Obesity and fertility

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

Obesity is defined as an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight.[1] 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.[2] 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.[3]

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.[4] Obesity can have particularly damaging effects in young women as they begin menstruating earlier than non-obese girls, essentially enhancing the defects associated with obesity and fertility.[4] Obesity also affects 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.[5] Leptin is also a product of the obese gene.[6] Leptins interaction with the hypothalamus decreases appetite, therefore a mutation in the obese gene would result in an increased appetite, leading to inevitable obesity.[7] 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.[5] Pre-pubertal individuals that lack leptin fail to reach the pubertal stage.[6] If given leptin administratively, the mutation would be reversed and puberty resumed.[6] Leptin is further expressed in mature follicles produced by the ovary,[5] suggesting it plays a role in oocyte maturation, hence embryo development.

Increasing body weight is also thought to be linked to the development of polycystic ovary syndrome (PCOS).[7] There are specific aspects associated with PCOS allowing an indication of diagnosis of the syndrome including hyperandrogenism (hirsutism), irregular periods, anovulation and subfertility.[citation needed] Obesity in PCOS sufferers amplifies hormonal and metabolic decline,[7] therefore damaging fertility and oocyte quality in women. PCOS can also have an effect if conception is successful through assisted reproductive technology (ART) in obese patients, leading to an increase in miscarriage rates.[8]

Polycystic ovarian syndrome[edit]

PCOS is a very common endocrine disorder among women who are reproductively active. Hyperandrogenism is a medical condition where there are excessive levels of androgens in the body. It is associated with PCOS. Studies have shown that hyperandrogenism could be caused by a reaction between ovarian theca cells and reactive oxygen species. Obesity interferes with the HPA axis and stops follicular maturation. Hyperandrogenism has a disturbing effect on this process and could cause anovulatory cycles. Currently, therapy is aimed at patients that need to improve their resistance to insulin so that hyperinsulinemia is reduced and ovulatory features in women are improved. According to recent studies, insulin-sensitiser drugs are the main type of therapy for women with irregular cycles that want to improve their fertility, although weight loss is normally the first step in overweight patients with PCOS.[9]


Obese men have a lowered sperm count which effectively lowers their chance of conceiving a child.
Sperm count and its relationship to pregnancy rate

Obese men have lower circulating testosterone which affects sperm production known as spermatogenesis.[10] This affects the quantity and quality of a mans sperm. Obese men have increased risk of oligozoospemia, having fewer than 15 million sperm per millilitre of semen, and far fewer motile sperm than a man of healthy weight.[11] Sperm with high amounts of damaged DNA are significantly more common in obese men than in normal weight men.[12] Ejaculate volume is also affected. Altered male hormones can also give erectile dysfunction which is the major cause of infertility in obese men.[13]



Preventing or treating obesity in women has a positive effect on fertility rates. As simple as modifying lifestyle choices in order to lose weight could lead to a recovery in fertility decline.[14] Taken into consideration firstly must be the weight of the individual before investigating further into complications surrounding fertility.[15] Initially, treatment should proceed for obesity, then if complications still arise with infertility then progression onto ART is required.[15] There are many other ways of reducing body fat including modifying diet or administrating diet pills, increasing energy expenditure, or surgically removing abdominal fat/surgical fitting of a gastric band in order to subside excess abdominal weight.[15] Restoration of fertility should follow these modifications. A weight-loss study was carried out of 13 individuals over a 6-month period.[14] 12 of the 13 previously infertile subjects restored ovulation whilst 11 subjects were able to conceive after the programme had ended. This study demonstrates weight loss to be the primary source of treatment for obesity and fertility problems before ART. A further study enhances this idea with 80% of females having regular menstrual cycles and conception rate was 29% after modifications.[16]


The effects of obesity on male fertility can be reversed, either with testosterone therapy, or weight loss.[10] Testosterone therapy is likely to improve hormone imbalances and treat erectile dysfunction.[13] Weight loss can be achieved through lifestyle changes such as a reduced calorie diet, regular exercise and quitting smoking. Trained healthcare professionals and weight loss groups may also be beneficial. People struggling to keep to these lifestyle changes may seek other methods such as medication known as orlistat or weight loss surgery.[17]



It is common practise for body condition scoring to be used in domesticated animals to assess the fatness of an animal and is often used by vets and livestock handlers to determine whether the animal need more or less energy. Both a low and a high score can reduce an animal's fertility.

