9 Weight Is The Main Nutritional Factor Influencing Fertility

Sabine Zempleni and Sydney Christensen

During the last few decades concerns grew about the ever increasing male infertility. Worldwide studies show that sperm count has been declining by 57% over a span of 35 years in most countries. Only a couple of countries, such as Australia, do not show this decline.

It is not entirely clear what lifestyle and environmental factors are causing this decline. Of course scientists are busy at work looking into the reasons. One factor may be the Western lifestyle which involves consumption of processed foods, sedentary behavior, and chronic stress.

Other factors such as obesity and endocrine disruptors may play a role. Endocrine disruptors are environmental chemicals such as some insecticides, fungicides, surfactants, plastics, dioxin, and DDT. It is thought that these chemicals we find increasingly in the environment modify hormone secretion.

Female fertility is being affected as well. We are seeing an increasing prevalence of PCOS (polycystic ovary syndrome) in women. PCOS causes hormonal imbalances which prevent ovulation and thus prevent the chance of becoming pregnant. It is the leading cause of infertility in women. Potential contributing factors tied to the increased prevalence are obesity, insulin resistance, and T2D.

The hormone connecting obesity and fertility is leptin. Here is a quick review slide from chapter 1:


The Main Points:

  • Infertility and sub-fertility in men and women is rising.
  • Underweight impairs fertility.
  • Obesity impairs fertility in men and women.
    • Growing adipose tissue changes the hormone balance in men and disrupts sperm production.
    • Growing adipose tissue changes hormone balance disrupting the menstrual cycle.
    • Low-grade inflammation reduces sperm, egg and embryo quality.
  • PCOS (polycystic ovary syndrome) is the leading cause for infertility in women.


Underweight Impairs Fertility

A successful pregnancy requires a lot from women. A pregnant woman needs to supply the energy and nutrients to grow her uterus, breast tissue, and the fetus all while maintaining her own baseline nutritional needs. The woman’s metabolism will profoundly change, steering nutrients to those tissues and the fetus sometimes at the cost of her own health.

For these reasons it makes sense that a woman needs to have sufficient nutrient resources to support the pregnancy. If this is not the case because the woman is undernourished, hormonal regulations will kick in to prevent a pregnancy.

Primary infertility refers to couples who have not become pregnant after at least 1 year of having sex without using birth control methods. Secondary infertility refers to couples who have been able to get pregnant at least once, but now are unable to get pregnant again.


The key regulator is leptin. Once a woman loses enough weight to have a BMI lower than 18 or if the woman is losing weight rapidly leptin secretion from the adipose tissue declines. The lack of leptin  interferes with the hypothalamic-pituitary-gonadal (HPG) axis.

The HPG axis becomes active during puberty. In girls and women, the proper cyclic hormonal secretion regulates female fertility. The main components are:

  • Hypothalamus: involved in secretion of GnRH (gonadotropin-releasing hormone) which acts on
  • Pituitary gland: a small gland underneath the brain, to release LH (luteinizing hormone) and FSH (follicle stimulating hormones).
  • Ovary: LH and FSH act on the ovary to stimulate maturation and release of an egg. Those two hormones also regulate the production of estrogen and progesterone by prompting the to secrete estrogen and progesterone which are needed to grow the lining of the uterus— the endometrium (more about that in the pregnancy module).

In normal weight individuals, leptin signals sufficient energy stores to the hypothalamus which releases GnRH starting a menstrual cycle. In underweight women or after rapid weight loss the leptin blood levels are low. The hypothalamus has leptin receptors and registers a lack of leptin as “a pregnancy would be unwise at this point.”

The hypothalamus stops the secretion of  GnRH. Lacking GnRH stimulation reduces the release of  LH and FSH from the pituitary gland. The ovaries do not receive the needed stimulation to mature and release an egg, and the endometrium is not growing. The underweight woman will not ovulate (anovulation) and may not have a period (amenorrhea).  She becomes temporarily infertile.

Depending on the degree of underweight the woman may have irregular periods or no period at all. For most underweight women gaining some weight is often sufficient to restore fertility. This should be done by establishing healthy eating habits rather than eating high-calorie foods to increase weight rapidly.  Establishing healthy, regular eating will help ensure a healthy pregnancy as well.

