The review states that the relationship between estrogen and obesity is bidirectional: estrogen deficiency can promote excessive fat accumulation, while obesity itself can alter estrogen receptors and the enzymes involved in estrogen synthesis. It also notes that in premenopausal women obesity is associated with higher estradiol synthesis in subcutaneous fat, whereas in postmenopausal women obesity is associated with increased estradiol in visceral fat.

The article says that menopause-related decline in estrogen is accompanied by a change in adipose tissue distribution and increased prevalence of obesity in women. It further states that data suggest excess adiposity is associated with decreased expression of estrogen receptors and key enzymes involved in estrogen synthesis, and that estrogen deficiency or impaired function may predispose to obesity.

In premenopausal women, obesity was associated with lower estradiol levels than in non-obese women. The paper reports that obese and overweight premenopausal women had significantly lower estradiol levels compared with non-obese women, but after menopause the association reversed and obese women had higher estradiol levels.

The review states that as women enter menopause, circulating estrogen declines, and this is accompanied by changes in energy homeostasis that result in increases in intra-abdominal body fat. It also notes that decreased estrogen levels in menopausal women are associated with loss of subcutaneous fat and increased abdominal fat.

Decreased estrogen levels after menopause, a pivotal factor in the biology of aging, and obesity were more associated with shorter telomere lengths in pre- and postmenopausal women than aerobic capacity and other CVD risk factors. The estrogen level… was higher in premenopausal women than in postmenopausal women.

For postmenopausal women, estrogen levels increase with increasing BMI, presumably because conversion of androgens to estrogen in adipose tissue is a primary source of estrogen. In premenopausal women, higher BMI was associated with lower estradiol levels early in the menstrual cycle, but higher estradiol levels in the late follicular phase.

In this postmenopausal cohort, both BMI and waist circumference were positively associated with all three blood estrogen levels. The study found the highest estrogen levels in obese women with large waists, and regression analyses confirmed significant associations between obesity measures and estrogen levels.

This review states that excess body fat increases androgen aromatization and, together with an obesity-related decrease in SHBG, is associated with mildly elevated levels of estrone and free estradiol in postmenopausal women. It adds that premenopausal obese individuals show the same tendency, but the much greater ovarian estrogen secretion overshadows the difference.

The article reports that obese premenopausal women had significantly lower estradiol and inhibin levels than non-obese premenopausal women, but that the associations reversed after menopause, when obese women had higher estradiol levels than non-obese women. This indicates the obesity-estrogen relationship differs by menopausal status.

The article states that obesity is associated with increased estrogen production secondary to increased peripheral aromatization. It adds that in postmenopausal women this effect is proportionately more significant because the ovaries no longer contribute to estrogen production.

The article explains that depletion of ovarian function after menopause in women induces estrogen deficiency leading to increased fat and decreased muscle mass. It notes that in climacteric women, decreased estrogen is accompanied by increased follicle-stimulating hormone, relatively increased testosterone, decreased basal metabolic rate, and decreased sex hormone binding globulin, resulting in impaired lipid metabolism and increased glucose uptake, thereby increasing body fat and causing obesity. It specifically states that "obesity occurring after menopause in women appears because estrogen is deficient." (translation from Korean).

The study found that postmenopausal women with circulating estradiol in a middle range had the best body-composition profile, while women with lower or higher estradiol had more body fat. The authors state that estrogen deficiency is postulated as a critical triggering factor for the rise in obesity after age 40.

The review says that as fat mass increases in obesity, aromatase expression and estrogen levels are elevated, especially in postmenopausal women because adipose tissue becomes the primary source of estrogen production after menopause. It also says adipose tissue can contribute up to 100% of circulating estrogen in postmenopausal women.

This Korean review on menopausal obesity states: "When estrogen is deficient at menopause, it induces excessive fat accumulation due to decreased lipid metabolism and increased glucose uptake." It describes "obesity induced by estrogen deficiency at menopause" and discusses mechanisms such as changes in energy expenditure, fat distribution, and insulin sensitivity. (translation from Korean).

The review notes that loss of estrogens after menopause increases total adiposity and decreases lean body mass, and that estrogenic hormone replacement therapy prevents this. This supports a link between low estrogen and increased obesity-related fat mass in women, especially after menopause.

This Korean conference paper notes: "The sharp increase in body fat and abdominal obesity in women after middle age is not a general aging phenomenon but rather due to menopause and the resulting decrease in estrogen concentration." It further states: "In middle‑aged postmenopausal women, the main cause of obesity is the compensatory mechanisms following estrogen decrease." (translation from Korean).

Before menopause, breast cancer incidence is relatively low and adiposity is erroneously regarded as a protective factor against this tumor conferred by the obesity-associated defective estrogen synthesis. In premenopausal cases, the results of clinical studies justify that obesity induces mild or moderate decrease in circulating estrogen levels reflected by their inclination to anovulatory infertility and long or irregular menstrual cycles. In premenopausal cases, obesity is associated with defective estrogen synthesis and decreased circulatory estrogen levels, particularly in the follicular phase.

