April 12, 2024

How minerals affect women’s fertility and menstrual health

In a recent review published in the journal Nutrients, researchers in Austria discuss the role of certain minerals in the female reproductive system.

Study: Minerals and the menstrual cycle: impact on ovulation and endometrial health. Image credits: Marko Aliaksandr / Shutterstock.com


The function of minerals in women’s reproductive health, especially during menstruation, is a complex area of ​​research that emphasizes the link between nutrition and female fertility. Despite the emphasis on micronutrients for the prevention of reproductive diseases, there remains a lack of systematic evidence on the effect of minerals during menstruation on female fertilization pathways.

Although researchers have extensively investigated minerals linked to male fertility, their involvement in women’s reproductive health has received less attention, with many studies overlooking the menstrual phase.

Overview of female reproductive regulation

Hormones are crucial in human reproduction as they control various processes such as menstruation, ovulation, implantation and pregnancy. Hormones also facilitate follicle maturation and ovulation, in addition to supporting the endometrium to provide ideal conditions for a fertilized egg.

The ovaries are essential to women’s reproductive health because they produce eggs for fertilization and synthesize hormones such as estrogen and progesterone. During the follicular phase, increased production of gonadotropin hormone-releasing hormone (GnRH) stimulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In comparison, GnRH secretion is suppressed as progesterone levels rise during the luteal phase.

Oxidative stress, which occurs when the body’s production of free radicals exceeds its ability to detoxify their harmful effects, can damage cell structures and potentially affect fertility. An excess of iron, a deficiency of selenium, a deficiency of zinc, insufficient magnesium intake and an imbalance of copper indirectly affect female fertility.

Impact of mineral intake on female fertility


Zinc is essential for hormone production, endometrial function and fertility because it regulates LH, FSH and steroid production and protects the egg from oxidative stress-related reactive oxygen species (ROS) damage.

Zinc finger proteins aid estrogen receptor function; therefore, maintaining proper zinc levels is critical for fertility. Zinc deficiency can cause reproductive health problems such as abnormal LH and FSH synthesis, irregular ovarian growth, menstrual cycle disruptions and preeclampsia.


Selenium is necessary for the production of selenoproteins, which convert thyroxine into its biologically active form, triiodothyronine (T3). Thyroid metabolism is critical for maintaining hormonal balance in the female fertility system, as hyperthyroidism and hypothyroidism can interrupt menstrual cycles and affect conception. Thus, maintaining optimal selenium levels is crucial for consistent and effective ovulation.


Iodine is essential for thyroid function and hormone production because this mineral interacts with reproductive hormones such as estrogen and progesterone. Iodine deficiency can cause hypothyroidism, infertility and reproductive abnormalities.

Adequate iodine consumption is vital for all menstrual phases. Animal studies have even shown that Lugol’s iodine therapy can increase fertility in cows with unexplained infertility.


Iron, a key component of hemoglobin, is necessary for oxygen transport of red blood cells and for physiological activities. Iron deficiency can cause anemia, reduced egg quality and reduced ovulation frequency.

Maintaining adequate iron levels is critical for women trying to conceive, as low levels can lead to infertility. In comparison, iron overload can reduce the number of eggs with assisted reproductive techniques.


Calcium is an essential part of the female reproductive system because it affects bone health, hormone production and sperm fusion. The release of calcium causes the pituitary gland to release LH and FSH, which stimulate the ovaries to produce estrogen and progesterone.

Calcium indirectly affects hormonal control by altering ovulation and ovarian function. Furthermore, balanced calcium levels are crucial for optimal cell division and embryo implantation.


Magnesium is essential for hormonal balance and female fertility. It is involved in enzymes such as aromatase, which converts androgens into estrogens. Magnesium is involved in approximately 600 enzymatic activities, including deoxyribonucleic acid (DNA) repair and glutathione metabolism.

Magnesium can also improve insulin sensitivity and minimize comorbidities. The antioxidant properties of this mineral indirectly improve fertility by protecting the body from oxidative damage, maintaining egg quality, modifying ovulation, and promoting endometrial health.


Copper is crucial for protecting the body against oxidative stress by functioning as a cofactor for the superoxide dismutase enzyme. Copper influences antioxidant systems, signal transduction and gene expression; However, excess copper can have pro-oxidative effects and impair endothelial function.


Manganese, a valuable trace element, acts as an antioxidant that scavenges free radicals to protect cell structures from oxidative stress and potentially improve female reproductive well-being. Oxidative stress damages the function and quality of egg cells, disrupting the hormonal regulation of female fertility.


Minerals play a crucial role in female fertility, especially in hormonal control, ovulation, oxidative stress and endometrial health. Certain minerals, such as selenium, calcium and zinc, are essential for the follicular phase and ovulation. Conversely, iron excess, zinc deficiency, inadequate magnesium consumption and copper imbalance can indirectly affect women’s fertility.

Magazine reference:

  • Kapper, C., Oppeit, P., Ganhor, C., et al. (2024). Minerals and the menstrual cycle: implications for ovulation and endometrial health. Nutrients 16(1008). doi:10.3390/nu16071008

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