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Obesity and fertility


Obesity is defined as an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. This is often described as a body mass index (BMI) over 30. However, BMI does not account for whether the excess weight is fat or muscle, and is not a measure of body composition. For most people, however, BMI is an indication used worldwide to estimate nutritional status. Obesity is usually the result of consuming more calories than the body needs and not expending that energy by doing exercise. There are genetic causes and hormonal disorders that causes people to gain significant amounts of weight but this is rare. People in the obese category are much more likely to suffer from fertility problems than people of normal healthy weight.

A report carried out by the Nurses Health Study demonstrated an increased risk of anovulation in women with an increasing BMI value. Its major effects include a reduction in ovulation rate, a decline in oocyte quality, menstrual irregularities, a decreased pregnancy rate and a rise in miscarriages. Obesity can have particularly damaging effects in young women as they begin menstruating earlier than normal girls, essentially enhancing the defects associated with obesity and fertility. Obesity also has an impact on fertility in men.

The hormones involved in the reproductive system are negatively affected with an increase of weight. In humans, via white adipocytes (fat cells), production of the hormone leptin (an adipokine) acts on the hypothalamus where reproductive hormone Gonadotrophin-releasing hormone (GnRH) is produced. Leptin is also a product of the obese gene. Leptins interaction with the hypothalamus decreases appetite, therefore a mutation in the obese gene would result in an increased appetite, leading to inevitable obesity. Leptin has been found to be linked to the HPG axis as it can induce the release of GnRH by the hypothalamus and subsequently follicle stimulating hormone (FSH) and leutinising hormone (LH) by the anterior pituitary.Pre-pubertal individuals that lack leptin fail to reach the pubertal stage. If given leptin administratively, the mutation would be reversed and puberty resumed. Leptin is further expressed in mature follicles produced by the ovary, suggesting it plays a role in oocyte maturation, hence embryo development.


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