diabetes research and clinical practice 1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1

Contents available at ScienceDirect

Diabetes Research
and Clinical Practice
journal homepage: www.elsevier.com/locat e/dia bre s

Review

The physiological and glycaemic changes in

breastfeeding women with type 1 diabetes mellitus

Naomi Achong a,b,*, Emma L. Duncan a,b,c, H. David McIntyre a,d, Leonie Callaway a,b
a
The University of Queensland, Brisbane, Queensland 4072, Australia
b
Royal Brisbane and Women’s Hospital, Herston, Queensland 4029, Australia
c
The Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia
d
Mater Health Services, Raymond Terrace, South Brisbane, Queensland 4101, Australia

A R T I C L E I N F O A B S T R A C T

Article history: The World Health Organisation recommends exclusive breastfeeding for the first six
Received 27 July 2017 months of life (Australian institute of health and welfare, 2011). Breastfeeding confers
Received in revised form many short- and long-term benefits for infants and mothers, including reduced childhood
11 October 2017 obesity and lower maternal body weight (Infant feeding survey, 2010; CDC National immu-
Accepted 7 November 2017 nization surveys, 2012 and 2013; Sorkio et al., 2010; Hummel et al., 2014; Finkelstein et al.,
Available online 14 November 2017 2013). Exclusive breastfeeding is also recommended in women with type 1 diabetes melli-
tus (T1DM), for at least four months (Nucci et al., 2017). However, the impact of breastfeed-
ing on mothers with T1DM, and, conversely, the impact of maternal T1DM on
Keywords:
breastfeeding, is not clear. This review summarizes current knowledge regarding the epi-
Breastfeeding
demiology and physiology of breastfeeding in women with T1DM. In particular, it high-
Type 1 diabetes mellitus
lights the relationship between breastfeeding and glycaemia. Potential areas for future
research are also identified.
Ó 2017 Published by Elsevier Ireland Ltd.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
2. Epidemiology of breastfeeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
2.1. Breastfeeding rates in the general population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
2.2. Breastfeeding rates in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3. Breastmilk production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3.1. Onset of lactogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3.2. Breastmilk constituency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
3.3. Rates of breastmilk production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95
4. Breastmilk production in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95

* Corresponding author at: PO Box 5006, Mt Gravatt East, Brisbane 4122, Australia.
E-mail address: nachong@uq.edu.au (N. Achong).
https://doi.org/10.1016/j.diabres.2017.11.005
0168-8227/Ó 2017 Published by Elsevier Ireland Ltd.
94 diabetes research and clinical practice 1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1

4.1. Onset of lactogenesis in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95

4.2. Breastmilk constituency in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95
5. Insulin in breastmilk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95
5.1. The rates of breastmilk production in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
6. Energy demands of lactation and effect on insulin requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
6.1. Insulin requirements in breastfeeding women. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
7. Acute glycaemic changes induced by suckling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
7.1. Effect of suckling on glucose levels in women without T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
7.2. Effect of suckling on glucose levels in women with T1DM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
7.3. Potential hormonal mechanisms underlying changes in glycaemia induced by suckling . . . . . . . . . . . . . . . . . . . 98
7.4. Areas for further research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
8. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Conflicts of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Funding sources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

