READY FOR FERTILITY is the product of the Rinehart Fertility Center and was designed to assist patients with PCOS and/or an elevated BMI to achieve healthier lifestyles through diet, exercise and one-on-one coaching. Learn more about this innovative program from patients who enrolled and are being highlighted here!

A 2017 study demonstrated that a 12-week diet and exercise program improved cumulative pregnancy rates in IVF from 30 % to 60%. The Rinehart Fertility Center recently launched just such a program – Ready for Fertility™ – to help patients achieve greater success.

Designed for patients with polycystic ovarian syndrome (PCOS) and an elevated BMI, this novel program is a three month exercise, diet, and mentoring program for patients undergoing ART.

More information on Ready for Fertility™ is available by calling 630-366-5100.

Diet Impacts Fertility in Patients who are Overweight and have Polycystic Ovarian Syndrome

A new study published in the October issue of the Journal of Clinical Endocrinology and Metabolism (1) confirms that: “diet is an effective, acceptable, and safe intervention for relieving insulin resistance ….” Why is this so significant? Because insulin resistance is a primary factor in the cause of polycystic ovarian syndrome (PCOS).

PCOS is a metabolic disease in women which impacts multiple systems. At its core, PCOS is a syndrome of increased intra-ovarian androgens. The pathway to that endpoint and the clinical manifestations of the result are very diverse but insulin resistance is a key road on that path.

Insulin resistance is simply when insulin becomes less effective in controlling blood glucose (sugar) levels. Usually, to maintain a normal glucose level, the body releases more insulin. This response is fine for the control of the blood sugar – but not so good for the ovary. Increased insulin causes the ovary to make increased amounts of testosterone, which may affect the development of the egg. Testosterone is also released into the blood stream where it is converted by adipose (fat) tissue into estrogen which interferes with the normal hormonal control of the menstrual cycles – leading to irregular menstrual cycles. So, eggs and cycles are not optimal for fertility. In addition, the altered hormonal pattern can affect the lining of the uterus (endometrium), such that the time when the endometrium is able to accept an embryo (implantation window) can be altered.

Finally, the increased amount of androgen released by the ovary may cause an increase in a woman’s inflammatory status. This is significant for late-onset disease complications such as the cardio-vascular risk from PCOS. For the infertile woman, the increased inflammatory state may also raise the risk that an embryo will not implant or increase the miscarriage rate.

Insulin resistance is directly related to obesity. Obesity reduces a woman’s chance to have a child in a direct relationship to the BMI. Simply, the greater the BMI, the lower the overall chance to have a child.

Obesity takes its toll

Obesity is a major health risk that is increasing in frequency. It is associated with several adverse health risks such as adult- onset diabetes, cardio- vascular disease, and hypertension. In the US today, over 25% of women in the reproductive age are obese and in Mexico, that number is closer to 50%. Considering how frequently obesity occurs and the serious health consequences of being obese, it is surprising (and for those of us with weight-control issues, it is infuriating) that there are no successful long-term treatments for obesity. So, who is considered “obese?” Obesity is an excess body weight for a given height. Body mass index (BMI) is the most frequently measurement used to define obesity. A BMI (Weight in kg/ height in m2) of over 25 is considered overweight, over 30 -34 obese class 1, 35-39 obese class 2, and > 39 as obese class 3 (sometimes referred to a morbidly obese). A 5’5” woman weighing 130 pounds has a BMI of 21.6. A woman of the same height weighing 150 has a BMI of 25 and is considered overweight.

The recently published study demonstrated that diet was significantly related to improvements in insulin resistance. Arguably, improving insulin resistance could reduce intra-ovarian androgens.  This may create a more normal physiology, which could significantly improve pregnancy rates.

(1)Yujie Shang, Huifang Zhou, Minghui Hu, Hua Feng, Effect of Diet on Insulin Resistance in Polycystic Ovary Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 105, Issue 10, October 2020, Pages 3346–3360,

(2)Espinós JJ, Polo A, Sánchez-Hernández J, Bordas R, Pares P, Martínez O & Calaf J. Weight decrease improves live birth rates in obese women undergoing IVF: a pilot study. Reproductive BioMedicine Online 2017 35 417–424. rbmo.2017.06.019 10 

Dr. John Rinehart MD, Ph.D. has been trained in both reproductive endocrinology and andrology at Brigham and Women’s Hospital of the Harvard Medical School. Dr. Rinehart is accepting new patients in his practices at the Oak Lawn (630-366-5100) and Hinsdale (630-366-5100) offices.

