Tips for Improving Breastfeeding with PCOS
This is part one of a 2 part series on breastfeeding and PCOS by Alex Walker.
Breastfeeding is best. We hear it all the time and for good reason. Breast milk provides babies with the perfect balance of nutrition and immune protection that ensure a healthy start to life. But for women diagnosed with PCOS, exclusive breastfeeding for the first six months of their baby’s life (the recommendation of the American Academy of Pediatrics) may not be possible. Many of you know all too well that PCOS can wreak havoc on a woman’s body, potentially causing obesity, insulin resistance, and even infertility. What you may not be aware of, and what your physician may not be telling you, is that PCOS can also lead to insufficient milk supply, or what I prefer to call impaired mammary organ function (IMOF).
Before we address IMOF, we ought to start with its predecessor: impaired mammary organ development (IMOD).
While almost all vital organs in the human body develop in utero, the mammary organ is different. Not until a girl begins puberty does the breast start its journey toward becoming a fully functioning organ. At the onset of puberty, continuous pulses of estrogen from a girl’s ovaries during each menstrual cycle will stimulate mammary organ growth. Estrogen, in concert with growth hormone (GH) and insulin-like growth factor (IGF-1), will initiate and maintain the development of the ductal network that forms the foundation for future lactating breasts. These ducts will function as canals that will carry breast milk from the milk-making cells, called lactocytes, within the breast to the nipple.
PCOS, which often begins in adolescence, can potentially disrupt the creation of this ductal network in two important ways. First, abnormally high androgen levels, which are common in PCOS, can potentially stunt estrogen-driven ductal growth and proliferation. Second, obesity, another common occurrence in PCOS, can inhibit normal development of the mammary organ by decreasing estrogen sensitivity.
In order to promote optimal mammary development in the face of high androgen levels and/or obesity, we can encourage adolescents to do the following:
- Receive timely screening and diagnosis for PCOS, ideally within the first two years of the first menstrual period
- Maintain a healthy BMI through a PCOS-friendly diet (IR or anti-inflammatory), regular exercise, avoiding inflammatory food, etc.
- Control high levels of androgens with dietary changes, exercises or natural supplements such as Ovasitol.
Pregnancy is the second stage of exponential mammary development. Under the influence of insulin, progesterone and prolactin, the milk-making cells of the breast (lactocytes) undergo substantial growth and proliferation. If you suffer from PCOS then it is likely that your cells, including the lactocytes, have become insulin and possibly progesterone resistant, making it difficult for these key hormones to initiate growth. Decreasing circulating androgens and restoring insulin sensitivity through diet, exercise and natural supplements are simple yet critical steps to support mammary development during this period.
In addition to progesterone and insulin, your breasts depend on the hormone prolactin to make milk. Although prolactin activity is muted during pregnancy, prolactin levels should be high enough for the lactocytes to start producing colostrum toward the end of the second trimester. Numerous studies have shown that obesity, a common comorbidity of PCOS, can blunt the prolactin response, causing the lactocytes to lose some of their necessary sensitivity to this vital hormone.
Given the possible barriers that PCOS women face for mammary organ development during pregnancy, we can encourage expectant moms to do the following:
- Increase insulin sensitivity (IR or anti-inflammatory diet, medication, supplements)
- Decrease free testosterone levels and thereby increase progesterone sensitivity (medication, supplement such as Ovasitol or vitamin D)
- Increase prolactin sensitivity through weight loss
We have covered methods for decreasing the risk of IMOD and increasing breastfeeding success before and during pregnancy. But now you may be wondering if there is anything you can do to decrease the chances of impaired mammary organ function (IMOF) once your baby is born? Fortunately, the answer yes!
Once your baby arrives, we want to make sure that two vital hormones during this stage, prolactin and insulin, can function optimally. Insulin and prolactin sensitivity are key and can be maximized by maintaining a normal BMI and nourishing your body with healthy foods, including whole grains, fresh fruits and vegetables and lean proteins. And if you haven’t already started a supplement such as Ovasitol or vitamin D, it’s never too late to start.
Another way to maximize production is to make your breasts think you are having twins or even triplets by expressing your breasts twice: once with the baby, and again with a pump. While you can certainly request a breast pump right after delivery, another option is hand expression. Studies have shown that early colostrum expression (within the first few hours after delivery) can possibly stimulate your milk supply better than pumping.
Some final tips:
- Stay hydrated and relaxed; stress and ensuing elevated cortisol levels can lower milk supply
- Take your baby on walks to keep your body moving; fresh air and nature can do a lot to recharge the body and lower cortisol levels
- Skin to skin contact with your baby can help spike your lactation hormones—enjoy it often!