1. Introduction

This paper reviews the important issues pertaining to breast-
feeding in women with type 1 diabetes mellitus (T1DM).
Firstly, it presents the epidemiology of breastfeeding, both
in the general population and in women with T1DM. Sec-
ondly, the physiology of lactogenesis is discussed, highlight-
ing changes to lactogenesis in women with T1DM. Finally
this review explores glycaemia in breastfeeding women with
T1DM with particular emphasis to the impact of breastfeed-
ing on maternal glycaemia and insulin requirements and
the effect of suckling on maternal glycaemia.
2. Epidemiology of breastfeeding
2.1. Breastfeeding rates in the general population
There is considerable variation in the regional rates of breast-
feeding in the general population. The rates of breastfeeding
initiation in Australia are 96% [1], England 83% [2] and in the
United States 79% [3]. In the first six months postpartum,
rates of breastfeeding reduce markedly. Interestingly, the
decline in breastfeeding is not proportional to the rates of
breastfeeding initiation. By six months, breastfeeding rates
are only 15% in Australia compared with 1% in the UK and
49% in the USA.
2.2. Breastfeeding rates in women with T1DM
Comparative rates of breastfeeding in women with or without
T1DM are inconsistent. Some studies have shown similar
rates of breastfeeding initiation in diabetic and non-diabetic
women (>90% in both groups in Sorkio et al. [4] and >95% in
Hummel et al.) [5]. However, other studies have suggested
lower rates of breastfeeding initiation in women with T1DM
compared with the non-diabetic population. A study con-
ducted in Ontario involving 107 women with T1DM showed
an odds ratio of 0.42 for breastfeeding initiation compared
with non-diabetic women [6]. The reported duration of
breastfeeding also varies; however, most studies suggest
shorter duration of breastfeeding in women with T1DM
[4,5,7–9]. A large international study of infant feeding in the
first six months of life showed breastfeeding rates in women
with T1DM were lower compared to the general population
(51–60% vs. 70–80%) [7]. In some but not all studies of the off-
spring of women with T1DM, shorter duration of breastfeed-
ing is predictive of higher body mass index in childhood
[8,10].
In the general population, the major determinants of long-
term breastfeeding are early initiation of suckling and mark-
ers of high socioeconomic status [4,6,9,11–14]. In women with
T1DM, initial breast contact is often delayed because of higher
rates of operative delivery and neonatal intensive care admis-
sions [4,9]. However, T1DM per se is not an independent pre-
dictor of long-term breastfeeding [4,9]. In almost 90% of
women, with or without T1DM, the main reason for ceasing
breastfeeding is perceived poor milk supply [11]. Only 6% of
women with T1DM reported fear of, or actual, hypoglycaemia,
as a factor determining breastfeeding initiation and/or
cessation.
3. Breastmilk production
3.1. Onset of lactogenesis
In women without diabetes, the progression from colostrum
production to the onset of lactogenesis generally occurs
within a week postpartum (mean day 2 postpartum) [15]. Lac-
togenesis is heralded by a postpartum rise in milk lactose and
fall in milk nitrogen concentrations.
3.2. Breastmilk constituency
Lactose, synthesised from glucose and galactose, is the major
carbohydrate in breastmilk and the main osmotic compo-
nent. As such, lactose concentration determines the volume
of milk produced.
The main glucose transporter in the mammary gland is
GLUT1, a passive glucose transporter, and the majority of glu-
cose transported into the mammary glands is used to synthe-
sise lactose. In non-diabetic women, the free glucose
concentration in breastmilk is constant regardless of the stor-
 diabetes research and clinical practice
age time in the breast [16]. Similarly, the lactose concentra-
tion of milk is constant over a 24 h period, unlike the fat con-
tent which is variable [17].
3.3. Rates of breastmilk production
Volumetric studies using computerised breast measurement
enable the assessment of milk production following an epi-
sode of suckling and the volume of milk ingested by the
infant [18]. This measurement technique shows good repro-
ducibility with a coefficient of variation of 1.6% between
repeated measurements over a 24-h period; and show good
correlation with infant weight changes before and after suck-
ling [18]. Studies using CT volumetric assessment indicate
that the rate of milk synthesis increases after suckling and
remains constant for 4–6 h [18,19]. However, the absolute rate
of milk synthesis varies after each feed, between the breasts
of the same woman and between different women [18–20].
Infants regulate their oral intake and do not empty the
breast completely of milk [19,20]. The rate of milk production
after suckling is increased by greater emptying of the breast
and more frequent suckling [19,20]. The time of day also
affects the rate of milk synthesis as most infants consume
