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Infertility on the rise

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Learn more about how our modern lifestyles affect both fertility and the health of our children in my book, Conversations with my Daughter:  How to Have a Healthy Baby.

Order your paperback copy today from True Medicine or e-book from Balboa Press.

 

 

In Australia, infertility rates are on the rise, with one couple in six experiencing infertility1. Multiple factors have been attributed to declines in fertility rates (worldwide). These include; trying to conceive later in life, obesity, metabolic diseases such as diabetes, and environmental toxins2.

The Australian Department of Health, has recorded a shift in the median age of mothers giving birth, with women having their first child later in life. The highest fertility rates were for women aged between 30 – 34 years3, this is important to note, as fertility peaks at 25 and then declines from 32 years, with another steep decline at age 374. The median age for men becoming fathers was 33 years5.

Obesity is also linked to infertility with 27.9% of Australians being obese6. In men, obesity has been linked to erectile dysfunction, a reduction in semen quality and changes in sperm proteomes7. While in women, obesity is associated with menstrual dysfunction, anovulation and higher miscarriage rates8.

Environmental toxin exposure has also been linked to infertility with researchers pointing to low dose, chronic exposure to combinations of toxins as a potential explanation for the increasing prevalence of impairment of spermatogenesis9. Negative impacts in female reproductive health have also been observed. For example dioxin exposure has been shown to inhibit transcription of mRNAs, aromatase and other steroidogenic enzymes responsible for oestrogen synthesis10.

An interesting key that underpins these factors is their association with mitochondrial dysfunction. Optimal mitochondrial function is paramount for fertility in both men and women.

Female

In female fertility, oocytes contain the most amount of mitochondrial DNA (mtDNA) than other types of cells, with mitochondria being an important contributor to oocyte quality4. Oogenesis utilises adenosine triphosphate (ATP) from oxidative phosphorylation in mitochondria at a number of steps and this continues after fertilisation to assist in chromatid separation, cell division, and spindle formation11.

In addition to this, the development of the zygote is reliant on the existing pool of mitochondria available and this existing pool will decrease with each cell division. Decreased numbers of mitochondria coupled with dysfunctional mitochondria during embryo development can lead to miscarriage11.

Male

Mitochondria are required for sperm motility and dysfunction of mtDNA may impact spermatozoa functionality. Sperm require ATP for the flagellum to move in fertilisation and as such quality of semen can be related to the functioning of the respiratory chain in sperm mitochondria12.

Spermatozoa in infertile men share a number of similar characteristics. These include; ROS production and reduced mitochondrial membrane potential12. Spermatozoa are particularly vulnerable to oxidative damage12.

Recommendation:

If you would like to start a family in the next five years, it is never too early to begin cleaning up your body.  This applies to both the mother and the father.  At True Medicine we specialise in individualised clinical detox programmes as well as educating you about how to remove the daily toxins you may be exposed to and how these affect your body. 

References:

  1. Fertility and Infertility [Internet]. 2011 Feb 7 [cited 2018 Dec 6]. Available from: http://www.health.gov.au/internet/publications/publishing.nsf/Content/womens-health-policy-toc~womens-health-policy-experiences~womens-health-policy-experiences-reproductive~womens-health-policy-experiences-reproductive-maternal~womens-health-policy-experiences-reproductive-maternal-fert
  2. Sharma R, Biedenharn KR, Fedor JM, Agarwal A. Lifestyle factors and reproductive health: taking control of your fertility. Reproductive Biology and Endocrinology. 2013 Dec; 11(1):66.
  3. Fertility Rates [Internet]. 2016 [updated 2017 Dec 13; cited 2018 Dec 16]. Available from:http://www.abs.gov.au/ausstats/abs@.nsf/Latestproducts/3301.0Main%20Features42016?opendocument&tabname=Summary&prodno=3301.0&issue=2016&num=&view
  4. Cecchino GN, Seli E, da Motta EL, Velasco JA. The role of mitochondrial activity in female fertility and assisted reproductive technologies: overview and current insights. Reproductive biomedicine online. 2018 Mar 8.
  5. Births [Internet]. 2014 [updated 2015 Oct 29; cited 2018 Dec 16]. Available from:http://www.abs.gov.au/ausstats/abs@.nsf/Previousproducts/3301.0Main%20Features32014?opendocument&tabname=Summary&prodno=3301.0&issue=2014&num=&view
  6. Overweight and Obesity [Internet]. 2015 Dec 08 [cited 2018 Dec 6]. Available from: http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/4364.0.55.001~2014-15~Main%20Features~Overweight%20and%20obesity~22
  7. Cabler S, Agarwal A, Flint M, Du Plessis SS. Obesity: modern man’s fertility nemesis. Asian journal of andrology. 2010 Jul;12(4):480.
  8. Dağ ZÖ, Dilbaz B. Impact of obesity on infertility in women. Journal of the Turkish German Gynecological Association. 2015;16(2):111.
  9. Gabrielsen JS, Tanrikut C. Chronic exposures and male fertility: the impacts of environment, diet, and drug use on spermatogenesis. Andrology. 2016 Jul;4(4):648-61.
  10. Hutz RJ, Carvan III MJ, Baldridge MG, Conley LK, Heiden TK. Environmental toxicants and effects on female reproductive function. Trends in reproductive biology. 2006;2:1.
  11. Chappel S. The role of mitochondria from mature oocyte to viable blastocyst. Obstetrics and gynecology international. 2013;2013.
  12. Kumar DP, Sangeetha N. Mitochondrial DNA mutations and male infertility. Indian journal of human genetics. 2009 Sep;15(3):93.
  13. Grindler NM, Moley KH. Maternal obesity, infertility and mitochondrial dysfunction: potential mechanisms emerging from mouse model systems. MHR: Basic science of reproductive medicine. 2013 Apr 23;19(8):486-94.
  14. Saini R. Coenzyme Q10: the essential nutrient. Journal of Pharmacy and Bioallied Sciences. 2011 Jul 1;3(3):466.
  15. Ben‐Meir A, Burstein E, Borrego‐Alvarez A, Chong J, Wong E, Yavorska T, Naranian T, Chi M, Wang Y, Bentov Y, Alexis J. Coenzyme Q10 restores oocyte mitochondrial function and fertility during reproductive aging. Aging cell. 2015 Oct;14(5):887-95.
  16. Safarinejad MR. Efficacy of coenzyme Q10 on semen parameters, sperm function and reproductive hormones in infertile men. The Journal of urology. 2009 Jul 1;182(1):237-48.
  17. González R, Ferrín G, Hidalgo AB, Ranchal I, López-Cillero P, Santos-Gónzalez M, López-Lluch G, Briceño J, Gómez MA, Poyato A, Villalba JM. N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes. Chemico-biological interactions. 2009 Sep 14;181(1):95-106.
  18. Ciftci H, Verit A, Savas M, Yeni E, Erel O. Effects of N-acetylcysteine on semen parameters and oxidative/antioxidant status. Urology. 2009 Jul 1;74(1):73-6.
  19. Mokhtari V, Afsharian P, Shahhoseini M, Kalantar SM, Moini A. A review on various uses of N-acetyl cysteine. Cell Journal (Yakhteh). 2017 Apr;19(1):11.
  20. Johnson JA, Johnson DA, Kraft AD, Calkins MJ, Jakel RJ, Vargas MR, Chen PC. The Nrf2–ARE pathway. Annals of the new York Academy of Sciences. 2008 Dec 1;1147(1):61-9.
  21. Dinkova-Kostova AT, Abramov AY. The emerging role of Nrf2 in mitochondrial function. Free Radical Biology and Medicine. 2015 Nov 1;88:179-88.