Insulin Resistance and Fertility: Part 1
Fertility, PCOS, Uncategorized | POSTED November 13, 2013
Part 1: of Insulin Resistance and Fertility
Originally published by Dr. Fiona McCulloch in Naturopathic Currents in September 2013, you can read the original article here.
This article has been broken down into a four part series, links to the other parts of this series are listed below:
- Part 2 covers How does Insulin Resistance affects Fertility
- Part 3 covers Diet and Exercise Interventions for Insulin Resistant Fertility Concerns
- Part 4 covers Supplements for Insulin Resistance and Fertility
Insulin Resistance and Fertility
Insulin resistance and fertility are linked in different ways. This 4 part series will go through in detail and with research driven information on how insulin, a key hormone, can seriously disrupt normal female hormonal balance and overall fertility. I will also go through naturopathic treatments which can help to restore healthful sensitivity to insulin. Insulin resistance is actually very common. It affects 10% of young adults and nearly 44% of adults in mid-life.(1) We now know that genetics play an important role in insulin resistance. Diet, exercise and body composition are also key factors, and modern lifestyle has definitely contributed to the sharp rise of this condition and it’s subsequent negative effects on fertility.
What is Insulin Resistance?
Insulin resistance is defined by a state where the cells in the body do not respond normally to insulin. Left unchecked over time, insulin resistance can result in what is known as metabolic syndrome, a constellation of problems including high blood pressure, high triglycerides, low HDL (good cholesterol), and abdominal obesity. Before it gets to this extreme point however, it can impact health and has been documented to have various negative effects on fertility.
Let’s start with a brief overview of the function of insulin in the body. Insulin is produced by the beta cells of the pancreas. Insulin causes fat, liver and muscle cells to take up and store glucose from the blood. In fat cells, glucose is stored as triglycerides, and in muscle and liver cells, it is stored as glycogen. In fat cells, insulin resistance causes the breakdown of stored triglycerides. In short, insulin takes the sugar from the blood and moves it into the cells to be stored.
When the body’s cells do not respond normally to insulin, the blood sugar levels also do not respond in an ideal way. The pancreas attempts to re-establish normal blood sugar by producing extra insulin in response to eating a meal – resulting in high blood insulin levels overall. High insulin can cause a variety of negative effects on female fertility including causing the section of higher levels of androgens (male hormones), other hormonal imbalances, and detrimental inflammatory effects. High insulin is thought to be an underlying cause of polycystic ovarian syndrome (PCOS), and it also contributes to fertility concerns such as recurrent miscarriage, inflammatory implantation failure, and obesity.
Diagnosis of Insulin Resistance
Insulin resistance can be measured by several methods. The gold standard is known as the hyperinsulinemic euglycemic clamp, which measures the amount of glucose necessary to compensate for increased insulin levels. This test is rarely performed in a clinic setting as it is a difficult test to perform.
Another method for measuring insulin resistance is the HOMA-IR index.(2) The HOMA-IR index is a special calculation that compares the fasting glucose and the fasting insulin levels. Oral glucose tolerance testing and HBA1C levels can also be used as assessments for insulin resistance. This is a simple test that I perform often in the clinical setting and it can give a good overview as to the level of insulin resistance in a patient.
Causes of Fertility Related Insulin Resistance
In PCOS, it is thought that there is an underlying, possibly genetic defect within the theca cells, the male hormone producing cells, of the ovary. This makes the ovary produce excessive amounts of male hormones when exposed to insulin. Patients with PCOS often have a family history of type 2 diabetes. There may also be other women in the family with PCOS, evidenced by irregular menstrual cycles or difficulty in conceiving.
High body mass index (BMI) and deposits of abdominal body fat are also associated with insulin resistance. Abdominal body fat is actually related to fat that is stored around the organs and inside the abdominal cavity.
Free fatty acids are released more easily from abdominal fat deposits than from other areas in the body where fat is stored. These fatty acids affect the liver, causing it to release glucose, produce LDL (bad) cholesterol, and block the removal of insulin from the body.(3) Together these contribute to insulin resistance even further.
Poor diet can also promote insulin resistance in the body. A high fat, high simple carbohydrate, and low fibre diet has been repeatedly documented to induce insulin resistance and metabolic syndrome.(4, 5) It has also been suggested that a high fructose diet (containing soda, candy, and other high fructose corn syrup products) causes the liver to make triglycerides, causing metabolic syndrome which is associated with serious health risks.(6, 7)
Insulin resistance is a common condition with a variety of causes ranging from genetics to lifestyle. High levels of insulin can create negative changes in our health that put us at risk for serious conditions including cardiovascular disease, diabetes, infertility, and obesity.
Part 2 of this article will focus on the specific ways that insulin resistance affects healthy fertility.
- Beck-Nielsen H. General characteristics of the insulin resistance syndrome: prevalence and heritability. EuropeanGroup for the study of Insulin Resistance (EGIR). Drugs. 1999;58Suppl 1:7-10; discussion 75-82.
- Haffner SM, Miettinen H, Stern MP. The homeostasis model in the San Antonio Heart Study. Diabetes Care. 1997 Jul;20(7):1087-92.
- Björntorp P. Visceral obesity: a “civilization syndrome”. Obes Res. 1993 May;1(3):206-22.
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