An energy deficit, which can occur independent of changes in body weight, appears to be the critical factor in both the weight loss and exercise-induced forms of functional hypothalamic amenorrhea. Patients with FHA typically have low or low-normal LH, normal FSH, low estradiol, and low progesterone. The guideline does not describe underweight status itself as causing excess androgens.

Polycystic ovary syndrome is the most common cause of persistent hyperandrogenism beyond early puberty in adolescent girls and women. In this syndrome, chronically elevated luteinizing hormone and insulin levels lead to increased androgen production within the ovarian theca. Weight loss in obese patients with hyperandrogenemia with or without PCOS has been shown to decrease androgen levels, increase sex hormone binding globulin, and reduce clinical hirsutism.

Hyperandrogenism is the most common endocrinopathy seen in women and may result from ovarian or adrenal overproduction of androgens, altered peripheral metabolism and/or end-organ hypersensitivity. The most common cause of clinical hyperandrogenism is polycystic ovarian syndrome (PCOS). Obesity is listed as a diagnosis of exclusion, not underweight.

Endogenous total and free testosterone, but not DHEAS, were lower in women with anorexia nervosa than in controls. In contrast, normal-weight women with hypothalamic amenorrhea had normal androgen and DHEAS levels. The authors concluded that androgen levels are low in anorexia nervosa and that oral contraceptives can reduce them further.

PCOS is by far the most common cause of hyperandrogenism in women. In obese women with PCOS, weight loss results in a small decrease in testosterone as measured by the free androgen index and a concomitant mild improvement in hirsutism. Once tumorous hyperandrogenism is excluded, the most common cause is PCOS.

Overall, this review states that obesity is associated with increased androgen levels in women, and that these changes are reversed with weight loss. It also notes that women with higher BMI had a blunted LH response compared with women with lower BMI, but the direction of the androgen association is toward higher BMI, not low BMI.

Our data demonstrate lower mean total testosterone and free testosterone, but not DHEAS, levels in women with anorexia nervosa compared with healthy controls and normal-weight women with hypothalamic amenorrhea. Androgen levels are low, appear to be even further reduced by oral contraceptive use, and are predictors of bone density and fat-free mass in women with anorexia nervosa.

The study found that low-BMI PCOS patients had significantly higher LH and LH/FSH ratio than high-BMI PCOS patients. It also reported that the frequency of hyperandrogenism by increased androstenedione, DHEA, and DHEAS was significantly higher in low-BMI PCOS patients compared with high-BMI PCOS patients.

This case report discusses an underweight woman with insulin resistance and hyperandrogenic features, and notes that body fat distribution strongly correlates with PCOS. The authors state that the discrepancy between total and free testosterone in the patient could be attributed to low BMI. This is a case-based inference, not population-level evidence that being underweight causes hyperandrogenism.

In both the hirsutism and PCOS groups, women with BMI at or above 25 kg/m² had significantly higher measured total testosterone, lower SHBG, and higher calculated androgen parameters than women with BMI below 25 kg/m². BMI was positively correlated with testosterone and negatively correlated with SHBG.

Polycystic ovary syndrome (PCOS) is rightly identified as the predominant cause of androgen excess, affecting up to 13% of women globally. Other aetiologies, including non-classic congenital adrenal hyperplasia, hormone-secreting adrenal or ovarian tumours, Cushing’s syndrome and severe insulin resistance syndromes, can mimic the clinical and biochemical phenotype of PCOS.

Hyperandrogenemia is common in women and is associated with increased metabolic risk. The prevalence of hyperandrogenemia increased with BMI category: 12% for BMI under 25 kg/m², 22% for BMI 25 to 30 kg/m², and 31% for BMI 30 kg/m² or higher. The study supports a positive association with higher BMI, not underweight as a cause.

Functional hypothalamic amenorrhea is a disorder of chronic anovulation caused by suppression of the hypothalamic-pituitary axis from body weight loss, excessive exercise, or stress and may result in infertility or bone density loss. Evaluation typically reveals low or low-normal LH and FSH and low estradiol. The article recommends measuring free and total testosterone and DHEAS only if there is evidence of hyperandrogenism.

