Several studies have established the effect of obesity (BMI >30 kg/m2) on female fertility as well as on ART treatment outcomes; however, the mechanism underlying the association is still obscure. Now, a recent study published in the journal Reproduction, sheds more light on the impact of obesity on the major reproductive mechanisms and infertility treatment.
The key study findings reported by Christopher James Brewer and Adam H Balen from The Leeds Centre for Reproductive Medicine, United Kingdom, are as follows:
• Reduced chances of conception per cycle, especially in those suffering from central obesity
• Disruptions in the hypothalamic-pituitary ovarian axis and irregular menstrual cycle
• Three-fold increased risk for oligo-/anovulation
• Altered in vivo hormonal milieu, which regulates follicular development and oocyte maturation
• Increased production of hormone leptin by adipocytes
• Association of increased leptin production with reduced fecundity
• Impaired endometrial development, ovulation, and implantation
• Defective response to ART treatments
The researchers observed a more severe phenotype and enhanced risk for subfertility in obese women suffering from polycystic ovary syndrome (PCOS). The study also substantiated the positive effect of weight reduction through lifestyle modification or bariatric surgery in re-establishing menstrual cyclicity, ovulation, as well as enhancing the chances of conception.
An earlier review published by Mitchell et al (Reproduction, 2005) suggested the role of adipokines, including adiponectin and resistin, apart from leptin, in causing fertility impairment in obese women. The researchers reported that defective leptin production contributes to altered gonadotropin-releasing hormone (GnRH) and gonadotropin secretion, and also affects the normal functioning of the ovary and endometrium. Resistin aids in maintaining placental and ovarian function. Additionally, its localization in the brain exerts peripheral and central effects in the regulation of fertility and energy metabolism. The researchers did not find any evidence to substantiate findings of adiponectin being vital in maintenance of fertility. However, the discovery of adiponectin receptors expression in the ovary, and the hormone signaling in other peripheral tissues, is expected to open up new avenues for further elucidating its role in reproduction.
Considering the adverse effects of obesity on reproductive outcomes, the British Fertility Society issued policy and practice guidelines in 2007, for treating such patients. The key guidelines are mentioned below.
• Prior to the initiation of any fertility treatment, the patient should take necessary steps to attain a normal BMI.
• The treatment should be postponed till the patient achieves a BMI of <35 kg/m2.
• In patients below 37 years of age with normal serum FSH level, the preferred BMI is <30 kg/m2.
However, several studies oppose the deferring of fertility treatment based on BMI. In one such recent study, Pandey et al (Human Reproduction, 2010) reported that considering BMI as criterion for limiting fertility treatment may contribute to increase in stigmatization, inequity, social tension, and injustice among obese infertile patients.
1. Brewer CJ, Balen AH. The adverse effects of obesity on conception and implantation. Reproduction. 2010 Apr 15. [Epub ahead of print]
2. Mitchell M, Armstrong DT, Robker RL, Norman RJ. Adipokines: implications for female fertility and obesity. Reproduction. 2005 Nov;130(5):583-97.
3. Balen AH, Anderson RA; Policy & Practice Committee of the BFS. Impact of obesity on female reproductive health: British Fertility Society, Policy and Practice Guidelines. Hum Fertil (Camb). 2007 Dec;10(4):195-206.
4. Pandey S, Maheshwari A, Bhattacharya S. Should access to fertility treatment be determined by female body mass index? Hum Reprod. 2010 Apr;25(4):815-20.