While there is no way to tell whether or not PCOS will affect your ability to produce milk, the key to success is starting as early as you can to remove potential barriers. With a little bit of planning, you can do a lot to help minimize the risk of IMOD and IMOF and ensure the best start to your breastfeeding relationship with your new baby.
References
Al-Biate, M. A. (2015). Effect of metformin on early pregnancy loss in women with polycystic ovary syndrome. Taiwan J Obstet Gynecol, 54(3), 266–269. http://doi.org/10.1016/j.tjog.2013.06.020
Badawy, A., & Elnashar, A. (2011). Treatment options for polycystic ovary syndrome. International Journal of Women’s Health, 3(1), 25–35. http://doi.org/10.2147/IJWH.S11304
Bailey, C. J., & Day, C. (2004). Metformin: Its botanical background. Practical Diabetes International, 21(3), 115–117. http://doi.org/10.1002/pdi.606
Barrett, E. S., & Sobolewski, M. (2014). Polycystic ovary syndrome: Do endocrine-disrupting chemicals play a role? Seminars in Reproductive Medicine, 32(3), 166–176. http://doi.org/10.1055/s-0034-1371088
Bertrand, K. a, Baer, H. J., Orav, E. J., Klifa, C., Shepherd, J. a, Van Horn, L., … Dorgan, J. F. (2015). Body fatness during childhood and adolescence and breast density in young women: a prospective analysis. Breast Cancer Research : BCR, 17(1), 95. http://doi.org/10.1186/s13058-015-0601-4
Blank, S. K., McCartney, C. R., Chhabra, S., Helm, K. D., Eagleson, C. A., Chang, R. J., & Marshall, J. C. (2009). Modulation of gonadotropin-releasing hormone pulse generator sensitivity to progesterone inhibition in hyperandrogenic adolescent girls – Implications for regulation of pubertal maturation. Journal of Clinical Endocrinology and Metabolism, 94(7), 2360–2366. http://doi.org/10.1210/jc.2008-2606
Blank, S. K., McCartney, C. R., Helm, K. D., & Marshall, J. C. (2007). Neuroendocrine effects of androgens in adult polycystic ovary syndrome and female puberty. Seminars in Reproductive Medicine. http://doi.org/10.1055/s-2007-984741
Buonfiglio, D. C., Ramos-Lobo, A. M., Freitas, V. M., Zampieri, T. T., Nagaishi, V. S., Magalhães, M., … Donato Jr., J. (2016). Obesity impairs lactation performance in mice by inducing prolactin resistance. Scientific Reports, 6(March), 22421. http://doi.org/10.1038/srep22421
Dimitrakakis, C., Dimitrakakis, C., Bondy, C., & Bondy, C. (2009). Androgens and the breast. Breast Cancer Research : BCR, 11(5), 212. http://doi.org/10.1186/bcr2413
Eagleson, C. A., Gingrich, M. B., Pastor, C. L., Arora, T. K., Burt, C. M., Evans, W. S., & Marshall, J. C. (2000). Polycystic ovarian syndrome: Evidence that flutamide restores sensitivity of the gonadotropin-releasing hormone pulse generator to inhibition by estradiol and progesterone. Journal of Clinical Endocrinology and Metabolism, 85(11), 4047–4052. http://doi.org/10.1210/jc.85.11.4047
El Maghraby, H. A., Nafee, T., Guiziry, D., & Elnashar, A. (2015). Randomized controlled trial of the effects of metformin versus combined oral contraceptives in adolescent PCOS women through a 24 month follow up period. Middle East Fertility Society Journal, 20(3), 131–137. http://doi.org/10.1016/j.mefs.2014.10.003
Flaherman, V. J., Gay, B., Scott, C., Avins, A., Lee, K. A., & Newman, T. B. (2011). Randomised trial comparing hand expression with breast pumping for mothers of term newborns feeding poorly. Archives of Disease in Childhood – Fetal and Neonatal Edition . http://doi.org/10.1136/adc.2010.209213
Forsbach, G., Güitrón-Cantú, A., Vázquez-Lara, J., Mota-Morales, M., & Díaz-Mendoza, L. M. (2000). Virilizing adrenal adenoma and primary amenorrhea in a girl with adrenal hyperplasia. Archives of Gynecology and Obstetrics, 263(3), 134–136. http://doi.org/10.1007/s004040050012
Kumar, P., Kale, R. K., & Baquer, N. Z. (2012). Antihyperglycemic and protective effects of Trigonella foenum graecum seed powder on biochemical alterations in alloxan diabetic rats. European Review for Medical and Pharmacological Sciences.