Fertility in underweight men is less researched. There is some evidence that sperm count is lower in underweight men which might be connected to reduced fertility. Similar to women, the fertility in men may be improved upon gaining weight.


Obesity Impairs Fertility in Men And Women

In obesity leptin blood levels are increased which should stimulate the hypothalamus sufficiently to release GnRH. But you also learned that chronically high leptin blood levels trigger a counter regulation, leptin resistance. Leptin action will not be as efficient in obese individuals.

Leptin Resistance

• Failure of high leptin levels to reduce body weight: Leptin efficiency declines with increasing adipose tissue and high blood levels.
• LEPR, the leptin receptor, is functioning normally in most obese individuals (in contrast to insulin resistance)
• Actual mechanism is not quite clear – may be due to a decrease in leptin crossing the blood-brain barrier or a less sensitive receptor



The HPG axis regulates sperm production as well as fertility. The interaction and hormone secretion between the hypothalamus (GnRH), pituitary (LH and FSH), and gonads are similar. While women are born with all of their egg cells, men are continuously producing sperm. FSH stimulates healthy sperm growth while LH stimulates the Leydig cells to produce testosterone.

The testosterone stimulates growth and maturation of sperm but also feeds back to the hypothalamus to regulate the production of GnRH.

Growing adipose tissue causes an increase in leptin blood levels. This leads to overall leptin resistance which means that leptin is less efficient in regulating the HPG axis. Less effective leptin means less secretion of GnRH, less LH and less FSH. Both hormones are necessary to stimulate testosterone and androgen production which is in turn necessary for sperm production and maturation.


Fertility is not just impacted by leptin inefficiency. Several other mechanisms modulate sperm production and quality as well.

Growing obesity combined with a genetic pre-disposition leads to insulin resistance in many people. This increases circulating insulin which is also known to disrupt the HPG axis.

Androgens are needed to stimulate sperm production. Adipose tissue has an enzyme that converts androgens into estrogen. The more adipose tissue, the less androgens and the more estrogen are circulating in the blood stream. Obese men tend to have higher estrogen blood levels and this reduces fertility. In men estrogen has a negative effect on the hypothalamus by altering the release of gonadotropin releasing hormone (GnRH), resulting in suppression of FSH and LH secretions. The consequence is a lower sperm count. The effect is proportional to the degree of obesity.

Sleep apnea is another concern for many obese people. Sleep fragmentation has been proposed as the mechanism by which sleep apnea disrupts nocturnal testosterone rhythm.

Large adipose cells especially in visceral obesity start an inflammatory cycle (review obesity chapter as needed). Inflamed adipocytes signal the inflammatory state to other tissues by secreting cytokines.  The consequence is chronic low-grade inflammation. Cytokines disrupt the HPG axis but also reduce sperm quality.

The HPG disturbance and typical high estrogen and low testosterone blood levels over time, lead to secondary hypogonadism. Secondary hypogonadism presents with a reduced sperm count, lower fertility, and changed anatomical features.



In addition, growing adipose tissue around the gonads can insulate the testes. This increases temperature. The testicles need to remain about 4 degrees cooler than the body temperature to produce sperm. Higher temperature in the testes can lead to less sperm production.

Lastly, obese men have increased fatty acids blood levels. As we already discussed during the obesity and T2D chapter, free fatty acids are cytotoxic. Sperm is made of cells and free fatty acids can damage sperm cells just like any other cell. This, along with chronic inflammation, can lead to lower sperm quality.

Of course not every obese man is infertile, but the risk of becoming infertile increases with weight. Studies from North Europe show that infertility in obese men is 36 to 53% higher than in normal weight men.



In women obesity can lead to sub-fertility due to several mechanisms.



Ovulation and menstrual cycle: Looking at the reproductive physiology of obese women, leptin resistance, high insulin blood levels, increased estrogen and increased androgen levels disrupt the HPG axis in a similar way that is discussed in men. Less GnRH secretion reduces LH and FSH production. The reduced blood levels of LH and FSH suppresses ovulation and a regular menstrual cycle.