the majority of their daily milk consumption during the day
[21].
4. Breastmilk production in women with
T1DM
4.1. Onset of lactogenesis in women with T1DM
The onset of lactogenesis is affected by a number of factors.
In women with and without diabetes, early initiation and fre-
quency of suckling are associated with higher breastmilk pro-
lactin levels, indicative of lactogenesis [22]. In women with
T1DM, early mother-baby separation is more common than
in the non-diabetic population due to higher rates of peripar-
tum complications, both maternal and neonatal (with more
frequent admissions to the special care nursery or neonatal
intensive care unit) [8,23].
Women with good glycaemic control have a similar onset
of lactogenesis as the non-diabetic population (average day
2). However, poor glycaemic control may delay the onset of
lactogenesis typically by a day [15,22,24,25]. This delay is seen
in women with T1DM and in women with other forms dia-
betes in pregnancy [26]. For example, up to one-third of
women with gestational diabetes requiring insulin have
delayed lactogenesis [27]. In this population, insulin treat-
ment, obesity, increasing maternal age and suboptimal initial
breastfeeding are independently associated with the delay in
lactogenesis [27].
4.2. Breastmilk constituency in women with T1DM
The lactose content of breastmilk from diabetic women is
similar to that of non-diabetic women [28]. Studies concern-
ing the glucose content are inconsistent. One suggested that
the glucose concentration in breastmilk in women with
T1DM [with average HbA1c of 8.1% (65 mmol/mol)] is higher
1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1 95
and more variable than in non-diabetic women; but the abso-
lute differences remain low (0.7 mg/g vs 0.3 mg/g) despite
comparable lactose content [28]. However, a second study in
women with similar glycaemic control showed no difference
in breastmilk glucose concentration between the two groups
(0.68 mmol/L vs. 0.66 mmol/L) [29].
It has been proposed that ingestion of milk from women
with diabetes and hyperglycaemia during breastfeeding may
affect their offspring’s development possibly due to differ-
ences in milk composition. Rat studies suggest that increased
exposure to glucose in the early postnatal period can cause
significant changes in the structure and function of key
hypothalamic nuclei involved in weight and appetite regula-
tion [30]. The volume of breastmilk ingested by an infant from
women with T1DM in the first postnatal week has been pos-
itively correlated with the risk of overweight in early child-
hood (at two years old) [31]. This study did not assess milk
composition as a contributing factor. In a study specifically
assessing the impact of using banked milk in early postnatal
life, infants from women with T1DM given banked milk
(obtained from non-diabetic mothers) during the first week
of postnatal life had reduced rates of overweight (at age two
years) compared with infants breastfed exclusively from their
diabetic mothers. [10]. These differences in rates of over-
weight were only evident with differential feeding in the first
postpartum week and not thereafter. The psychomotor and
language skills of this cohort of children were also assessed,
with a suggestion that higher volumes of ingestion of breast-
milk from women with T1DM in week one were associated
with the early attainment of psychomotor milestones but
later language development (manifesting as a delay in speak-
ing), both when compared within the group of breastfeeding
T1DM mothers and compared with banked milk feeding
[30,32]. These studies collectively suggest an adverse effect
on the infant from the ingestion of hyperglycaemic breast-
milk. However, these early postpartum studies have not been
replicated and any contribution from differences in milk com-
position has not been assessed.
5. Insulin in breastmilk
In women with normal glucose tolerance delivering at term,
milk insulin concentration decline from days 3 to 7 postpar-
tum [33]. The initial concentrations seen at day 3 were greater
than the normal fasting serum concentration. Whitmore
compared the insulin concentration in a small cohort of
women (five women without diabetes, four women with
T1DM and five women with type 2 diabetes mellitus not trea-
ted with insulin) during established lactation (1–6 months
postpartum) [34]. This study showed comparable insulin
levels in all groups of women noting that women with
T2DM would be expected to have higher serum concentra-
tions of insulin compared to women without diabetes and
T1DM. In women with T1DM insulin levels were variable
solely attributable to administration of exogenous insulin.
However the C-peptide concentrations in breastmilk were sig-
nificantly lower than the serum levels which suggests an
active transport for insulin. In women without diabetes insu-
lin levels in breastmilk have been associated with varying
96 diabetes research and clinical practice 1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1