Weight and Fertility

Weight seems to have a negative influence on fertility. There certainly are women who are overweight, achieve a pregnancy easily, and have children. But if a woman is having problems conceiving and she is overweight, she may want to consider that her weight is part of the problem.

Does increased weight reduce a woman’s chance of conceiving?

What does it mean to be overweight? The World Health Organization (WHO) defines overweight as a Body Mass Index (BMI) as > 25 kg/m2 and obese as a BMI >30 kg/m2. Presently, in the US it is estimated that >25% of the women in the reproductive age range are obese. Obesity is associated with a problem where women have either no periods (menses) or very irregular menses. Most of these women have polycystic ovarian syndrome (PCOS). For women with PCOS who are obese, over 70-90% have weight-related insulin resistance, which just means that because of their weight their insulin is inefficient and they release more insulin than they should. However, women who have fairly regular menses but are overweight also have a reduced chance of conceiving due to their weight. A study by van der Steeg  (Hum,. Reprod. 2008)  established a reference range for women of a BMI between 21 And 29 kg/m2. Compared to this reference range, women with a BMI >35 had a 26% less chance of spontaneously conceiving. For women whose BMI was >40 kg/m2, the reduction in the chance of having a spontaneous pregnancy was 43%. Looked at in a different way, even if a woman’s BMI was >40 kg/m2, she had a 57% chance of conceiving. However, when woman conceive spontaneously, they do so quickly- usually within three to six months. So, if a woman has been trying for over a year to conceive, and she has not been successful AND her BMI is >35 or 40 kg/m2, it just might be the weight that is the problem. In practical terms, if a woman has been trying to conceive for over year and there is nothing else wrong, but she is 5’3” and weighs more than 165 lbs., her weight might be preventing her from conceiving. For a woman 5’5”, the critical (maximum) weight is about 175 lbs., and for women 5’7”, the critical weight is 185 lbs.

Notice that one of the caveats is that all other things are normal. Achieving a successful pregnancy requires a number of things to be normal. Therefore, before deciding that weight is the problems, a woman needs to eliminate male factor as part of the problem. Also, she needs to have normal anatomy (structure) to conceive, so some form of an evaluation of the structure of the uterus, ovaries, and fallopian tubes is required. Sometimes there will be more than one factor reducing a woman’s chance of conception, so attention to all factors will increase the person’s chance for conception.

Why is weight control such a problem?

A major factor influencing weight is genetic. Some studies show that up to 60-70% of obesity is hereditary. For hereditary factors, there has to have been an evolutionary reason for the problem. A commonsense explanation would be that the early ancestors of humans lived in an environment of calorie scarcity, so there was no need to regulate…no one was obese. However, comforting that explanation is, it seems to be wrong. Currently there are three major theories about the evolutionary genetic control of weight. The most comprehensive sees the genetic evolution of weight as a balance between calorie seeking and weight reduction. The argument for weight reduction suggests that as weight increases, animals become slower and thus more susceptible to predators. While that seems fantastical, there is evidence that early hominids were a favorite food for saber-tooth tigers, so looking at the problem from an early Sapiens perspective, being overweight might just be a fatal flaw. On the other hand, increased weight has been associated with increased ability to fight disease. Again, not such a big deal today, but as an early Sapiens, staying healthy was no minor feat. The hypothesis says that the two situations are controlled by different mechanisms. The drive to gain weight involves the hormone Leptin, and suggests that there is a set-point weight below which leptin will drive calorie seeking. The control of the upper limit is not leptin dependent, but the actual control is not currently defined. The sum of this theory is that weight control is much like a wide highway where weight can vary between extremes, but that overall, there is a constant genetically determined direction.

The significance of these theories is that for the short term, people can control their weight. However, over the long- haul, weight is genetically determined and very difficult to alter.