Laurie A Nommsen-Rivers. (2016). Does Insulin Explain the Relation between Maternal Obesity and Poor Lactation Outcomes? An Overview of the Literature. Advances in Nutrition, 7, 407–414. http://doi.org/10.3945/an.115.011007
Lemay, D. G., Ballard, O. A., Hughes, M. A., Morrow, A. L., Horseman, N. D., & Nommsen-Rivers, L. A. (2013). RNA Sequencing of the Human Milk Fat Layer Transcriptome Reveals Distinct Gene Expression Profiles at Three Stages of Lactation. PLoS ONE, 8(7). http://doi.org/10.1371/journal.pone.0067531
Marzouk, M., Soliman, A. M., & Omar, T. Y. (2013). Hypoglycemic and antioxidative effects of Fenugreek and Termis seeds powder in streptozotocin-diabetic rats. European Review for Medical and Pharmacological Sciences, 17(4), 559–565.
Neville, M. C., Neville, M. C., & Morton, J. (2016). Lactogenesis : The transition from pregnancy to Symposium : Human Lactogenesis II : Mechanisms , Physiology and Endocrine Changes Underlying Human Lactogenesis II 1 , 2, (MARCH 2001), 3005–3008.
Neville, M. C., Webb, P., Ramanathan, P., Mannino, M. P., Pecorini, C., Monks, J., … MacLean, P. (2013). The insulin receptor plays an important role in secretory differentiation in the mammary gland. American Journal of Physiology. Endocrinology and Metabolism, 305(9), E1103–14. http://doi.org/10.1152/ajpendo.00337.2013
Ohyama, M., Watabe, H., & Hayasaka, Y. (2010). Manual expression and electric breast pumping in the first 48 h after delivery. Pediatrics International, 52(1), 39–43. http://doi.org/10.1111/j.1442-200X.2009.02910.x
Olson, L. K., Ph, D., Tan, Y., Zhao, Y., Aupperlee, M. D., & Haslam, S. Z. (2011). Pubertal Exposure to High Fat Diet Causes Mouse Strain- dependent Alterations in Mammary Gland Development and Estrogen Responsiveness, 34(9), 1415–1426. http://doi.org/10.1038/ijo.2010.51.Pubertal
Parker, L. A., Sullivan, S., Krueger, C., Kelechi, T., & Mueller, M. (2012). Effect of early breast milk expression on milk volume and timing of lactogenesis stage II among mothers of very low birth weight infants: a pilot study. J Perinatol, 32(3), 205–209. Retrieved from http://dx.doi.org/10.1038/jp.2011.78
Perla, V., & Jayanty, S. S. (2013). Biguanide related compounds in traditional antidiabetic functional foods. Food Chemistry, 138(2-3), 1574–1580. http://doi.org/10.1016/j.foodchem.2012.09.125
Savaris, R. F., Groll, J. M., Young, S. L., DeMayo, F. J., Jeong, J. W., Hamilton, A. E., … Lessey, B. A. (2011). Progesterone resistance in PCOS endometrium: A microarray analysis in clomiphene citrate-treated and artificial menstrual cycles. Journal of Clinical Endocrinology and Metabolism, 96(6), 1737–1746. http://doi.org/10.1210/jc.2010-2600
Shen, Z.-Q., Zhu, H.-T., & Lin, J.-F. Reverse of progestin-resistant atypical endometrial hyperplasia by metformin and oral contraceptives., 112 Obstetrics and gynecology 465–467 (2008). http://doi.org/112/2/465 [pii]\r10.1097/AOG.0b013e3181719b92
Solorzano, C. M. B., Collins, J. S. P., Beller, J. P., Anderson, A. D., Bhabhra, R., McCartney, C. R., & Marshall, J. C. (n.d.). Metformin Improves Hypothalamic Progesterone Insensitivity in Hyperandrogenic Girls. Endocrine Reviews, MON–559–MON–559. http://doi.org/10.1210/endo-meetings.2013.RE.5.MON-559
Xie, Y., Wang, Y.-L., Yu, L., Hu, Q., Ji, L., Zhang, Y., & Liao, Q.-P. (2011). Metformin promotes progesterone receptor expression via inhibition of mammalian target of rapamycin (mTOR) in endometrial cancer cells. The Journal of Steroid Biochemistry and Molecular Biology, 126(3-5), 113–120. http://doi.org/10.1016/j.jsbmb.2010.12.006
Note: The views and recommendations shared by PCOS Diva LLC and pcosdiva.com, as well as the information contained in this email, if any, are for general health information only and do not constitute, and are not intended to be a substitute for professional medical advice regarding an individual’s specific health condition. The information is intended to provide accurate and helpful health information. The information is not intended as medical advice for individual problems or for making a diagnosis of a medical condition or an evaluation as to the risks and benefits of taking a particular drug or product.