Cattle that are over-conditioned are also more insulin resistant compared to their leaner counterparts.[18] As demonstrated in mice, insulin resistance is a factor in poor fertility as it has an effect on oocyte development.[19] This in turn means that less oocytes are suitable for fertilisation and fertility is impaired.

Another reason for decrease in fertility is to do with leptin. Leptin is a hormone which production is increased in obese animals. In cows, leptin can inhibit thecal cells from producing adrostenediol and progesterone.[20] Androstenediol is important in fertility as it is the precursor to oestrogen. Without oestrogen production, the balance of hormones is affected and there is no LH surge which is required for ovulation.[21]

Domestic Fowl[edit]

Domestic fowl has previously been researched on and it was found that by over feeding but not force feeding the male birds, there was no effect on fertility.[22] However, more recently a study has shown that obesity induced by force feeding can affect the number of spermatozoa and their motility in the male birds. It was also found that in two of the three birds, there was an decrease in testosterone and an increase in LH which suggests the pathway of why there might be reduced spermatozoa.[23]


Many women who have PCOS are also obese and it is estimated that the prevalence of obesity in women with PCOS is 35 - 63%.[24] It has also been shown that there is a relative risk of anovulatory infertility in amongst the obese population is 2.7%. For those who are obese and are ovulatory, for each unit increase in BMI over a BMI of 32 kg/m2 at the age of 18, there is a reduction of spontaneous conception rate by 5%.[7]