changes in infant gut microbial composition [35]. Higher

Insulin requirements
breastmilk insulin has also negatively correlates with infant

Lower postpartum

Lower postpartum

Lower postpartum
pre-pregnancy vs.
postpartum in AF
weight and lean mass [36]. However this needs to be inter-
preted in view of the increased risk of intrauterine growth
restriction seen in infants of mothers with diabetes. No stud-
ies have specifically examined the effect of exogenous insulin
on infant parameters.
N/A

N/A

N/A
N/A
N/A
M

M
5.1. The rates of breastmilk production in women with
T1DM
Insulin requirements

postpartum

postpartum

postpartum
postpartum
pre-pregnancy vs.

Both hypo- and hyperglycaemia have a deleterious effect on

postpartum in BF

lactogenesis. The rate of lactose synthesis is reduced by more

N/A: not assessed; M no significant difference; T1DM: type one diabetes mellitus; controls: non-diabetic women; BF: breastfeeding; AF: artificially-feeding.
than 50% during hypoglycaemia [16]. Similarly, hypergly-
caemia accounts for more than 60% of the variance in milk
Lower

Lower

Lower
Lower
production in T1DM [22].
N/A

N/A
N/A
N/A
M
M

6. Energy demands of lactation and effect on

insulin requirements
breastfeeding (BF) vs artificially-

Lactogenesis increases maternal energy requirements

because of the caloric content of milk and the energy required
Insulin requirements in

for milk production. Exclusive breastfeeding within the first

six months postpartum increases maternal caloric demands
feeding (AF) women

by approximately 450 kJ/day [37].

6.1. Insulin requirements in breastfeeding women

BF < AF

BF < AF

The insulin requirements in women with T1DM who breast-

N/A
N/A

feed compared with those who artificially feed, has been vari-
M
M
M

M
M
M
M
Table 1 – Insulin requirements in postpartum women with type 1 diabetes mellitus.

ably reported (Table 1). Most studies show either reduced or

comparable insulin requirements in women who beastfeed
compared with those who artificially feed, with no clear rela-
Number of participants

14 T1DM, 25 controls

30 T1DM, 30 controls

tionship to the duration of time postpartum. Of note,

artificial-feeding has been reported to have reduced insulin
requirements compared to the pre-pregnancy requirement,
for up to three months postpartum; the reasons for this are
13 BF, 21 AF

13 BF, 21 AF

27 BF, 15 AF
55 BF, 33 AF
18 BF, 6 AF

18 BF, 6 AF

12 BF, 6 AF

8 BF, 8 AF

unclear [12,38]. (Table 1). A major limitation of some of these

58 T1DM

studies was the use of intermittent self-monitoring of blood

glucose levels, rather than continuous glucose monitoring
(CGMS), which may affect accurate ascertainment of hypogly-
caemia and hence the recognition of the need to reduce insu-
lin doses.
Time postpartum

Stage et al. [11] showed that at four months postpartum

total insulin doses in exclusively lactating women with
T1DM were lower than their pre-pregnancy doses, and lower
(weeks)

than artificially feeding women. In artificially feeding women,

8–16

the dose of insulin was comparable postpartum compared to

12
16
1
1
1
1
6
6
8
8

pre-pregnancy. However, in this study insulin doses were not

adjusted for weight; and breastfeeding women may have had
greater weight loss than artificially feeding women [39–41]. A
Saez-de-Illbarra et al. [37]

Saez-de-Illbarra et al. [37]

later study by Rivello et al. [42] assessed insulin requirements

Whichelow et al. [17]

in a relatively homogenous population of 18 women with

Murtaugh et al. [27]
Rayburn et al. [43]

Achong et al. [44]

T1DM (12 breastfeeding, 6 artificially feeding). Within the first

Riviello et al. [41]
Davies et al. [42]

