As emerging research sheds light on possible reasons for lactation trouble even when mothers receive competent support, insulin resistance, or IR, is rising to the forefront of the discussion of possible causes. The following is an adapted-for-the-blogosphere excerpt of my upcoming book, Finding Sufficiency: Breastfeeding with Insufficient Glandular Tissue, which will be available this summer from Praeclarus Press.
Can maternal body mass index be a warning sign for lactation trouble?
This question has been studied, and the answer is yes—maternal overweight has been identified as a potential risk factor for delayed onset of lactation (Chapman & Pérez-Escamilla, 1999), which can generate a snowball effect of early supplementation and poor breastfeeding management in those critical early hours and days. However, we are reminded that high BMI does not always predict lactation difficulty. Many women with a high body mass index go on to produce plenty of milk, even overproduce in some cases, and not all women with milk production issues have a BMI over 30, though it seems a growing percentage does. There is also scientific literature that suggests overweight or obesity during adolescence can affect pubertal development (Burt Solorzano & McCartney, 2010).
More research is needed to explore the possible relationship between adolescent body mass index, or, perhaps, adolescent diet and mammary gland development. Today’s new mothers grew up during what some call “the Snackwell’s era,” referring to a popular brand of snacks that were, as dietary recommendations of that time encouraged, processed to be low in fat. In order to be appealing, however, these products had—and perhaps still have—there are many “low fat” products still marketed as “healthy” foods even though current science suggests that dietary fat doesn’t cause body fat, more sugar and simple carbohydrates do—way more sugar than their regular-fat counterparts.
Does this matter for breast development?
A relevant study of rabbits examined the role of adolescent diet on mammary gland development during mid-pregnancy. Researchers fed an “obesogenic diet” (high fat, high sugar) to pre-pubertal rabbits, then compared their mammary gland development at mid-pregnancy to that of the rabbits fed the control diet. What they found was that the rabbits fed the high sugar diet had more rapid pubertal breast development, but lower capacity for lactation after the glandular development of pregnancy (Hue-Beauvais, Chavatte-Palmer, Aujean, Dahirel, Laigre, Pechoux, Bouet, et al. 2011). Longitudinal research on humans that measures nutritional status and dietary intake in pre-pubertal girls, then follows them into adulthood and examines such outcomes as weight status, reproductive axis functioning, and lactation, is sorely needed. For now, we can look to our rabbit friends for possibilities into what is going wrong for us.
Another consideration regarding higher BMI and lactation is the possible reduced effect of infant suckling on prolactin levels in the early days postpartum. Ostrum and Ferris (1993) found lower prolactin levels in mothers with insulin-dependent diabetes. These findings suggest that additional care should be taken to ensure these mothers have good control over their blood sugar, and are feeding their babies or stimulating their breasts appropriately and frequently. This is, of course, good guidance for all new breastfeeding mothers, but is of special importance for mothers with diabetes (who may or may not have a BMI > 30—it is the insulin dependence that seems significant here).
Through observation and study of over 1,000 mothers with lactation insufficiency, as well as a review of the available literature about glandular development and lactation, it becomes evident that the hormone insulin is a key player in this drama. The work of Marasco, Marmet, and Shell (2000) and West and Marasco (2008) has already informed the lactation support community of practitioners about the relationship between PCOS and breastfeeding problems—insulin resistance is part of that syndrome.
The Role of Insulin Resistance
Insulin resistance, which precedes type-2 diabetes, is a condition in which the body uses insulin (to regulate blood sugar) less effectively. More and more insulin is needed to regulate blood sugar, until, if not resolved, the body stops being able to produce enough insulin to keep blood sugar levels in a normal range (diabetes). A person might have insulin resistance for years before ever developing diabetes, and have no idea—insulin resistance is not always a condition with obvious symptoms.
A recent, groundbreaking study revealed that when a mother is insulin resistant, a particular gene is expressed more prominently than in insulin-sensitive individuals. This genetic expression suggests a relationship between insulin resistance and insufficient milk supply (Lemay, Ballard, Hughes, Morrow, Horseman, & Nommsen-Rivers, 2013). While not always comorbid—an individual can be insulin resistant and appear lean and thin, just as a person with higher BMI may be appropriately insulin sensitive and healthy—insulin resistance and high BMI are often seen together. But, does high BMI impair the ability of the existing glandular tissue to lactate properly, or was insulin resistance during puberty to blame for inadequate and incomplete development of the breast glands?
