweetened beverages was inversely associated with SHBG and positively associated with free testosterone levels. Women consuming at least 10 g/day had a higher risk of biochemical hyperandrogenism (odds ratio 1.018; 95% CI 1.010 to 1.026). The authors also reported that total fructose intake was associated with lower total and free testosterone in women, so the direction of effect depended on the sugar source.

In response to hyperinsulinemia ovarian theca cells which normally support growing follicles and the generation of mature oocytes become hyper-responsive to excess insulin, causing them to proliferate and subsequently increase further androgen secretion.[19] Hyperinsulinemia further aggravates PCOS by ... reducing the production of sex-hormone-binding globulin (SHBG), thereby leading to increased free testosterone levels, further exacerbating symptoms of hyperandrogenism.[20]

Postprandial glucose, fasting insulin and insulin resistance were elevated in women with PCOS.[5] Elevated insulin level and HOMA-IR in women with PCOS who had higher BMI values in the present study could contribute to the increases in serum testosterone and FAI. Therefore, it is reasonable to suspect that increased BMI in women with PCOS impairs insulin sensitivity which can further influence hyperandrogenism.

Insulin resistance is another common finding in PCOS, that is thought to promote hyperandrogenism through compensatory hyperinsulinemia.[7,28] Glucose ingestion stimulated atherothrombotic inflammation in women with PCOS and was associated with higher insulin and inflammatory markers compared with controls, supporting a link between glucose intake, hyperinsulinemia and PCOS-related endocrine and vascular abnormalities.

As previously discussed, PCOS is also characterized by insulin-related hyperandrogenemia, which implies an important role of insulin in the regulation of ovarian androgen biosynthesis.[41,90,91] These results suggest that even in non-obese normoinsulinemic PCOS women, hyperandrogenemia is related to insulin action and might result from increased insulin action on androgen biosynthesis.[49]

Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, according to a study in mice and human liver cell cultures. The mechanism described was reduced SHBG production, which would increase the fraction of free sex steroids in circulation.

It is commonly established that the participation of IR and hyperinsulinemia in the development of PCOS is crucial for molecular mechanisms underpinning the endocrine hypersecretion feature of PCOS.[35] Insulin resistance/hyperinsulinemia in women with PCOS encourages androgen synthesis directly in ovarian and ductless glands, increasing follicular maturation and leading to anovulatory infertility. The decrease in the level of fasting insulin recorded by PCOS-treated women with insulin-sensitizing medicine appears to decrease androgenemia while increasing ovarian functionality.[36]

High carbohydrate intake and low-grade inflammation cooperate with insulin resistance and hyperandrogenism to constitute an interactive continuum acting on the pathophysiology of polycystic ovary syndrome (PCOS). In vitro, insulin increases androgen production, while in vivo circulating and molecular markers of oxidative stress and inflammation are highly correlated with circulating androgens.[76] Studies by Dunaif & Graf demonstrated that circulating androgens are influenced by insulin levels independent of variations of gonadotropin release, but only in PCOS women.[77]

This controlled observational study of healthy, eumenorrheic women concludes that "dietary carbohydrate and diet quality do not appear to relate to these subclinical endocrine characteristics in women without overt PCOS." The authors state that "no associations were identified between dietary carbohydrate intake, with the exception of dietary fiber, and occurrences of a mild PCOS-like phenotype, defined here as having relatively elevated testosterone and AMH combined," and that their data "does not support a relationship between dietary patterns in healthy women with subclinical manifestations of an aberrant insulin, AMH, and testosterone milieu."

The study used a mouse model and human liver cell cultures and found that increased lipid production shut down SHBG, reducing SHBG protein in blood. Because SHBG binds sex hormones, lower SHBG can increase free testosterone and estrogen activity.

Direct insulin infusion measurably increases androgen production by binding to insulin or insulin-like growth factor-1 receptors in the ovary.[15] The response to insulin was graded; higher levels of insulin infusion yielded higher levels of androgen production.[15] Insulin directly inhibits liver production of SHBG, and therefore increases the levels of free and bioavailable androgens.[18] Thus, excessive insulin causes both the overproduction of testosterone and decreased SHBG levels, both of which collaborate in creating an increased testosterone effect.

Chronic combined hyperandrogenemia and western-style diet (WSD) in young female rhesus macaques causes greater metabolic impairments compared to either treatment alone. Log transformed fasting insulin and HOMA-IR were significantly increased in T + WSD animals at 3 years of treatment compared to all other groups. This preclinical model suggests that chronic hyperandrogenemia beginning at puberty may exacerbate metabolic dysfunction in females consuming a WSD, but it does not show that the diet alone increases androgens.

This review on insulin and androgen excess notes that in severe insulin resistance syndromes "hyperinsulinemia promotes ovarian androgen synthesis independently of gonadotropins." It explains that "abnormally increased insulin levels cross-react with insulin and IGF receptors on the ovary, leading to androgen overproduction." The authors also state that insulin "inhibits hepatic synthesis of SHBG, which leads to increased amounts of unbound, biologically active" testosterone, describing a mechanistic link between high insulin (often driven by excess sugar intake) and higher ovarian androgen production in women with insulin resistance or PCOS-like conditions.