Davies et al. [42]

Ferris et al. [26]

Stage et al. [16]

two weeks postpartum, breastfeeding women had an

increase in the frequency of hypoglycaemia, compared to arti-
ficially feeding women, particularly overnight and fasting,
despite being advised to increase their caloric intake by 300
kcal/d. The insulin requirement, particularly basal insulin,
 diabetes research and clinical practice 1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1 97

was reduced in breastfeeding women compared to their pre-

p value comparing
pregnancy doses and to insulin requirements in artificially
feeding women. From weeks 3–8 of the study, there was no
difference in the rate of hypoglycaemia in these two groups.

BF and CC
However, both these studies were limited by the use of finger-
prick BGL testing and absence of dietary record.

0.02

0.64

0.02
0.70
0.03

0.70
0.87

0.84
0.02
0.3
In a separate study in a larger group of women with T1DM,
insulin requirements were significantly lower from 1 to 8
weeks postpartum in all women, with no difference seen
between breastfeeding and artificially feeding women [38]. A

Clinic controls,
number of older studies have also explored the changes in

13.64 (3.12)

10.00 (6.92)

14.80 (3.75)
7028 (2194)
insulin requirements postpartum, recognising that the appli-

5.06 (3.67)

6.06 (6.95)

4.59 (3.02)
cability of these studies is limited by the lack of use of insulin

CC (6)
analogs, incomplete recording of dietary intake, variable

4.31

3.66

4.29
advice regarding carbohydrate demands of breastfeeding,
and use of fingerprick BGLs only. These studies from the
1980s also showed no difference in the insulin requirements
at 2–3 months postpartum in breastfeeding compared with

p value comparing
artificial feeding women [12,23,24]. Fasting glucose levels
were, however, reported to be lower in the breastfeeding

Table 2 – Summary of the glycaemia parameters of breastfeeding, artificial feeding and clinic control women [45].
women compared to the artificially feeding or combined feed-

BF and AF

There were no significant differences between the artificially-feeding women and clinic controls for any of the above parameters.
ing women at six weeks postpartum [23]. Other studies have
also shown a reduction in insulin requirements within the

0.06

0.52

0.05
0.04

0.72
0.02

0.24
0.22

0.79
0.02
first postpartum week in breastfeeding women compared to
artificially feeding women that was not sustained at six
weeks postpartum [43]. However, a similar study failed to
Artificially-feeding

show a difference in insulin requirements in breastfeeding

women postpartum compared with pre-pregnancy [44].
women, AF (8)

We recently published a prospective observational study

16.26 (5.96)

14.17 (9.17)

16.02 (5.99)
6433 (1914)

5.10 (4.21)

4.35 (4.36)

5.41 (4.48)
comparing glycaemia (assessed using a continuous glucose
monitoring system, CGMS) and insulin requirements in 4.45

3.81

4.47
breastfeeding women compared to artificially feeding women
and compared to clinic-based women with T1DM but no

SD: standard deviation; LBGI: low blood glucose index; HBGI: high blood glucose index.
recent history of pregnancy or breastfeeding [45]. Somewhat
unexpectedly, we demonstrated that breastfeeding women
Breastfeeding women,

with T1DM had more stable glycaemic patterns than either

artificially feeding women or clinic-based women. This was
evidenced by a reduced rate of hyperglycaemia but compara-
ble hypoglycaemia. This was seen both in women during nor-
mal daily activities (with no restrictions on diet or insulin
5.77 (2.87)
9.52 (2.59)

7.46 (5.56)
9.46 (4.71)

4.91 (2.64)
9.42 (2.70)
8143 (790)

intake) and also after a controlled meal with or without asso-

BF (8)

ciated suckling (Table 2). Our study was performed in women

3.45

3.32

3.40

at 2–4 months postpartum. Similar studies are needed to

examine the influence of breastfeeding particularly in the
early postpartum period.
Duration monitoring in hours, mean (SD)

