Nutrition to Optimise Fertility
Being fertile and having the ability to conceive is indeed a blessing, as the culture in most of the social communities are continuously looking at infertility as an agony. This ‘adverse’ mindset against infertility has been there for generations, and probably arouses from the old belief of “the future belongs to those who procreate”, which may refer to the incredibly satisfying and rewarding lifelong experience of raising a child.
Conceiving a baby begins from the early stage of a complex process called fertilization. Fertilization is the fusion of both the male (paternal) and female (maternal) germ cells in order to form a new individual. The paternal gamete is called sperm, while the maternal gamete is called the oocyte (also known as ovum, ova, egg cell, etc.). Sperm is the smallest cell in the human body, whereas oocyte is the largest.
Spermatogenesis is the process of sperm production that takes place in the testicles. It started when the spermatogenic stem cells, known as spermatogonia, replicate themselves by mitosis forming two daughter cells that is known as primary spermatocytes. However, only one of the primary spermatocyte continues with the cell replication by meiosis. Upon completion of meiosis I at telophase I, two secondary spermatocytes will be produced. Each of the secondary spermatocytes will then continue with the second meiosis (meiosis II) and produces two spermatids (total of four spermatids from two secondary spermatocytes). Next, the maturation of spermatids into fully functioning spermatozoa will occur through the process of spermiogenesis [1-2].
Primary spermatocytes are formed and entered into early prophase I during the embryonic development; however spermatogenesis is arrested at this point until puberty, when testosterone is being produced. Testosterone is required for completion of meiotic division and during the early stages of spermatid maturation. Whereas, the later stages of spermatid maturation during puberty requires the presence of follicle stimulating hormone (FSH). FSH is required for the production of androgen binding protein (ABP) by testicular Sertoli cells, which functions to concentrating testosterone in levels that are high enough to initiate and maintain the process of spermatogenesis. Besides, the testes also produce a number of paracrine regulators such as transforming growth factor, insulin-like growth factor-1, inhibin and others to help in regulating the spermatogenesis [1-2].
Process of oocyte production is known as oogenesis and it occurs in the ovaries. Oogenesis started when the germ cells migrate into the ovaries and multiplies, resulting in about 6 – 7 million of oogonia being produced in ovaries during the embryonic development (about 5 months of gestation). However, most of the oogonia will die through apoptosis and the production of new oogonia stops at this time and never resumes again. Development of oogonia begins through meiosis during the end of gestation, producing primary oocytes that are contained within the primary follicles. The growths of the primary follicles are stimulated by FSH, where some of the oocytes and follicles will get larger. Besides, the follicular cells will divide to produce layers of granulosa cells that surround the oocyte and fill the follicle. Furthermore, some of the primary follicles will be stimulated to grow still more and develop into the secondary follicles that contain a number of fluid-filled cavities called vesicles. Continuous growth of one of the secondary follicles will involve the fusion of the vesicles to form a single fluid-filled cavity called an antrum. At this stage, the follicle is known as Graafian follicle. On the other hand, as the follicle develops, the primary oocyte completes the process of meiosis, producing the secondary oocyte. Upon the time of ovulation, the Graafian follicle will become so large that it forms a bulge on the ovarian surface. And under the proper hormonal stimulation; the Graafian follicle will rupture and extrude its oocyte into the uterine tube, and this process is known as ovulation [1-2].
Reasons for Poor Fertility
Significant risk factors of poor fertility include poverty, high percentage of older mothers, greater frequency of consanguineous marriages and low survivability rate against malaria for carriers of sickle cell, thalassemia, and glucose-6-phosphate dehydrogenase (G6PD) deficiency genes . Besides, poor fertility can be also caused by multifactorial inheritance, environmental teratogens, micronutrient deficiencies and maternal infectious diseases such as syphilis and rubella. Moreover, poor maternal health status including iodine and folic acid deficiency, and exposure to recreational drugs, alcohol and tobacco are also contributing to infertility problems .
Supplements for Fertility
The importance of having the sufficient amount of micronutrients in pregnancy and embryonic development has been reported previously. This is due to their roles in modulating oxidative stress (OS), enzyme functions, signal transductions and transcription pathways that occur during fertilization and early pregnancy . These include the major micronutrients including folate, vitamin A, vitamin B6, vitamin B12, iron, zinc and copper that has been reported to affect pregnancy outcomes through alterations in both maternal and foetal metabolism [5-12].
