‘To[o] much eating stifles the child’: fat bodies and reproduction in early modern England : Fat bodies and reproduction in early modern England

To examine the relationship between body mass index (BMI) and semen quality among young men from the general population. Cross-sectional study. Danish young men were approached when they attended a compulsory physical examination to determine their fitness for military service. From 1996-1998, 1,558 (19%) young men (mean age 19 years) volunteered. Semen volume (in milliliters), sperm concentration (in million per milliliter), percentage of motile spermatozoa, percentage of spermatozoa with normal morphology, total sperm count (in million), and testis size (in milliliters). In addition, serum reproductive hormones were measured. Serum T, sex hormone-binding globulin (SHBG), and inhibin B all decreased with increasing BMI, whereas free androgen index and E(2) increased with increasing BMI. Serum FSH was higher among slim men. After control for confounders, men with a BMI 25 kg/m(2) had a reduction in sperm concentration and total sperm count of 21.6% (95% CI 4.0%-39.4%) and 23.9% (95% CI 4.7%-43.2%), respectively, compared to men with BMI between 20-25 kg/m(2). Percentages of normal spermatozoa were reduced, although not significantly, among men with high or low BMI. Semen volume and percentage of motile spermatozoa were not affected by BMI. High or low BMI was associated with reduced semen quality. It remains to be seen whether the increasing occurrence of obesity in the Western world may contribute to an epidemic of poor semen quality registered in some of the same countries. If so, some cases of subfertility may be preventable. Show more

The 2009 Institute of Medicine (IOM) Committee to Reevaluate Gestational Weight Gain Guidelines concluded that there were too few data to inform weight-gain guidelines by obesity severity. Therefore, the committee recommended a single range, 5-9 kg at term, for all obese women. We explored associations between gestational weight gain and small-for-gestational-age (SGA) births, large-for-gestational-age (LGA) births, spontaneous preterm births (sPTBs), and medically indicated preterm births (iPTBs) among obese women who were stratified by severity of obesity. We studied a cohort of singleton, live-born infants without congenital anomalies born to obesity class 1 (prepregnancy body mass index [BMI (in kg/m(2))]: 30-34.9; n = 3254), class 2 (BMI: 35-39.9; n = 1451), and class 3 (BMI: > or =40; n = 845) mothers. We defined the adequacy of gestational weight gain as the ratio of observed weight gain to IOM-recommended gestational weight gain. The prevalence of excessive gestational weight gain declined, and weight loss increased, as obesity became more severe. Generally, weight loss was associated with an elevated risk of SGA, iPTB, and sPTB, and a high weight gain tended to increase the risk of LGA and iPTB. Weight gains associated with probabilities of SGA and LGA of < or =10% and a minimal risk of iPTB and sPTB were as follows: 9.1-13.5 kg (obesity class 1), 5.0-9 kg (obesity class 2), 2.2 to <5.0 kg (obesity class 3 white women), and <2.2 kg (obesity class 3 black women). These data suggest that the range of gestational weight gain to balance risks of SGA, LGA, sPTB, and iPTB may vary by severity of obesity. Show more

The obesity pandemic has grown to concerning proportions in recent years, not only in the Western World, but in developing countries as well. The corresponding decrease in male fertility and fecundity may be explained in parallel to obesity, and obesity should be considered as an etiology of male fertility. Studies show that obesity contributes to infertility by reducing semen quality, changing sperm proteomes, contributing to erectile dysfunction, and inducing other physical problems related to obesity. Mechanisms for explaining the effect of obesity on male infertility include abnormal reproductive hormone levels, an increased release of adipose-derived hormones and adipokines associated with obesity, and other physical problems including sleep apnea and increased scrotal temperatures. Recently, genetic factors and markers for an obesity-related infertility have been discovered and may explain the difference between fertile obese and infertile obese men. Treatments are available for not only infertility related to obesity, but also as a treatment for the other comorbidities arising from obesity. Natural weight loss, as well as bariatric surgery are options for obese patients and have shown promising results in restoring fertility and normal hormonal profiles. Therapeutic interventions including aromatase inhibitors, exogenous testosterone replacement therapy and maintenance and regulation of adipose-derived hormones, particularly leptin, may also be able to restore fertility in obese males. Because of the relative unawareness and lack of research in this area, controlled studies should be undertaken and more focus should be given to obesity as an etiolgy of male infertility. Show more