The Impact of High BMI on Anti-Müllerian Hormone (AMH) Levels
The prevalence of obesity is significantly higher among women than men worldwide. This is of particular importance for women of reproductive age, as obesity affects not only overall health but also has a substantial impact on reproductive health and fertility.
Obesity has been associated with lower rates of spontaneous conception as well as reduced pregnancy rates following in vitro fertilization (IVF).¹
How Does Obesity Affect Fertility? Obesity exerts a multifactorial effect on female reproductive physiology through increased oxidative stress, lipotoxicity, and the activation of pro-inflammatory pathways. One of the principal mechanisms is the disruption of the hypothalamic–pituitary–ovarian (HPO) axis, which has been well established as a key factor through which excess body weight contributes to menstrual cycle disturbances.² In addition, obesity has a direct and independent effect on the endometrium, resulting in impaired decidualization in response to hormonal stimulation and a reduction in the number of potential implantation sites.³ Furthermore, the adverse effects of hyperestrogenism on the endometrium and its impact on reproductive function are well recognized and extensively documented.
In addition, the direct effects of obesity on the ovaries and oocytes have become an area of considerable scientific interest. Human studies have demonstrated morphological abnormalities and reduced developmental competence in the oocytes of women with a high body mass index (BMI). Of particular significance is the growing evidence suggesting that obesity is associated with altered levels of anti-Müllerian hormone (AMH), a key marker of ovarian reserve.⁴
Several recent large-scale studies have demonstrated significantly lower AMH levels in women with a high body mass index (BMI), regardless of whether they have polycystic ovary syndrome (PCOS).
In fact, women with a high body mass index (BMI) have been shown to exhibit a 23.7% reduction in AMH levels, along with a lower antral follicle count (AFC), compared with women of normal body weight.³⁻⁵
In the context of assisted reproductive treatment, women with a high body mass index (BMI) appear to have a reduced response to ovarian stimulation medications, produce fewer oocytes, and achieve lower clinical pregnancy and live birth rates compared with women of normal body weight.²
More specifically, oocytes retrieved from women with obesity undergoing in vitro fertilization (IVF) are often smaller in size and have a lower developmental potential following fertilization. The resulting embryos have also been shown to exhibit metabolic alterations, including reduced glucose uptake and increased triglyceride content.⁶
Furthermore, obesity has been associated with a lower rate of oocyte maturation and alterations in meiotic spindle formation. The follicular fluid of women with obesity also demonstrates changes in its biochemical composition, including altered levels of adipokines, inflammatory markers such as C-reactive protein (CRP), and free fatty acids.⁷⁻⁸ In addition, the elevated leptin levels commonly observed in women with obesity are also reflected in their follicular fluid and have been shown to be associated with lower AMH levels.²
Scientific evidence suggests that the effects of obesity on ovarian function may be cumulative over time. Women who were already obese at the age of 18 have been shown to have lower AMH levels than women who became obese later in life after having a normal body weight at age 18. Although improvements in dietary habits and metabolic health may partially restore the metabolic environment, abnormalities in meiotic spindle formation and mitochondrial function appear to persist. These findings suggest that obesity may induce long-lasting—and potentially irreversible—changes in ovarian function.²
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