  1. ^ "obesity". The Free Dictionary.
  2. ^ "Obesity and overweight". World Health Organization. Retrieved 2016-09-28.
  3. ^ Pasquali R, Patton L, Gambineri A (December 2007). "Obesity and infertility". Current Opinion in Endocrinology, Diabetes and Obesity. 14 (6): 482–7. doi:10.1097/MED.0b013e3282f1d6cb. PMID 17982356.
  4. ^ a b Brannian JD (July 2011). "Obesity and fertility". South Dakota Medicine. 64 (7): 251–4. PMID 21848022.
  5. ^ a b c Mitchell M, Armstrong DT, Robker RL, Norman RJ (November 2005). "Adipokines: implications for female fertility and obesity". Reproduction. 130 (5): 583–97. doi:10.1530/rep.1.00521. PMID 16264089.
  6. ^ a b c Johnson MH (2012-12-14). Essential Reproduction. John Wiley & Sons. ISBN 9781118423882.
  7. ^ a b c d Pandey S, Pandey S, Maheshwari A, Bhattacharya S (May 2010). "The impact of female obesity on the outcome of fertility treatment". Journal of Human Reproductive Sciences. 3 (2): 62–7. doi:10.4103/0974-1208.69332. PMC 2970793. PMID 21209748.
  8. ^ Wang JX, Davies MJ, Norman RJ (December 2001). "Polycystic ovarian syndrome and the risk of spontaneous abortion following assisted reproductive technology treatment". Human Reproduction. 16 (12): 2606–9. doi:10.1093/humrep/16.12.2606. PMID 11726582.
  9. ^ Laganà AS, Rossetti P, Buscema M, La Vignera S, Condorelli RA, Gullo G, et al. (2016-08-04). "Metabolism and Ovarian Function in PCOS Women: A Therapeutic Approach with Inositols". International Journal of Endocrinology. 2016: 6306410. doi:10.1155/2016/6306410. PMC 4989075. PMID 27579037.
  10. ^ a b Stokes VJ, Anderson RA, George JT (May 2015). "How does obesity affect fertility in men - and what are the treatment options?". Clinical Endocrinology. 82 (5): 633–8. doi:10.1111/cen.12591. PMID 25138694.
  11. ^ Hammoud AO, Wilde N, Gibson M, Parks A, Carrell DT, Meikle AW (December 2008). "Male obesity and alteration in sperm parameters". Fertility and Sterility. 90 (6): 2222–5. doi:10.1016/j.fertnstert.2007.10.011. PMID 18178190.
  12. ^ Chavarro JE, Toth TL, Wright DL, Meeker JD, Hauser R (May 2010). "Body mass index in relation to semen quality, sperm DNA integrity, and serum reproductive hormone levels among men attending an infertility clinic". Fertility and Sterility. 93 (7): 2222–31. doi:10.1016/j.fertnstert.2009.01.100. PMC 2864498. PMID 19261274.
  13. ^ a b Pasquali R, Patton L, Gambineri A (December 2007). "Obesity and infertility". Current Opinion in Endocrinology, Diabetes and Obesity. 14 (6): 482–7. doi:10.1097/MED.0b013e3282f1d6cb. PMID 17982356.
  14. ^ a b Clark AM, Ledger W, Galletly C, Tomlinson L, Blaney F, Wang X, Norman RJ (October 1995). "Weight loss results in significant improvement in pregnancy and ovulation rates in anovulatory obese women". Human Reproduction. 10 (10): 2705–12. doi:10.1093/oxfordjournals.humrep.a135772. PMID 8567797.
  15. ^ a b c Zain MM, Norman RJ (March 2008). "Impact of obesity on female fertility and fertility treatment". Women's Health. 4 (2): 183–94. doi:10.2217/17455057.4.2.183. PMID 19072520.
  16. ^ Hollmann M, Runnebaum B, Gerhard I (September 1996). "Effects of weight loss on the hormonal profile in obese, infertile women". Human Reproduction. 11 (9): 1884–91. doi:10.1093/oxfordjournals.humrep.a019512. PMID 8921059.
  17. ^ "Treating Obesity". NHS. 2017-10-23.
  18. ^ Sinclair K. "Declining fertility, insulin resistance and fatty acid metabolism in dairy cows : Developmental consequences for the oocyte and pre-implantation embryo". Acta Scientiae Veterinariae. 38 (supl 2): 545–557.
  19. ^ Ou XH, Li S, Wang ZB, Li M, Quan S, Xing F, et al. (July 2012). "Maternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes". Human Reproduction. 27 (7): 2130–45. doi:10.1093/humrep/des137. PMID 22556376.
  20. ^ Spicer LJ, Francisco CC (January 1998). "Adipose obese gene product, leptin, inhibits bovine ovarian thecal cell steroidogenesis". Biology of Reproduction. 58 (1): 207–12. doi:10.1095/biolreprod58.1.207. PMID 9472942.
  21. ^ Baird DT, Swanston IA, McNeilly AS (June 1981). "Relationship between LH, FSH, and prolactin concentration and the secretion of androgens and estrogens by the preovulatory follicle in the ewe". Biology of Reproduction. 24 (5): 1013–25. doi:10.1095/biolreprod24.5.1013. PMID 6791711.
  22. ^ Parker JE, Arscott GH (February 1972). "Obesity and fertility in a light breed of domestic fowl, Gallus domesticus". Journal of Reproduction and Fertility. 28 (2): 213–9. doi:10.1530/jrf.0.0280213. PMID 5058261.
  23. ^ Nir I, Waites GM, Cunningham FJ (September 1975). "Obesity induced by force-feeding and accompanying changes in body temperature and fertility in the male domestic fowl". British Poultry Science. 16 (5): 505–15. doi:10.1080/00071667508416219. PMID 1156930.
  24. ^ Wilkes S, Murdoch A (July 2009). "Obesity and female fertility: a primary care perspective". The Journal of Family Planning and Reproductive Health Care. 35 (3): 181–5. doi:10.1783/147118909788707995. PMID 19622210.