Glucose ingestion caused significantly more hyperinsulinemia than did protein, and it stimulated cortisol and DHEA. These findings provide mechanistic support for increasing protein intake and restricting the simple sugar intake in a PCOS diet, as simple sugars acutely increase insulin and adrenal androgen (DHEA) responses compared with protein.

Another effect of insulin is to decrease sex hormone binding globulin (SHBG) synthesis in the liver, resulting in elevated levels of free androgens.[17] Investigations of metabolic abnormalities in patients with PCOS revealed significantly higher plasma insulin levels two hours after glucose was given to women in the lean subgroup compared with lean controls, supporting the concept of insulin-related hyperandrogenemia even in lean PCOS.[Lean PCOS review]

Results: The intervention based on a low-glycemic index diet with anti-inflammatory elements and slight energy deficit decreased total testosterone levels (p < 0.003), increased SHBG levels (p < 0.001), and decreased the free androgen index (FAI; p < 0.001) in women with polycystic ovary syndrome. The authors conclude that dietary modification with lower glycemic index can improve menstrual and fertility-related outcomes by reducing androgen levels and FAI. This clinical trial indicates that lowering glycemic load is associated with decreased androgens, but does not directly test high sugar intake increasing androgens.

Approximately 70% of women with PCOS are phenotypically insulin-resistant.[28] The HSCA diet caused insulin resistance and high testosterone levels, which contribute to the development of PCOS, and affected folliculogenesis by altering follicular maturation. Our findings showed that HSCA promoted insulin resistance, increased testosterone levels, and reduced Enterobacteriaceae colonies. Increased insulin resistance as well as a high level of testosterone were observed in HSCA rats and may be associated with excessive sucrose and cholic acid ingestion.[14,28]

This study evaluated dietary carbohydrate intake and hormone levels in healthy, regularly menstruating women. The authors reported that dietary carbohydrate and overall diet quality did not appear to relate to androgen-related endocrine characteristics in women without overt PCOS.

Thus, although dietary interventions have been reported to have an impact in managing PCOS in some studies, dietary intake in women without PCOS was not associated with PCOS-related hormones including testosterone, AMH, and insulin. There was no association identified here between any dietary carbohydrate factors typically associated with promotion of insulin resistance and hormone concentrations in the highest quartile levels of both testosterone and AMH combined. Therefore, despite previous evidence in PCOS, dietary carbohydrate and diet quality did not relate to subclinical elevations of androgens in healthy, nonobese women.

We showed that metformin proved to be effective in reducing total testosterone levels, and the same was observed for free androgen index (FAI) values. Metformin’s insulin-lowering effect is one mechanism proposed for its influence on androgen levels in women with PCOS. This supports the concept that reducing insulin, which is stimulated by high carbohydrate/sugar intake, can decrease hyperandrogenism, although the study does not directly manipulate sugar intake.

Hyperinsulinemia inhibits hepatic SHBG secretion, which increases free testosterone in circulation. Insulin and luteinizing hormone can also stimulate androgen production in ovarian theca cells, providing a biologic pathway by which insulin resistance related to diet could raise androgen activity.

Emerging evidence suggests that diets high in sugar consumption may be implicated in the development of polycystic ovary syndrome (PCOS), but the causal nature of these associations remains unclear. Experimental and epidemiologic data indicate that diets rich in added sugars promote hyperinsulinemia, visceral adiposity, and impaired glucose tolerance, all of which are established contributors to reproductive and metabolic disturbances in women of reproductive age.

According to the "gut microbiota" theory put forth by Tremellen et al., a high sugar and fat diet-induced imbalance in the gut bacterial flora causes hyperandrogenism by increasing gut mucosal permeability, which allows for the passage of lipopolysaccharide (LPS). This generates an immunological response that disrupts the operation of insulin receptors and causes insulin resistance; elevated circulating insulin promotes increased androgen synthesis in ovarian theca cells and disruption of follicle development. The review notes that these dietary patterns may worsen PCOS symptoms including hyperandrogenism, insulin resistance, and menstrual irregularities.

This lay summary describes the Chen et al. European Journal of Endocrinology study, stating that "fructose in the form of added sugar may have adverse effects on lipid metabolism in the liver and impair the production of a protein called sex hormone-binding globulin (SHBG), which causes an increase in the free testosterone levels in the body." It notes that the study "reported that fructose intake from sugar-sweetened beverages (SSBs) is associated with elevated androgen levels and increases the risk of hyperandrogenism in women," highlighting that added-sugar beverages specifically were linked to higher free testosterone in women in the cohort.

In women with overweight, a low-glycemic-index intervention with anti-inflammatory elements decreased total testosterone, increased SHBG, and decreased the free androgen index. This is relevant because it shows that lowering glycemic load and improving diet quality can move androgen markers in the opposite direction.

