Obesity and Reproduction

Obesity and Reproduction

Obesity seems to have a significant impact on the ability of a woman to become pregnant. The chances of having an ovulatory problem, receiving infertility treatment, and miscarriage increases by three-fold in the obese population. The problem does not stop there. In pregnancy, obese women have 3-4x greater chance of developing gestational diabetes, preeclampsia, and experiencing preterm birth. Their babies have 3-4x higher incidence of birth defects and macrosomia (large body size). The chance of stillbirth doubles.

There have been several studies confirming these observations. One of them found that for obese women with regular menstrual cycles, the time to achieve pregnancy was prolonged by 5 % for every 10 pounds of body weight increase. Even advanced fertility treatment is not as successful for obese women with or without polycystic ovaries, resulting in a 15 – 22 % reduction in live birth rate. Therefore, it is important to improve the chances of becoming pregnant by reducing body weight (BW). How to do that has become a persistent question. Can insulin help create obesity? Is insulin responsible for obesity?

Obesity is not uncommon in patients that have infertility, especially those who have been diagnosed with polycystic ovaries (PCO). They are asked to reduce their BW in order to increase their chances of becoming pregnant. In many instances, this task is placed on them. The patients have to select one of the available diets and an exercise program to reduce caloric intake and increase energy expenditure. In the recent past, medications such as Ozempic, that were originally designed to combat diabetes and have unpredictable side effects, have been utilized.

It goes without saying that no one willingly becomes overweight or obese. So what is the underlying cause?. It was noticed that several patients that are either overweight or obese and have PCO appearing ovaries, are also insulin resistant (IR). That means they produce more insulin than is required for their metabolic needs. Could the insulin be the culprit?

A genetic technique was used to study the role of insulin in the increase of the BW. The instructions for the functions of our body are in our DNA, in the form of genes. For each instruction, there are two identical genes, just in case something goes wrong with one of them. In this event, the other copy is present and fulfills the assigned function of the body. Of course when only one gene is available (expressed) that function is not in full capacity.

When one of the two genes is defective, this is called a mutation. Indeed, mutations happen spontaneously in nature and several mutations are known to exist. Scientists can remove one gene, causing an artificial mutation for that particular gene. This technique has been used for several years in laboratory animals to study the functions of the genes and is called ‘Knockout”. There are several laboratory knockout mice lines that are used for that purpose.

The mouse species has the same gene that is identical to that of the human insulin gene. Recently, scientists at the University of Columbia studied two groups of mice. One that had both gense of insulin expressed and another one that had only one functioning gene. One that produced a normal amount of insulin and another one that produced less than a normal amount. They fed them with a diet that typically leads to obesity, fat accumulation in the liver, and increased insulin level. Both groups of mice consumed the same amount of food, but only the mice with both functioning genes experienced the results of high caloric intake. The mice with only one gene did not become obese and did not have any of the expected results of their diet. Surprisingly their glucose levels were normal, despite their food intake and the decreased amount of insulin produced.

After looking further into the underlying mechanism that caused this unexpected discrepancy, they found that the mice with only one gene had a higher level of uncoupling protein 1 (UP1) in their adipose tissue, leading to an increase in burning and waste of the nutrients, rather than storing them into their fat. So, it seems that a decreased amount of insulin favors burning of extra calories rather than storing them. This is the first time that insulin was associated with an adverse effect on energy expenditure. Up until this time, it was believed that insulin causes fat storage directly. By decreasing insulin, the BW can be decreased and caloric restrictions alone through diets are not effective.

The high levels of UP1 can be achieved as well through Irisin, a hormone that is produced from the muscle during exercise. If one exercises systematically for 10 days the level of Irisin doubles in the blood.

Based on this information, it is incredibly important to determine if a woman produces excessive amounts of insulin and how to manage this condition appropriately with medical nutrition therapy (MNT), rather than trying to achieve the same results via one of the available commercial diets. A prescribed exercise program and medications that decrease the insulin production may be used in conjunction to help patients achieve more rapid results.

At DVIFG, we implement a program that encompasses these three approaches simultaneously. Over the years, we have been successful in achieving our goal of BW reduction, and a significant improvement in fertility treatment.