Title: Body size and fertility


Key words: body weight, fertility, pregnancy, reproduction, reproductive failure, weight disorders, hunger, protein, foetal, development, placental development, protein, carbohydrate, fat, micronutrients, macronutrients, live birth weight, starvation, ovulation, anorexia, obesity, diet, exercise, infertility, diabetes, abortion, macrosomia, abnormalities, polycystic ovary syndrome, pre-eclampsia, preeclampsia, BMI, vitamin C, folate, zinc, calcium, iron, homocysteine, preconceptual, supplementation, reproductive health, leptons, neuropeptide Y, GnRH, hypothalamus, ovulation, undernutrition, exercise


Date: Sept 2006


Category: Reproduction


Nutrimed Module:


Type: Article


Author: Morgan, G


Body size and fertility


Both low and high body weight are known to effect fertility and the outcome of pregnancy. Eating disorders in this country are now widespread leading to an increasing problem of reproductive failure. This review will comment on the nutritional and hormonal factors that are operative across the wide range of weight disorders. The interaction of undernutition and weight loss in humans is hard to quantify owing to the nature of the studies required to establish scientific validity.


Experiments in rats looking at protein restriction have shown early foetal and placental development to be sensitive to significant protein restriction (Kwong 2000, Joshi 2003). In humans, restricted protein, carbohydrate, fat, and micro- and macronutrients occurring at times of war have been studied. The Dutch hunger study of Stein (Stein 1975) showed a higher incidence of unfavourable outcomes of pregnancy, though the mean reduction in live birth weights was only around 300G. The ability of starvation or long-term weight loss to suppress ovulation is well described and may also be associated with anorexia and high-intensity athletic training (Norman 1998, Goldberg 1997)).


The more prevalent form of weight dysregulation, obesity, is also strongly associated with fertility problems. Just losing weight has been reported to increase fertility in up to 30% of cases (Crosignani 2002). The combination of diet and exercise has been proved to be especially beneficial in restoring ovulation and fertility (Norman 1998). Several medical conditions are known to be associated with obesity and infertility. Firstly, diabetes, which if untreated leads to infertility and miscarriage, and even when treated is still associated with an increased rate of first trimester abortion, macrosomia and foetal abnormalities (Spellacy 1990). Secondly, polycystic ovary syndrome which is associated with a number of nutritional and hormonal disturbance (Goldberg 2003), as well as possibly having a genetic component (Tapanainen 1999). Thirdly, preeclampsia, increasingly common when the BMI exceeds the ideal mean by 20% (Sibai 1995), is 3-6 fold more likely with obesity (Roberts 1994). Preeclampsia is associated with a 5 fold increase in foetal mortality (Roberts 1994).


Both low and high body weight have been associated with deviations from optimum nutrition. Thus, in the case of nutritionally deprived groups, low levels of vitamin C have been reported (Matthews 1999). In the case of obesity, as during the Hackney study, low levels of folate, calcium, iron and zinc have been found (Doyle 1990). Large scale dietary surveys have consistently shown these deficiencies to be more prevalent in the lower socio-economic groups (Gregory 1990). Raised homocysteine levels, associated with deficiencies of several of these micronutrients, may be a factor in the higher incidence of reproductive failure (Quere 1998, Nelson 2000, Doyle 2001). The beneficial effects of preconceptual vitamin supplementation has helped to establish a cause-effect relationship between these deficiencies and fertility (Scholl 1997, Czeizel 1998).


Consideration of the above facts leads to the conclusion that reproductive health is critically dependent on optimum weight and nutritional status. Frisch (Frisch 1997) hypothesised that it was necessary to exceed a critical fat mass, i.e. during adolescence, for regular ovulation and fertility to be instituted. Leptins released by fat cells have subsequently been shown to possess a key role in modulating the hormonal changes associated with ovulation, fertility and pregnancy through stimulating neuropeptide Y and GnRH release via the hypothalamus (Magni 2000, Baldelli 2002, Coad 2003). Disturbances of leptin production and responses have been linked to both obesity and the polycystic ovary syndrome, a not uncommon cause of infertility (Coad 2003).


The interaction of diet, obesity, hormonal changes and reproductive failure is illustrated, for example, in the case of preeclampsia where intakes of vitamin C lower than 85mgs a day have been associated with a doubling of the rate of preeclampsia (Zhang 2000) and, in the case of the polycystic ovary syndrome, where low copper and selenium status has been reported (Coad 2003) and weight loss has led to an increase in fertility (Lefebvre 1997). Drawing from work in rats, these findings have led to the theory that hormonal changes and nutritional factors in the periconceptual period may lead to poor implantation, placental and foetal development, and increased foetal loss (Godfrey 1998, Coad 2002).