It is obvious that we are dealing with a very complex web of interdependent factors. One piece of the puzzle, which is related to high BMI, may be leptin, a hormone that is secreted by fat cells. Its short-term purpose is to regulate appetite and its long-term purpose is to regulate body weight. Brannian, Zhao, and McElroy (1999) also found that leptin may limit or inhibit the production of progesterone by the ovaries, but only when insulin was also present. If we think about what we know to be true–that regular, cyclic exposure to progesterone is necessary for glandular development, it makes sense that excess leptin plus excess insulin might result in insufficient progesterone each month to stimulate glandular growth of the breasts, even if ovulation and regular menstrual cycles are occurring.
How can I know if I have IR?
Insulin resistance is prevalent in Western societies and often goes unrecognized until type-2 diabetes emerges. In many people with insulin resistance, there are no outward symptoms. Some may have a condition called acanthosis nigricans, which is a darkening of skin either around the neck or in patches in places like the elbows, knees, knuckles, and armpits. Just over a decade ago, the means to assess for insulin resistance was complicated and difficult, requiring repeated blood samples over a period of a few hours to measure blood glucose, insulin, or both. A simple explanation of this procedure, called hyperglycemic (high blood sugar), hyperinsulinemic (high insulin), or euglycemic (normal blood sugar) glucose clamps, can be found at this link: https://www.diabeteshealth.com/whats-a-glucose-clamp-anyway/
While the glucose clamp techniques are the gold standard and the only way to assess exactly how insulin is being secreted and used in an individual’s body, recent and ongoing research has revealed simpler techniques for assessing insulin sensitivity, however, which technique offers the most precise and reliable result for which individuals varies widely. The labs that gave one mother a result might not be the same labs you need to get yours–there are several factors to consider and this is not a one-size-fits-all sort of thing.
All of these techniques for assessing insulin sensitivity use variables that should be easy to test for in a routine fasting blood test, such as triglyceride level, insulin, and glucose; as well as easily obtained values, such as waist circumference and body mass index (BMI). Assessments that have been compared to the euglycemic clamp technique include:
- Fasting insulin level
- Homeostasis model assessment (HOMA)
- Insulin-to-glucose ratio
- Bennett index
- McAuley index
Your healthcare provider can help you determine which assessment will tell you about your insulin sensitivity. However, if you have had issues with blood sugar, including gestational diabetes, hypoglycemia, or high blood sugar at any time, it is probably safe to assume you may be insulin resistant and adopt a lifestyle that corrects this problem. Even if you’re not insulin resistant, a conscious diet and regular physical activity certainly won’t hurt, so trying to determine whether you are, indeed, insulin resistant may not really be all that important. If you are insulin resistant enough that it causes problems (for example, you do not ovulate), you should already be under the care of a physician who will recommend dietary changes, prescribe medication, or both. If you merely suspect insulin resistance, “acting as if” may improve your health and well-being in ways you didn’t even realize you were suffering. It’s worth a try.
So, Does Insulin Resistance Prevent Me from Making Milk? Can I Still Have IGT?
This is a complicated question, and another topic area where more research is definitely needed, because there are insulin resistant women who make plenty of milk (perhaps their pubertal breast development was robust?), and a confirmed relationship between insulin resistance and low milk output. We do know that insulin is important. Insulin has a direct action on the mammary gland during breast development and is vital to the production and secretion of colostrum (lactogenesis I), in lactogenesis II (when lots of milk arrives after the placenta is born, usually around day 2 or 3 postpartum), and continued lactation.
Berlato and Doppler (2009) examined the action of insulin and insulin-like growth factors on mammary gland development and the ability of those cells to secrete milk in mice. They found that particular cells in the breast must remain insulin sensitive to develop properly and function in the presence of other hormones of lactation. While this doesn’t address insulin and glandular development directly, it does provide some insight into why we might be seeing so much insulin resistance among mothers with full, but perhaps slightly hypoplastic-appearing breasts (see Huggins, Petok, and Mireles, 2000). It provides some support for what we know to be true about herbs and supplements that seem to help with milk production—they enhance blood sugar metabolism and insulin sensitivity.