Based on the available reports, an earlier study has reported that increase in vitamin A intake can possibly reduce the risk of maternal mortality . Besides, the increase in calcium and magnesium intake during pregnancy may reduce the risk of pregnancy-induced hypertensive disorders, whereas sufficient intake of iron, zinc, iodine and folic acid during pregnancy can improve the pregnancy outcomes [14-15]. In addition, the consumption of folic acid-containing supplements have been reported to reduce the occurrence of neural tube defects, as the low concentrations of dietary and circulating folate are associated with the increased risks of preterm delivery, infant low birth weight and foetal growth retardation .
Fertility can be affected by several factors including environmental, chemical or physical factors that lead to the problems of infertility. However, there are possibilities of improving the infertility problems through the proper nutrients/supplements intake in daily meal consumptions as well as by having a healthy lifestyle.
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1. Tortora G.J, Derrickson B.H. (2009), Principles of Anatomy and Physiology. 12th Edition (International Student Version), John Wiley & Sons.
2. Marieb E.N., Hoehn K. (2010), Human Anatomy & Physiology. 8th Edition, Pearson International Edition (Benjamin Cummings).
3. Christianson , A.L., Howson, C. P, & Modell, B. (2006). March of dimes global report on birth defects: The hidden toll of dying and disabled children. White Plains, New York: March of Dimes Birth Defects Foundation
4. McArdle, H. J., & Ashworth, C. J. (1999). Micronutrients in fetal growth and development. British Medical Bulletin, 55(3), 499-510.
5. Scholl, T. O., & Johnson, W. G. (2000). Folic acid: Influence on the outcome of pregnancy. The American Journal of Clinical Nutrition, 71(5 Suppl), 1295S-1303S.
6. Ross, A. C. Vitamin A and carotenoids. (2006) In: Shils, M.E., Shike, M., Ross, A. C., Caballero, B., Cousins, R. J. (Eds.). Modern Nutrition in Health and Disease. (10th Edition) (pp. 351-375). USA: Lippincott Williams & Wilkins.
7. Mackey, A. D., Davis, S. R., Gregory, J. F. I. (2006). Vitamin B6. In: Shils, M.E., Shike, M., Ross, A. C., Caballero, B., Cousins, R. J. (Eds.). Modern Nutrition in Health and Disease. (10th Edition) (pp. 452-461). USA: Lippincott Williams & Wilkins.
8. Ryan-Harshman, M., & Aldoori, W. (2008). Vitamin B12 and health. Canadian Family Physician, 54(4), 536-41.
9. Beard, J. (2003). Iron deficiency alters brain development and functioning. The Journal of Nutrition, 133(5 Suppl 1), 1468S-1472S.
10. Wood, R. J., & Ronnenberg, A. G. Iron. (2006). In: Shils, M.E., Shike, M., Ross, A. C., Caballero, B., Cousins, R. J. (Eds.). Modern Nutrition in Health and Disease. (10th Edition) (pp. 248-270). USA: Lippincott Williams & Wilkins.
11. Hambidge, M. (2000). Human zinc deficiency. The Journal of Nutrition, 130(5S Suppl), 1344S-1349S.
12. Turnlund, J. R. Copper. (2006). In: Shils, M.E., Shike, M., Ross, A. C., Caballero, B., Cousins, R. J. (Eds.). Modern Nutrition in Health and Disease. (10th Edition) (pp. 286-299). USA: Lippincott Williams & Wilkins.
13. West, K. P. Jr., Katz, J., Khatry, S. K., LeClerq, S. C., Pradhan, E. K., Shresta, S. R., Connor, P. B., Dali, S. M., Christian, P., Pokhrel, R. P., & Sommer, A. (1999). Double blind, cluster randomized trial of low dose supplementation with vitamin A or β carotene on mortality related to pregnancy in Nepal. The NNIPS-2 Study Group. BMJ, 318(7183), 570-575.
14. Ladipo, O. A. (2000). Nutrition in pregnancy: Mineral and vitamin supplements. The American Journal of Clinical Nutrition, 72(1), 280S-290S.
15. Diaz, J. R., de las Cagigas, A., & Rodriguez, R. (2003). Micronutrient deficiencies in developing and affluent countries. European Journal of Clinical Nutrition, 57(Suppl 1), S70-S72.