In the vast majority of cases, the underlying aetiology is polycystic ovary syndrome (PCOS), a common chronic condition that affects up to 10% of all women. Previous work from our group has also highlighted the role of insulin in adipose androgen generation in women with PCOS through upregulation of AKR1C3 expression and activity; indeed, adipose tissue itself is a source of androgen production in simple obesity. Hyperinsulinaemia in PCOS and simple obesity is therefore likely to be a key driver of the androgen excess phenotype in these conditions.

Weight loss in patients with hyperandrogenism, with or without the clinical presence of PCOS, should be the first therapeutic option because it decreases androgen levels, increases SHBG, and may restore ovulation. As little as a 7% reduction in body weight can restore fertility, decrease hirsutism in some women with androgen excess, and improve the response to induction of ovulation.

Hormones can contribute to underweight in women, but underweight itself is not presented as a cause of androgen excess. The article emphasizes that PCOS is the most common cause of hyperandrogenism and that obesity and insulin resistance are associated with higher androgen levels.

This paper reports that higher current BMI was associated with higher concentrations of DHEAS and other androgen-related metabolites, and that BMI at age 18 was inversely associated with adrenal androgens including DHEA, DHEAS, androstenedione, and testosterone.

FHA women with normal BMI present an unfavorably altered hormonal profile reflected by hyperandrogenemia, with higher total testosterone and 17-hydroxyprogesterone and no differences in DHEA-S concentration compared with the remainder. The study reports increased androgens in a subgroup of FHA patients, showing that elevated androgens can occur in FHA, but this is not framed as a general effect of being underweight.

Hyperandrogenism in women is defined by clinical signs (hirsutism, acne, alopecia) and/or biological signs (elevated total or free testosterone). Polycystic ovary syndrome is the most common cause of hyperandrogenism in women (70% of cases) but must remain a diagnosis of exclusion. Other causes include non-classic congenital adrenal hyperplasia, androgen-secreting tumours, Cushing’s syndrome and severe insulin resistance syndromes.

Ovarian tumors and polycystic ovary syndrome can both cause too much androgen production. Women who have polycystic ovary syndrome can reduce their chances of long-term complications by maintaining a normal weight through healthy diet and regular exercise.

Hyperandrogenemia may be associated with obesity in peripubertal girls, even prior to thelarche, with observed elevations of serum A4, T, and free T levels. In prepubertal obese girls, weight loss is associated with improved insulin resistance and decreased A4 and T levels.

The article reports that total physical activity was negatively associated with estrone, estradiol, and androstenedione, and that women with high BMI/low physical activity had higher estrone than the low-BMI groups. The findings do not support a simple pattern of low BMI causing excess androgens.

In women with hypothalamic amenorrhea and polycystic ovarian morphology, the quiescence of the hypothalamic-pituitary-ovarian axis most likely explains their normal baseline androgen status. The article further notes that hyperandrogenism emerges in association with weight gain and recovery of hypothalamic function, implying that low weight does not simply cause high androgen levels.

A clinical epidemiological survey cited in this article found that patients with PCOS who have a high BMI are more susceptible to clinical or biochemical hyperandrogenism. This points in the opposite direction from the claim that being underweight causes excess androgen levels.

Rapid weight loss and undernourishment lead a woman’s body into a state of emergency. Excess training, undernourishment and low BMI adversely affect reproductive function and fertility. The paper discusses low BMI as a reproductive disruptor, but the cited mechanism for androgen excess in the article is obesity-related insulin resistance and hyperinsulinemia, not underweight causing hyperandrogenism.

The authors report that lean women had statistically significant higher increments of free estradiol index than overweight women after low-dose hormone therapy. This paper concerns sex-steroid response to therapy, not baseline hyperandrogenism, but it shows BMI-related differences in free sex-steroid measures.

The processes by which GnRH is suppressed by weight loss, exercise or stress are multifactorial. Diagnosis of hypothalamic amenorrhea is based on amenorrhea, low estradiol, and normal or low gonadotrophins. This review does not describe underweight status as a cause of excess androgens; instead it frames weight loss as a cause of hypothalamic suppression.