Another mouse model that offers some insight is presented by Sun, Shushanov, LeRoith, and Wood (2011). These researchers found that when receptors for insulin-like growth factor were decreased (such as, perhaps, when there was too much insulin-like growth factor circulating during adolescent breast development), the body adapted by making fewer receptors, resulting in fewer alveoli (milk-making sites in the breast—glandular tissue). However, in the mice, this did not seem to have a significant effect on whether the mouse pups gained sufficient weight (which was how they measured sufficient milk output in the mice). The study does not account for whether the baby mice fed more frequently, or whether the dam’s (mamma-mouse’s) milk was somehow adapted to give her pups a better chance at survival.
So, there are likely some women with lactation trouble who are insulin resistant but have adequate glandular development, and others who are insulin resistant and have insufficient glandular development. It’s likely possible to have IGT and IR at the same time. There are also women without insulin resistance who have insufficient glandular development for other (theorized) reasons (this is covered further in my book, as well as in this blog post).
What Can I Do If I’m Insulin Resistant?
The problem most of us who’ve struggled with insulin resistance know all too well is that losing weight will help normalize insulin sensitivity, but being insulin resistant makes losing weight more challenging a task than it is for those who aren’t insulin resistant. It’s not as simple as “calories in, calories out,” and frustration comes quickly to a person who is eating meticulously (often feeling hungry all the time and fighting sugar cravings), and exercising through a feeling of sheer exhaustion, but seeing no results at all. Those who have been successful losing weight and beating insulin resistance have found that a counted-carbohydrate diet, perhaps difficult to get used to at first, can be very effective. Western culture’s portions of carbohydrate foods are quite large, much more than we need, and the message that we need a certain number of servings of whole grains every day is pervasive and misleading. If you ever had gestational diabetes, perhaps you were put on a daily eating plan that utilized this strategy to normalize blood sugar and insulin levels until your baby was born—three meals and two or three snacks, with prescribed carbohydrate counts. A nutritionist or dietician can help you determine what daily meal plan is best for you.
Look for ways to eat whole, real foods, and be wary of chemically engineered “food-like products,” such as artificial sweeteners, that may have fewer calories but often contain ingredients that can have a negative effect on overall health. A dietician or physician who works with insulin resistant patients can provide guidance. Will counting carbs or adopting a “paleo diet” definitely increase your milk production? There is some research to suggest that possibly, it could (Matsuno, Esrey, Perrault, & Koski, 1999; Mohammad, Sunehag, & Haymond, 2009). Clinical observations indicate that it probably won’t hurt your milk supply, and improved health is always a good idea. Whether this way of nourishing your body leads to improved health remains to be seen: there is also evidence to support improved overall health on diets that are nothing like the paleo diet. Perhaps different individual physiologies respond to different macronutrient balances? This is another area that needs more research.
Along the same lines of good health, daily exercise is especially vital for those with insulin resistance. You don’t have to run a marathon: just 30 minutes each day of walking or other focused movement can help improve your insulin sensitivity and may improve your milk production over time. Even if your milk supply doesn’t seem to change, the daily exercise is indisputably good for your overall health, your mood, and your quality of sleep (even if your baby isn’t letting you sleep as much as you used to!), and sets a positive example for your child or children, who want to do everything you do.
Many women with insulin resistance are prescribed metformin to normalize insulin sensitivity and keep blood sugar in a normal range. Some mothers have found that metformin, either through pregnancy, postpartum, or both, has improved their ability to make milk, and this makes a lot of sense given what we know about insulin and lactation. While anecdotal and clinical experience supports improvement in milk production for women with insulin resistance who start or resume metformin, Vanky and colleagues (Vanky, Nordskar, Leithe, Hjorth-Hansen, Martinussen, & Carlsen, 2012) reported after a randomized, controlled trial that metformin had no effect on breast changes/size increase in pregnancy or breastfeeding in women who were obese. However, in this study, the metformin was not continued after delivery, and this may (or may not) have been a factor in the outcome. If insulin is an issue for you, discuss your options with your doctor and the potential of these options to help you boost your milk production. Your milk supply troubles may be the only “symptom” you have that something else is not working properly in your body.
Metformin is not well-tolerated by all women. Many stop taking it because the side effect of gastro-intestinal distress/diarrhea interferes with daily life too much. There is another option that may be promising for insulin-resistant mothers, and it may also improve ovarian function in women with PCOS. Myo-inositol, a naturally occurring substance that our bodies produce, that is also available in foods (a member of the B-complex vitamin group) like beans, fruits, and nuts, has been shown to have an effect on how our insulin receptors work. Gerli, Papaleo, Ferrari, and DiRenzo (2007) found that myo-inositol helped women with PCOS who were not ovulating to begin ovulating again (in women with a BMI under 37). The study also noted weight loss among those who were taking the myo-inositol (the experimental dose was 4 grams per day, which is 8 500mg capsules), but weight gain among the placebo group.