This article explains that "high levels of insulin can affect the normal workings of a women’s ovaries, resulting in the production of the hormone testosterone." It states that "whilst excess sugar in the diet can raise testosterone levels in women, contradictorily it may lower testosterone levels in men," and links high sugar intake to insulin spikes and consequent ovarian testosterone production as a contributor to symptoms like acne and menstrual irregularities, reflecting clinical observations rather than controlled trial data.

The paper found that high-fat, high-sugar diet exposure in rodents altered basal testosterone levels and induced cystic ovaries. It does not directly establish the same effect in women, but it is experimental evidence that a high-sugar diet can affect ovarian and androgen-related physiology in animals.

In multiple meta-analyses, medications that reduce insulin levels or improve insulin action (metformin, troglitazone and rosiglitazone) were no more effective than placebo in treating hyperandrogenism in PCOS. Therefore, metformin should be reserved for the treatment of prediabetes or type 2 diabetes in women with PCOS, as it is not as effective as other medications for cosmetic concerns or for uterine protection in the case of irregular menses. This review underscores that although insulin and diet are mechanistically linked to androgen production, evidence that insulin-lowering alone effectively treats hyperandrogenism is mixed.

This longitudinal study on hyperandrogenemia and glucose metabolism notes that "insulin acts synergistically with LH, increasing testosterone (T) production from ovarian theca cells and inhibiting hepatic synthesis of SHBG, which leads to increased amounts of unbound, biologically active T." Although the study focuses on the metabolic consequences of hyperandrogenemia, it reinforces the mechanistic pathway whereby elevated insulin—often driven by high sugar intake and insulin resistance—can increase circulating free androgen levels in women.

In healthy women without overt PCOS, this study found no association between dietary carbohydrate intake and androgen-related hormone concentrations. This is relevant counterevidence because it suggests that higher carbohydrate intake alone was not linked to higher androgens in that population.

In rats, early exposure to a high-sucrose diet caused ovarian dysfunction. The authors note that possible mechanisms include hyperinsulinemia leading to higher ovarian androgen production, but they also state that the relationship to women remains inferential.

The study showed statistically significant differences in the hormonal levels of dehydroepiandrosterone (P = 0.045), luteinizing hormone (P = 0.017) and follicle-stimulating hormone (P = 0.014) when comparing the carbohydrate-reduced diet associated with lifestyle intervention (LCDE) and standard diet and exercise (SDE) groups. The intervention used can promote an improvement in the clinical presentation of PCOS, especially in hormonal parameters, suggesting benefit of carbohydrate restriction on the endocrine profile. The study does not directly isolate sugar intake, but supports lower carbohydrate diets as potentially improving androgen-related abnormalities in women with PCOS.

This patient-oriented article on hormone imbalance and sugar notes that "insulin also increases the production of testosterone" and that "when you eat excess amounts of sugar, the body copes with it by turning it into fat cells," which then produce estrogen. It explains that for women, excess testosterone can lead to symptoms such as "acne, hair loss and mood swings" and suggests that sugar-driven insulin surges may contribute to these androgen-related symptoms, though it does not cite specific clinical trials in women.

Objective and hypothesis: The purpose of this research study is to compare different diets for treating PCOS. We hypothesize that a low-glycemic load diet - designed to lower blood levels of glucose and insulin - will be more beneficial than a low-fat diet in obese adolescents and young adults with PCOS. The trial is designed to test whether dietary manipulation of glycemic load (largely driven by carbohydrate/sugar content) affects PCOS-related outcomes, which include hyperandrogenism, but results are not reported in this registry entry.

This article for a general audience claims that "elevated blood sugar levels can disrupt the delicate balance of these hormones [estrogen and testosterone], leading to estrogen dominance or testosterone suppression." It notes that in women, such imbalances may manifest as "irregular menstrual cycles, polycystic ovary syndrome (PCOS), or fertility issues," suggesting that sugar can influence sex hormones but describing both potential increases and decreases rather than a uniform rise in androgens.

This narrative review focuses mainly on men but notes that "excessive intake of sugar and confectionery products adversely affects testosterone regulation" and that chronic high-sugar intake, especially of sweetened beverages, "has been linked to metabolic dysfunction, insulin resistance, inflammation, and oxidative stress," which in turn impair steroidogenesis. While centered on male reproductive function, it supports the broader concept that high added sugar intake can dysregulate testosterone through metabolic pathways that are also relevant to women with insulin resistance or hyperandrogenic disorders.

In women with PCOS, higher protein intakes may be superior at suppressing androgen levels when compared to high carbohydrate diets. This trial description notes that the study will test the effects of a high-protein diet (30% of total energy from protein) on cardiometabolic health in women with PCOS, with interest in whether this macronutrient pattern improves body composition and metabolic markers including androgens. While not yet reporting results, it reflects the hypothesis that relatively higher carbohydrate (often including sugar) intake is less favorable for androgen suppression than higher protein intake in PCOS.