Adipomastia, or lipomastia, also known colloquially as fatty breasts, is a condition defined as an excess of skin and adipose tissue in the breasts without true breast glandular tissue. It is commonly present in men with obesity, and is particularly apparent in men who have undergone massive weight loss. A related/synonymous term is pseudogynecomastia. The condition is different and should be distinguished from gynecomastia ("women's breasts"), which involves true glandular breast development in a male. The two conditions can usually be distinguished easily by palpation to check for the presence of glandular tissue. Another difference between the conditions is that breast pain/tenderness does not occur in pseudogynecomastia. Sometimes, gynecomastia and pseudogynecomastia are present together; this is related to the fact that fat tissue expresses aromatase, the enzyme responsible for the synthesis of estrogen, and estrogen is produced to a disproportionate extent in men with excessive amounts of fat, resulting in simultaneous glandular enlargement.

Estrogen insensitivity syndrome (EIS), or estrogen resistance, is a form of congenital estrogen deficiency or hypoestrogenism which is caused by a defective estrogen receptor (ER) – specifically, the estrogen receptor alpha (ERα) – that results in an inability of estrogen to mediate its biological effects in the body. Congenital estrogen deficiency can alternatively be caused by a defect in aromatase, the enzyme responsible for the biosynthesis of estrogens, a condition which is referred to as aromatase deficiency and is similar in symptomatology to EIS.

EIS is an extremely rare occurrence. As of 2016, there have been three published reports of EIS, involving a total of five individuals. The reports include a male case published in 1994, a female case published in 2013, and a familial case involving two sisters and a brother which was published in 2016.

EIS is analogous to androgen insensitivity syndrome (AIS), a condition in which the androgen receptor (AR) is defective and insensitive to androgens, such as testosterone and dihydrotestosterone (DHT). The functional opposite of EIS is hyperestrogenism, for instance that seen in aromatase excess syndrome.

In 1994, a 28-year-old man with EIS was reported. He was fully masculinized. At 204 cm, he had tall stature. His epiphyses were unfused, and there was evidence of still-occurring slow linear growth (for comparison, his height at 16 years of age was 178 cm). He also had markedly delayed skeletal maturation (bone age 15 years), a severely undermineralized skeleton, evidence of increased bone resorption, and very early-onset osteoporosis. The genitalia, testes, and prostate of the patient were all normal and of normal size/volume. The sperm count of the patient was normal (25 million/mL; normal, >20 million/mL), but his sperm viability was low (18%; normal, >50%), indicating some degree of infertility. The patient also had early-onset temporal hair loss. He reported no history of gender identity disorder, considered himself to have strong heterosexual interests, and had normal sexual function, including morning erections and nocturnal emissions.

Follicle-stimulating hormone and luteinizing hormone levels were considerably elevated (30–33 mIU/mL and 34–37 mIU/mL, respectively) and estradiol and estrone levels were markedly elevated (145 pg/mL and 119–272 pg/mL, respectively), while testosterone levels were normal (445 ng/dL). Sex hormone-binding globulin levels were mildly elevated (6.0–10.0 nmol/L), while thyroxine-binding globulin, corticosteroid-binding globulin, and prolactin levels were all normal. Osteocalcin and bone-specific alkaline phosphatase levels were both substantially elevated (18.7–21.6 ng/mL and 33.3–35.9 ng/mL, respectively).

Treatment with up to extremely high doses of ethinylestradiol (fourteen 100-µg patches per week) had no effect on any of his symptoms of hypoestrogenism, did not produce any estrogenic effects such as gynecomastia, and had no effect on any of his physiological parameters (e.g., hormone levels or bone parameters), suggesting a profile of complete estrogen insensitivity syndrome.