Another study (Artini, DiBerardino, Papini, Genazzani, Simi, Ruggiero, & Cela, 2013) offered similar positive results on ovarian function, as well as improvement of insulin sensitivity in women with PCOS who were taking myo-inositol (in this study, the dosage was only 2g per day). Myo-inositol, in very high doses, has also been shown to help with the treatment of obsessive-compulsive disorder and depression (Brink, Viljoen, deKock, Stein, & Harvey, 2004), which may be of interest to women who bear the dual suffering of lactation difficulty and depressive illness.
It is important to note that myo-inositol has not been formally studied in pregnancy but, due to its observed ability to stimulate oxytocin release, may cause uterine contractions. The ideal time to see if this supplement might benefit you is not when you are pregnant, but before you become pregnant. Along those lines, it is decidedly more advisable to improve any insulin issues you may have before you become pregnant. It is wise to find a healthcare practitioner you trust and discuss options like myo-inositol with him or her. Often, printing out an abstract to a study (such as those cited here), and bringing it to your doctor or midwife can prompt her to explore an option that might be new, but beneficial to you.
Hopefully, this post offers a primer for your future discussions with your healthcare providers as you try to solve the mystery of your lactation issues. I encourage you to more thoroughly examine the resources that are cited in this post, and to share the ones that seem relevant to your situation with your healthcare provider.
Artini, P. G., DiBerardino, O. M., Papini, F., Genazzani, A. D., Simi, G., Ruggiero, M., & Cela, V. (2013, Jan 22). Endocrine and clinical effects of myo-inositol administration in policystyc ovary syndrome. A randomized study. Gynecological Endocrinology. Advance online publication. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23336594
Berlato, C., & Doppler, W. (2009). Selective response to insulin versus insulin-like growth factor-I and -II and up-regulation of insulin receptor splice variant B in the differentiated mouse mammary epithelium. Endocrinology, 150(6), 2924-2933. doi: 10.1210/en.2008-0668
Brannian, J. D., Zhao, Y., & McElroy, M. (1999). Leptin inhibits gonadotrophin-stimulated granulosa cell progesterone production by antagonizing insulin action. Human Reproduction, 14(6), 1445-1448. doi: 10.1093/humrep/14.6.1445
Brink, C. B., Viljoen, S. L., deKock, S. E., Stein, D. J., & Harvey, B. H. (2004). Effects of myo-inositol versus fluoxetine and imipramine pretreatments on serotonin 5HT2A and muscarinic acetylcholine receptors in human neuroblastoma cells. Metabolic Brain Disease, 19(1-2), 51-70.
Burt Solorzano, C. M., & McCartney, C. R. (2010). Obesity and the pubertal transition in boys and girls. Reproduction, 140(3), 399-410. doi: 10.1530/REP-10-0119
Chapman, D. & Pérez-Escamilla, R. (1999). Identification of risk factors for delayed onset of lactation. Journal of the American Dietetic Association, 99(4), 450-454.
Gerli, S., Papaleo, E., Ferrari, A., & DiRenzo, G. C. (2007). Randomized, double blind placebo-controlled trial: Effects of myo-inositol on ovarian function and metabolic factors in women with PCOS. European Review for Medical and Pharmacological Sciences, 11(5), 347-354.
Hue-Beauvais, C., Chavatte-Palmer, P., Aujean, E., Dahirel, M., Laigre, P., Pechoux, C., Bouet, S. … Charlier, M. (2011). An obesogenic diet started before puberty leads to abnormal mammary gland development during pregnancy in the rabbit. Developmental Dynamics, 240(2), 347-356.
Huggins, K. E., Petok, E. S., & Mireles, O. (2000). Markers of lactation insufficiency: A study of 34 mothers. Current Issues in Clinical Lactation. Sudbury, MA; Jones & Bartlett, 25-35.
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), e67531. doi: 10.1371/journal.pone.0067531
Marasco, L., Marmet, C., & Shell, E. (2000). Polycystic ovarian syndrome: A connection to insufficient milk supply? Journal of Human Lactation, 16(2), 143-148.
