Onset of lactation in women can be influenced by a variety of factors like, diabetes mellitus, premature delivery, obesity, prolactin deficiency and delayed progesterone withdrawal, and hormonal changes during pregnancy and anesthetic therapeutic agents administered during child birth. Obesity is a risk factor for delayed onset of lactation and because GDM is most common in obese women, it is possible that the diabetes or the obesity could alter the onset of lactation following delivery in these women. It appears that lactation markers (lactose, citrate and total nitrogen) in the milk of women with diabetes mellitus take an additional 24 h to attain the concentrations of normal women.
Birth interventions such as scheduled induction before indications that baby is ready to be born, epidural with high fluid load, restriction of movement during labour and frequently resulting c-section can affect lactogenesis timing. As can separation of mother and baby in the first hours or days after birth with reduced opportunities for suckling at the breast and increased likelihood of non-mother's milk feeds, and general lack of support to establish lactation in the first 24 hours. Often women with diabetes and their infants are routinely treated as medical patients who happen to give birth.
You didn't mention what her estimated blood loss with the delivery. Postpartum hemorrhage and resultant hypotension may result in the pituitary gland's failure to produce gonadotropins leading to Sheehan syndrome (Panhypopituitarism). Hemorrhage leads to pituitary thrombotic infarction and necrosis and hypoperfusion. Because of the increased size of the pituitary during late gestation, this organ is more senstive to hypoperfusion. Even milder cases of blood loss can result in a delay of milk synthesis.
--Delayed lactogenesis may be due to lower prolactin concentrations that are found with maternal obesity and insulin resistance;
-- Longer separation of newborns from diabetic mothers or greater use of non-breast milk liquids in the neonatal period to treat hypoglycemia.
-- Decreased insulin sensitivity may delay milk production as a result of protein tyrosine phosphatase, receptor type F (PTPRF) over-expression in the mammary gland .
1. Lemay DG, Ballard OA, Hughes MA, Morrow AL, Horseman ND, Nommsen-Rivers LA. RNA Sequencing of the Human Milk Fat Layer Transcriptome Reveals Distinct Gene Expression Profiles at Three Stages of Lactation. PLoS ONE 2013;8:e67531
2. Matias SL, Dewey KG, Quesenberry CP Jr, Gunderson EP. Maternal prepregnancy obesity and insulin treatment during pregnancy are independently associated with delayed lactogenesis in women with recent gestational diabetes mellitus. Am J Clin Nutr. 2013 Nov 6. [Epub ahead of print] PubMed PMID: 24196401.
In keeping with above, you did not state long lactation was suppressed before becoming normal. Certainly depression is not something that is common or our midwifery lactation team have experienced unless the patient was uncertain to breastfeed in the first instance or delivery was by C/S in which case bonding / Contact with baby was delayed or there are complications as PPH leading to Sheehans syndrome as suggested above. Whilst above references are acknowledged, I am afraid this is not an issue that has been identified with patients in my unit with 3400 deliveries per annum and initiation of breastfeeding of over 60%.
If diabetes is not well controlled may be some differences in the composition of milk (low lactose concentration, higher nitrogen content and lower milk production by low levels of prolactin).
Hi Jose, do you have a reference for research showing clinically relevant differences in milk composition in mothers with diabetes? I have seen some materials (aimed at mothers) that says milk would be high in lactose if poorly controlled! And how poorly controlled before there is a difference? Thanks
Yes. The reference is : Peptides. 2010 Dec;31(12):2236-40. doi: 10.1016/j.peptides.2010.08.021. Epub 2010 Sep 8.
The presence of the peptides apelin, ghrelin and nesfatin-1 in the human breast milk, and the lowering of their levels in patients with gestational diabetes mellitus.
Hi Jose. Can you be more specific about where in the article you suggest there is research findings on clinically relevant difference in the milk for lactose, nitrogen or prolactin? In this article I can only see a laboratory investigation for the presence of some specific peptides and no mention of any effect of higher or lower levels of these peptides on the milk, mother or child.
People usually say that lactation is delayed in women with diabetes in pregnancy, rather than suppression, which sounds like the milk might not 'come in' at all. We have just started recruiting women without diabetes to compare to the women with diabetes in pregnancy in our DAME trial. In most of the old studies, there was separation of mother and baby, so we wanted to see if there is delayed lactogenesis in a Baby Friendly hospital today.
Hi Lisa. It will be very useful to have this research that explores what are physiological issues and what are hospital practice issues that affect establishment of lactation. Best wishes with your research. Genevieve
Hi Genevieve. It's a medical student project - so won't answer everything! But we plan to recruit 200 women without diabetes. I think we're aiming for half primips and half multis; and equal numbers of vaginal and Caesarean births. We're recruiting on the postnatal wards at the Women's Hospital.
Research in dairy animals (e.g., see my publication on the effect of LPS) have shown that in times of conflict between the needs of the whole body for glucose and non-essential functions (to the host), lactation, there is saving of glucose utilization by the mammary gland for the benefit of essential tissues (immune cells, heart, brain). This is achieved by converting the metabolism of mammary epithelial cells into glycolysis, on the account of mitochondrial respiration (the Warburg-like effects). The physiological signs for such shift are reduction in milk concentrations of lactose and glucose and increase in the concentrations of lactate and malate.
JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
Volume: 19
Issue: 1
Pages: 100-108
DOI: 10.1097/00005176-199407000-00017
Published: JUL 1994
View Journal Information
Abstract
The concentrations of lactose, glucose, glucose 6-phosphate (G6P), glucose 1-phosphate (GIP), UDPglucose (UDPglc), UDPgalactose (UDPgal), and inorganic phosphate (P(i)) (metabolites in the lactose synthesis pathway) were measured in mammary secretion from nondiabetic (ND) and insulin-dependent diabetic (IDD) mothers during the first 10 days postpartum to determine their relationship with the amount of lactose synthesized and their association with the delay in lactose synthesis in IDD mothers. For all mothers the concentrations of all metabolites were low initially, and in ND mothers the first increases occurred as follows: lactose-day 2; glucose, G6P and P(i)-day 3; GIP and UDPglc-day 4; and UDPgal-day 6. The first increases for IDD mothers occurred 1-4 days later than for ND mothers. The concentrations of glucose, G6P, G1P, UDPglc, and P(i) were related to the amount of lactose synthesized. Since the rate of lactose synthesis and concentrations of other metabolites were less than half-maximal while the concentration of glucose was low, and since there was a delay in the increase in mammary gland concentrations of glucose in IDD mothers, it is concluded that glucose availability has the potential to play a role in the regulation of the rate of lactose synthesis at lactogenesis II.
I wonder if these mothers have more interventions around birth and more separation from their babies, causing a delay in milk coming in. Another factor may be that GDM is often associated with high BMI, and these mothers have self-image/psychological factors that may inhibit them from offering their babies free access to the breast from birth. It would be interesting to distinguish outcomes depending on whether the GDM was diet controlled and the labour was spontaneous and the birth unassisted, compared to the alternatives.
I agree with Megan. Effective lactation support and management in this case is most important. Gestational diabetes, in effect, resolves itself after the birth of baby (and the placenta). These GDM mothers may need more help with breastfeeding, specifically latching on technique, to ensure effective suckling, mother-baby interaction, and of course, let-down reflex. The article by Arthur et al. (1994) suggested a delay in increase of lactose in breast milk of women with insulin dependent diabetic mothers, not GDM mothers.