We found that in postmenopausal women, serum and tissue estradiol levels were increased in those who were overweight, and serum FSH levels were decreased in obese status. Breast tissue estradiol (E2) levels were higher in overweight women compared to normal-weight women in postmenopausal women, but did not differ among all three groups of premenopausal women. Generally, breast tissue estrone (E1) and estradiol (E2) levels were lower in postmenopausal women than in premenopausal women.

The review states that a reduction in estradiol levels, as found in menopause, would be expected to increase food intake, and that loss of estradiol post-menopause may contribute to the development of obesity and insulin resistance. It also says that abnormally high or low estradiol can both increase insulin resistance.

The study reports a non-linear relationship between body fat and estradiol in healthy women. Women with very low and high body fat had lower estradiol than women with low and average body fat, and the authors note that the hypothesis that body fat simply raises estradiol is not strongly supported in healthy women of reproductive age.

A Korean clinical explanation of obesity and sex hormones states: "Increase in body weight and fat cells causes various disturbances in the balance of female hormones." It explains that with obesity, insulin resistance increases insulin secretion, and the resulting high insulin reduces sex hormone-binding globulin (SHBG), which impairs transport of sex hormones to tissues. "Decrease of SHBG affects both female and male hormones; tissues perceive a deficiency of male hormones and increase male hormone secretion. As a result, in women, increase of male hormones and deficiency of female hormones lead to anovulation." It concludes that obesity can be associated with "female hormone deficiency" in this endocrine context. (translation from Korean).

This Korean science policy article summarizing basic research reports: "The research team experimentally demonstrated that the female hormone estrogen is the cause of obesity in menopausal women." They describe that to confirm the relationship between estrogen receptors and obesity, "when the ovaries of mice were removed to reduce the amount of estrogen, obesity was induced," whereas administration of estrogen that reacts with both alpha and beta receptors prevented obesity even after ovariectomy. (translation from Korean).

This Korean news report on research by a Frontier R&D program and Georgetown University states that "estrogen, a female hormone, is the main cause of obesity in women after menopause." It explains that estrogen, acting via estrogen receptor alpha (ERα), plays an important role in obesity induction and reports animal experiments in which surgical removal of ovaries decreased estrogen and led to obesity, while estrogen administration prevented obesity. (translation from Korean).

This review describes estrogen and obesity as bidirectionally related and says that menopause-associated estrogen decline correlates with increased obesity prevalence in women. It also states that available studies suggest excess adiposity is associated with decreased expression of estrogen receptors and key enzymes involved in estrogen synthesis, but that the human data are limited.

Another Korean pharmaceutical news article similarly reports that a joint research team found "estrogen is a major cause of female obesity after menopause" and that in most menopausal women, rapid decrease in estrogen triggers obesity. The team emphasized that estrogen receptor alpha is "directly related to obesity" based on experiments where ovariectomy-induced estrogen reduction led to obesity in mice. (translation from Korean).

This paper reports that reducing estrogen receptor alpha in female mice induced obesity in the female mice but not the males. It is relevant as mechanistic evidence that impaired estrogen signaling can contribute to obesity, although it is animal data rather than direct evidence in women.

A Korean article citing work from the University of Texas Southwestern Medical Center reports that researcher Deborah Clegg found estrogen plays an important role in regulating energy expenditure, appetite, and body weight. It notes that when estrogen receptor alpha signaling is deficient in specific hypothalamic centers in mice, they become obese and develop obesity‑related diseases, indicating a metabolic regulatory role for estrogen in body weight control. (translation from Korean).

The report says a research team tested the idea that estrogen deficiency in aged females may trigger obesity and high blood pressure, and that their rat study suggested loss of estrogens after menopause may contribute to obesity and hypertension. This is animal evidence, not direct human evidence.

This secondary report says a study found that estrogen and other hormone levels dropped when overweight and obese women lost weight. The article also states that extra body fat likely increases estrogen levels, and that losing weight lowered estradiol, estrone, and free estradiol.

A Korean pharmaceutical/health news site reports research presented to the American Physiological Society showing that decreased estrogen is a cause of obesity in menopausal women. The article states that "decrease of the female hormone estrogen becomes a cause of obesity in menopausal women" and highlights that estrogen receptor alpha is closely related to obesity, based on ovariectomized mice experiments where reduced estrogen led to obesity unless estrogen reacting with both alpha and beta receptors was administered. (translation from Korean).

Paradoxically, in menopause, a woman's estrogen levels are inversely related to her weight. In a study of newly menopausal healthy women over a four-year period, women showed an increase in weight and body fat (primarily as visceral adipose tissue), which coincided with a drop in estradiol levels and a decrease in physical activity and energy expenditure. The absence of both estrogen and these crucial elements leads to progressive obesity.

From background endocrinology knowledge: In general, obesity in women is associated with complex alterations in sex hormones: peripheral aromatization in adipose tissue can increase estrogen levels, while obesity-related insulin resistance and decreased sex hormone-binding globulin can lower circulating bioavailable estrogens in some contexts. In premenopausal women, obesity is linked with lower estradiol levels compared with normal-weight women in several studies, but obesity is not typically described as a universal primary cause of "estrogen deficiency"; rather, it contributes to dysregulation of reproductive hormones and conditions such as anovulation and polycystic ovary syndrome.