Matsuno, A. Y., Esrey, K. L., Perrault, H., & Koski, K. G. (1999). Low intensity exercise and varying proportions of dietary glucose and fat modify milk and mammary gland compositions and pup growth. Journal of Nutrition, 129, 1167-1175
McAuley, K. A., Williams, S. M., Mann, J. I., Walker, R. J., Lewis-Barned, P. J., Temple, L. A., & Duncan, A. W. (2001). Diagnosing insulin resistance in the general population. Diabetes Care, 24(3), 460-464. Retrieved from http://care.diabetesjournals.org/content/24/3/460.full#T3
Mohammad, M. A., Sunehag, A. L., & Haymond, M. W. (2009). Effect of dietary macronutrient composition under moderate hypocaloric intake on maternal adaptation during lactation. American Journal of Clinical Nutrition, 89(6), 1821-1827. doi: 10.3945/ajcn.2008.26877
Ostrum, K. M., & Ferris, A. M. (1993). Prolactin concentrations in serum and milk of mothers with and without insulin-dependent diabetes mellitus. American Journal of Clinical Nutrition, 58(1), 49-53.
Sun, Z., Shushanov, S., LeRoith, D., & Wood, T. L. (2011). Decreased IGF type 1 receptor signaling in mammary epithelium during pregnancy leads to reduced proliferation, alveolar differentiation, and expression of insulin receptor substrate (IRS)-1 and IRS-2. Endocrinology, 152(8), 3233-3245. doi: 10.1210/en.2010-1296
Vanky, E., Nordskar, J. J., Leithe, H., Hjorth-Hansen, A. K., Martinussen, M., & Carlsen, S. M. (2012). Breast size increment during pregnancy and breastfeeding in mothers with polycystic ovarian syndrome: A follow-up study of a randomized controlled trial on metformin versus placebo. BJOG: An International Journal of Obstetrics and Gynaecology, 119(11), 1403-1409. doi: 10.1111/j.1471-0528.2012.03449.x
West, D. & Marasco, L. (2008). The breastfeeding mother’s guide to making more milk. New York: McGraw-Hill.
27 thoughts on “Insulin resistance and lactation insufficiency: FAQ”
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Is inositol safe to use when breastfeeding?
Thank you. Happy Holidays.
It’s a nutrient found in food and it’s also produced by the body. There may be reasons it’s not appropriate for certain people, so checking with a healthcare provider who knows your and your baby’s full health histories is always a good idea before you use any supplement.
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In your experience have you seen women who have shown signs of insulin resistance in their first pregnancy and has trouble Breast feeding. Then lose weight and make better lifestyle choice and were able to breast feed their second pregnancy.
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I just wanted to let you know that there are studies wherein Myo-Inositol was used during pregnancy to prevent Gestational Diabetes. Here is an example of one such study: http://www.ncbi.nlm.nih.gov/pubmed/23327487.
There are also studies that looked at what percentage of Myo-inositol crosses the placenta during pregnancy. http://care.diabetesjournals.org/con…77.full#ref-19
“Metformin, for example, is concentrated on the fetal side of the placenta (18), and it is unclear whether fetal effects are harmful, beneficial, or neutral. Measurements of fetal levels of maternally infused stable isotope-labeled myo-inositol in normal pregnancies at term demonstrated that less than 10% of fetal inositol was maternally derived, suggesting little placental transport in late pregnancy (19)”
And another: http://www.ncbi.nlm.nih.gov/pubmed/2…?dopt=Abstract
This is fabulous! Thank you!
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Wow. I am so happy I found this article.
With both babies, around 3 mo PP I go from an oversupplier to an undersupplier. While lactating with my first I had a blood test come back pre diabetic, but a follow up test said I was “normal” (although looking back I was on the high end of normal, a1c of 5.2). When the same issues started this time, I had blood levels checked but again, “normal.” Whenever I binge on sweets I’d notice a sharp decrease usually the following day. I started to make a connection, have adjusted my diet and begin to see improvement. I’ve had two doctors tell me this can’t be related, but I still suspected I was having insulin issues. Your comment that low milk supply could be the ONLY indicator tells me I am not crazy. I do have a history of diatebes in my paternal family.
Would love to know if this sounds on par with what you’ve studied. I have also wondered if metafirmin would help me make more milk but have been nervous to try.
Thank you for this article!
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