Obesity Can Cause Women Not to Ovulate Regularly

By Urbanaveed
7 Min Read

Obesity, being high in fat content, is more unhealthy than one can assume. Besides its ominous effects on overall well-being, it can disrupt the hormonal balance of sex hormones. Women are prone to this dysregulation. Accumulation of excess fats in the adipose tissue interferes with the signaling process of hormones. Obesity can be a menace to women’s fertility. Nutrition has a pronounced impact on reproductive health and excess of anything upsets the balance. It can affect the Hypothalamus-pituitary-ovarian (HPO) axis, leading to the disturbance in the secretion of sex hormones. Obesity, directly or indirectly, is the cause of many reproductive irregularities, for example, PCOS, menstrual cycle imbalance, infertility, gestational diabetes, etc.

The Complex Interplay of Obesity and The Tendency to Ovulate

Advancement to ovulatory dysfunction from being high weight is a complex interplay. It involves a progression of events, each leading to the successive one, from the accumulation of fats to the imbalance of sex hormones. Ovulatory dysfunction is the lack or irregular occurrence of ovulation. Ovulation is the release of an egg from the ovary that occurs every month. Any fluctuation in the rhythmic cycle of sex hormones can affect the ovulatory process. A series of events lead to the disturbance in the HPO axis. Let’s learn them stepwise.

Interference of Obesity with Insulin Signaling

Excess accumulation of Adipose tissues releases chemicals like adipokines that interfere with the insulin pathway. Obesity also causes adipose tissues to undergo inflammatory pathways, releasing inflammatory chemicals into the bloodstream. The combined effect of adipokines and inflammatory chemicals hampers insulin signaling and minimizes insulin uptake by cells. Adiponectin is secreted by adipose tissue that enhances the insulin-sensitizing properties. Obesity causes the adipocytes to increase in size. These oversized adipocytes are inefficient in producing normal levels of adiponectin. Decreased adiponectin plays a contributory role in the above paradigm of insulin resistance. Insulin resistance is generally a condition in which cells become less sensitive to insulin uptake, directing high blood glucose levels and no glucose in cells.

Results in High Insulin Levels

Insulin resistance makes glucose degradation difficult as cells become insensitive to insulin uptake. This insensitivity leads to increased blood glucose levels. As cells cannot respond to insulin, it imparts the false impression that insulin is insufficient for the cells, causing the pancreas to secrete more insulin. Over-secretion of insulin leads to the medical condition -of hyperinsulinemia (high levels of insulin in the blood). Hyperinsulinemia acts as a compensatory mechanism to optimize insulin uptake, but in reality, it aggravates the situation. Higher insulin levels in the blood act on the ovarian theca cells and urge them to secrete more androgen in response.

Ovarian Cells Begins to Release More Androgens

Insulin binds to its receptors on the surface of ovarian theca cells. Theca cells, in response to insulin, initiate the synthesis of androgens, mainly testosterone. Androgens are a class of sex hormones that have a primary role in the development of male secondary sexual characters. They are also secreted in females but in small amounts. Hyperinsulinemia stimulates theca cells to produce excess androgens in females which can potentially upset the hormonal balance. Hyperinsulinemia also triggers theca cells’ sensitivity to Leutinizing hormone (LH). LH is a gonadotropin secreted by the pituitary gland. LH sensitization of theca cells further promotes androgen synthesis. As a result, excess androgens imbalance the HPO axis and lead to ovulatory problems.

HPO Axis Impairment

Excess androgen secretion, directly or indirectly, impacts the hypothalamus in optimizing the GnRH factor. GnRH (Gonadotropin-Releasing-Hormone) controls the secretion of gonadotropins from the anterior pituitary gland. FSH and LH are the two primary sex hormones that play their part in the development of ovulatory dysfunctions. LH secretion increases as explained above and this in turn causes LH/FSH to become high, disrupting the HPO axis.

How  obesity leads to ovulatory dysfunction
Progression of ovulatory complications due to excess fats.

No Ovulation or Eggs Get Entrapped

Excess androgen synthesis and triggered LH sensitization of theca cells impair the follicular development in ovaries. It results in anovulation (no ovulation at all) or the lack or irregular periods of ovulation. A disrupted HPO axis can potentially cause follicular arrest (a condition in which follicles stop developing further) or the formation of multiple, small-sized, non-functional follicles. Excess LH can boost follicular development and result in the formation of multiple cysts in ovaries, leading to PCOS.

Consequence of gonadotropin disturbances due  to obesity
Obesity leads to ovulatory dysfunction due to excess androgen production. It affects the maturation of ovarian follicles.


After reading the above physiology related to obesity, one cannot underestimate the excess fats in her body. Ovulatory dysfunction is only a single consequence of obesity on female reproductive health. Besides ovulatory dysfunction, many other reproductive irregularities are associated with obesity. Being heavy with fats has more drastic outcomes in females than in males. As females have the utmost responsibility of producing a generation, they have to take care of their health more vigilantly.

Other than reproductive health, obesity is equally fatal in the context of cardiovascular health for both males and females. High cholesterol is the leading cause of heart attacks in both populations. Super-processed foods contain trans-fats that directs the accumulation of LDL cholesterol, leading to obesity. So, it is significant to control obesity, not only for women but for men too.

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Student of BSc MLT at NUMS, and Content Writer in Health, Medicine, and Wellness. Finding soothe in writing and spreading knowledge.
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