Secondly, low-grade inflammation and lipotoxicity due to increased free fatty acid blood levels, impact not only the HPG axis, but also reduce the egg or oocyte quality by damaging the DNA. We know this because obese women undergoing fertility treatment might ovulate, but the embryo resulting from this ovulation is of lower quality. This lower quality embryo is less likely to survive when implanted.

A proper balance of estrogen and progesterone stimulates the growth of a healthy endometrium (uterus lining) during the menstrual cycle. The disruption of the HPG axis leads to an endometrium that is less functional in supporting an early pregnancy. If the implantation is successful the placental function in obese women is often lower leading to a loss of the fetus or premature birth.


What can couples do if getting pregnant is not as easy due to obesity? The first step to restoring full fertility is starting a healthy lifestyle. An increase of fresh vegetables, fruits, legumes, and whole grains and a decreased intake of fast and processed foods should trigger a slow weight loss. Keep in mind that rapid weight loss will trigger a reduction of leptin blood levels and might reduce fertility in women for a while.

In addition, increased aerobic physical activity supports the dietary changes. Increased plant food intake and exercise will also reduce chronic inflammation and improve sperm and oocyte quality.

The discussion of fertility increasing foods is as old as humanity. However, scientific evidence only supports measures that help improve chronic systemic inflammation and oxidative stress. Next to antioxidants from plant food and aerobic exercise, evidence supports an increased intake of omega-3 fatty acids from seafood and some nuts. Both strategies are included in the Mediterranean diet which is sometimes recommended to improve fertility.


PCOS Is the Leading Cause For Infertility in Women

So far we have discussed how metabolic changes in obese women lower fertility. Sub-fertility does not mean that obese women cannot get pregnant at all, just that it is not as easy.

In the US up to 20% of women are affected by PCOS. 80% of women with PCOS are obese and the majority of those women have fertility problems. Now, the question is if the syndrome causes the obesity or if obesity causes the syndrome. This is an important question scientists haven’t answered yet, but for health care professionals this doesn’t matter as we will try to help the woman regardless.

PCOS is an endocrine disorder with a hormonal imbalance. Women with PCOS have increased androgen production while estrogen and progesterone production is decreased.

Visibly, women tend to have unusual hair growth in the face (hirsutism) and acne. Irregular periods and cysts (fluid filled sacks) on the ovaries reduce fertility.  Many women with the disorder have a family history of PCOS. They may also have a genetic disposition for insulin resistance and low-grade inflammation.

From studies, we know that a weight loss of 5–10 % will help many women with PCOS to restore fertility. Since those women tend to be insulin resistant, a low GI diet is recommended along with regular low to moderate intensity exercise.


Keep in mind that “weight” or “obesity” are a jargon term for us in metabolic health. By using these words we squeeze the entire adipose tissue chapter into those short words. We know that obesity and metabolic health are connected, but this is a development over years and with many other factors involved.

Obese 20-year old women and men might still be sufficiently metabolically healthy to conceive without a problem. When the same individuals try to get pregnant in their 30s they might have reached the threshold of metabolic health where fertility is impacted.

Weight certainly plays a role in fertility. There are additional controllable and uncontrollable factors that impact whether or not a couple can become pregnant. Couples can control various lifestyle factors such as alcohol consumption and smoking, but they do not necessarily have control over their access to health care, their age, and whether or not they have had previous pregnancies.

Other factors such as diet will be considered in the following chapter as we discuss how to prepare for a healthy pregnancy.


Interested In More Information?

Gaskins AJ, Chavarro JE. Diet and fertility: A review. Am J Obstet Gynecol. 2018; 218(4): 379 – 389

Editors: Nicole Legler, Sydney Christensen

NUTR251 Contributors:

  • Spring 2020: Justin Porreca, Kalen Codr, Dylan Fruhling, Bryce Heiser, Rose Davidson, Tim Gillespie
  • Fall 2020: Bryson Krull, Clare Caraghar



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Nutrition Through the Life Cycle by Sabine Zempleni and Sydney Christensen is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, except where otherwise noted.

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