In conclusion, normal reproductive capacity is critically dependent on optimum weight and nutrition during the preconceptual period. Fertility and fertility are closely associated with hormonal changes and these in turn to both loss and gain in weight beyond the norm and to undernutrition. Secondary lifestyle changes, such as the moderation of obesity through exercise, also need to addressed if fertility is to be instituted and optimised.



1. Kwong WY, Wild AE, Roberts P, Willis AC, Fleming TP (2000) Maternal undernutrition during the preimplantation period of rat development causes blastocyst abnormalities and programming of postnatal hypertension. Development 127: 4195

2. Joshi S, et al. (2003) Maternal protein restriction before pregnancy affects vital organs of offspring in Wistar rats. Metabolism 52: 13-18

3. Stein ZA, Susser M, Saenger G, Marolla F (1975) Famine and Human Development: The Dutch Hunger Winter of 1944-1945. New York : Oxford University Press

4. Norman RJ, Clark AM (1998) Obesity and reproductive disorders: a review. Reproduction, Fertility and Development 10: 55-63

5. Goldberg G (1997) Reproduction: a global nutritional challenge. Proc Nutr Soc 56, 1B: 319-313

6. Crosignani PG, Vegetti W, Colombo M, Ragni G (2002) Resumption of fertility with diet in overweight women. Reproductive Medicine Online 5: 60-64

7. Spellacy WN (1990) Diabetes Mellitus and Pregnancy. In: Scott JR, DiSaia PJ, Hammond, Spellacy, eds. Danforth’s Obstetrics and Gynecology, 6th ed. pp 403-410. Lippincott Co, Pa.

8. Goldberg G (2003) Lecture notes. Surrey University

9. Tapanainen JS, et al. (1999) A new contributing factor to polycystic ovary syndrome: the genetic variant of luteinizing hormone. J Clin Endocrinol Metab 84: 1711-15

10. Sibai B, et al. (1995) Risk factors for preeclampsia in healthy nulliparous women: a prospective multicenter study. Am J Obs Gynecol 172: 529-555

11. Roberts JM (1994) Pregancy-related hypertension. In:Creasy RK, Resnik R, eds. Maternal-Fetal Medicine: Principles and Practice. Philadelphia, Pa.

12. Matthews F, Yudkin P, Neil A (1999) Influence of maternal nutrition on outcome of pregnancy: prospective cohort study. BMJ 319: 339- 343

13. Doyle W, Crawford MA, WynnAHA, Wynn SW (1990) The association between maternal diet and birth dimensions. J Nutr Med 1: 9-17

14. Gregory J, et al. (1990) The dietary and nutritional survey of British adults. Office of population censuses and surveys. London, HMSO

15. Quere I, et al. (1998) A woman with five consecutive fetal deaths: case report and retrospective analysis of hyperhomocysteinemia prevalence in 100 consecutive women with recurrent miscarriages. Fertility & Sterility 69: 152-4

16. Nelson WL, Bloom HJ, Steegers EA, den Heiger M, Eskes TK (2000) Hyperhomocysteinemia and recurrent early pregnancy loss: a meta- Analysis. Fertility & Sterility 74: 1196-9

17. Doyle W, et al. (2001) Inter-pregnancy folate and iron status of women in an inner city population. Br J Nutr 86: 81-87

18. Scholl TO (1997) Use of multivitamin/mineral prenatal supplements: influence on the outcome of pregnancy. Am J Epidemiol 146:134-41

19. Czeizel AE (1998) Periconceptual folic acid containing multivitamin supplementation. Eur J Clin Gynecol Repro Biol 78: 151-61

20. Frisch RE (1997) Critical fatness hypothesis. Am J Physiol 273:E231- E232

21. Magni P, Motta M, Martini L (2000) Leptin: a possible link between food intake, energy expenditure, and reproductive function. Regulatory Peptides 92: 51-56

22. Baldelli R, Dieguez C, Casanueva FF (2002) The role of leptin in reproduction: experimental and clinical aspects. Ann Med 34: 5-18

23. Coad J (2003) Lecture notes. Surrey University

24. Zhang C, et al. (2002) Vitamin C and the risk of preeclampsia. Epidemiology 13: 409-16

25. Lefebvre P, et al. (1997) influences of weight, body fat patterning and nutrition on the management of PCOS. Human Reproduction 12, Suppl 1: 72-81

26. Godfrey K & Robinson S (1998) Maternal nutrition, placental growth and fetal programming. Proc Nutr Soc 57: 105-11

27. Coad J, Al-Rasasi B, Morgan J (2002) Nutrient insult in early pregnancy. Proc Nutr Soc 61: 51-59