The presence and severity of ovarian hyperandrogenism seem to be primarily related to common risk factors such as age, low birth weight, overweight, and obesity in adolescents and young women. In this cohort, overweight and obesity were associated with higher androgen levels, whereas being underweight was not identified as a risk factor for ovarian hyperandrogenism.

The review states that metabolic, hormonal, and haematological derangements exist in lean PCOS, although they are usually equal to or less obvious than in obese PCOS. It also says insulin resistance is inherent in PCOS regardless of BMI.

Prevalence of type 2 diabetes and free androgen index did not differ between the two groups. This underweight-vs-normal-weight comparison does not show that underweight causes excess androgen levels.

Reasons your hypothalamus may stop secreting hormones include not eating enough food, poor nutrition, excessive exercise, emotional or psychological stress, low body fat, and having an eating disorder such as anorexia nervosa. The page presents hypothalamic amenorrhea as a consequence of low energy availability rather than as a condition caused by excess androgens.

PCOS is the underlying cause of androgen excess in the vast majority of women presenting to primary and secondary care and is associated with a significant metabolic risk burden. Obesity exacerbates PCOS manifestations via insulin resistance and proinflammatory cytokine excess; excess adipose tissue also forms testosterone. The data to date are consistent with the hypothesis that PCOS is a complex genetic trait whose expression is amplified by obesity and insulin-resistant hyperinsulinaemia.

The article states that BMI was negatively associated with testosterone levels and positively associated with estradiol levels. This is a broader BMI-hormone association study, but it does not support a claim that low BMI causes excess androgens.

There were no clinical manifestations of hyperandrogenism, and biochemical androgen levels were normal. This abstract is an example of hypothalamic amenorrhea presenting without elevated androgens, rather than supporting the claim that underweight causes hyperandrogenism.

High levels of circulating male sex hormones in females may arise from disease of the ovaries (including polycystic ovary syndrome and ovarian tumours), disease of the adrenal gland (congenital adrenal hyperplasia and adrenal tumours), disease of the pituitary gland (Cushing syndrome, acromegaly, prolactinoma), obesity and the metabolic syndrome, and medications such as testosterone and anabolic steroids. Obesity and the metabolic syndrome increase adrenal and body fat androgen production via insulin and IGF-1; underweight is not listed among causes.

Hyperandrogenemia is common in asymptomatic women and is often associated with low sex hormone-binding globulin (SHBG). Indeed, hyperandrogenemia may be a consequence of low SHBG, which results in increased non-SHBG bound testosterone, the leading cause of hyperandrogenemia in our cohort. Factors such as obesity and insulin resistance are known to reduce SHBG levels, thereby increasing free androgen levels.

Polycystic ovary syndrome causes most cases of hyperandrogenism in women. Insulin resistance often drives this process: when cells become resistant to insulin, the body produces more insulin, and high insulin levels signal the ovaries to make extra androgens. Obesity worsens hyperandrogenism because fat tissue produces hormones that increase androgen levels. There is no mention of underweight status as a cause of excess androgen levels.

High androgen levels in females may be due to polycystic ovary syndrome, congenital adrenal hyperplasia, insulin resistance, hyperprolactinemia, Cushing's disease, certain cancers, and certain medications. Obesity can play a role in insulin resistance, making thecal cells more responsive to luteinizing hormone and thereby increasing ovarian androgen production. Underweight status is not cited as a cause of hyperandrogenism.

In anorexia nervosa, clinical studies have found low total testosterone and low free testosterone rather than excess androgen levels, and normal-weight women with hypothalamic amenorrhea can have normal androgen and DHEAS levels. This review-like summary in a university reading list cites free testosterone and DHEAS testing to rule out hyperandrogenism.

This reference text states that functional hypothalamic amenorrhea is characterized by decreased or absent endogenous GnRH secretion, resulting in very low to undetectable LH and FSH levels. It does not state that being underweight causes excess androgen levels; rather it describes central suppression of reproductive hormones.