7. Acute glycaemic changes induced by

suckling
Glycaemic parameters – overnight
Glycaemic parameters – overall

7.1. Effect of suckling on glucose levels in women without

Glycaemic parameters – day

T1DM
SD of glucose, mean

SD of glucose, mean

SD of glucose, mean

The literature regarding the influence of suckling on maternal

HBGI, mean (SD)

HBGI, mean (SD)

HBGI, mean (SD)

LBGI, mean (SD)

LBGI, mean (SD)

LBGI, mean (SD)

glycaemia is also unclear. Using CGM in women with normal

glucose tolerance, no effect of suckling on glycaemia in the
following 60 mins was observed [46,47]. The duration of mon-
itoring may have been insufficient to detect glycaemic
changes due to the lag between changes in serum and inter-
stitial glucose concentrations. Further, glucose transferred
98 diabetes research and clinical practice
into the breast is utilised for milk production which continues
for hours after suckling. Finally, hypoglycaemia is uncommon
in individuals with normal glucose tolerance because of pre-
served counter-regulatory responses.
7.2. Effect of suckling on glucose levels in women with
T1DM
Self-reported hypoglycaemia in women with T1DM post-
suckling has been reported [48]. However, studies confirming
this are limited. Saez et al. [38] compared glycaemia in breast-
feeding and artificially feeding women with T1DM. Mean glu-
cose levels were lower in the breastfeeding group in the first
week postpartum (p = .05) but were comparable at one and
two months postpartum. Hypoglycaemia was self-reported
and considered related to suckling if occurring within thirty
minutes of suckling. Hypoglycaemia was more commonly
unrelated to suckling than related to suckling. Overall, there
was no difference in hypoglycaemia (BGLs < 3.0 mmol/L),
HbA1c or insulin dose between breastfeeding and artificially
feeding groups. This study was limited by the detection of
hypoglycaemia by fingerprick BGLs (rather than CGM) and
unrecorded oral intake.
Murtagh et al. [24] considered the effect of breast pumping
on glycaemia in women with T1DM compared to non-diabetic
women two weeks postpartum. BGLs declined after breast
pumping in both groups; however the change was 55% greater
in women with T1DM. In all women, BGLs remained >5.6
mmol/L. The decline in BGLs was exaggerated after a second
episode of breast pumping the time between episodes of
breast pumping was not provided). In the women with
T1DM, three of the four women had a BGL of <2.8 mmol/L
whereas BGLs remained >3.9 mmol/L in the non-diabetic
women.
In a separate study by these authors, BGLs were analysed
80 mins after a non-standard breakfast in women with
T1DM and without diabetes 2–84 days postpartum [24]. The
decline in glucose was greater in women with T1DM com-
pared to non-diabetic women. However, only 3% (3/95)
women with T1DM had a glucose of <2.8 mmol/; and all epi-
sodes occurred within the first two weeks postpartum. In this
study, oral intake was not standardised and insulin doses
were not recorded. Finally, milk content and production dif-
fered at day 2 postpartum compared with day 84 postpartum.
The hormonal changes of pregnancy can also persist for up to
six weeks postpartum. As such, the study population may
have been heterogeneous with regard to milk production
and hormonal status.
In our recent study, acute suckling reduced the maternal
serum glucose level but was insufficient to cause hypogly-
caemia in the majority of episodes [49]. The lowest mean glu-
cose concentration occurred at 90–120 min (mins) after the
onset of suckling, with an average BGL of 8.3 mmol/L. Follow-
ing a controlled meal, suckling reduced the maternal serum
glucose – though without casing hypoglycaemia; in contrast,
refraining from suckling resulted in a rise in maternal serum
glucose. The study was performed in women at 2–4 months
postpartum and may not be applicable to the early postpar-
tum period.
1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1
7.3. Potential hormonal mechanisms underlying changes
in glycaemia induced by suckling
Suckling could influence glycaemia directly through glucose
uptake into the breast (as discussed above) or indirectly via
the action of lactogenic hormones. Oxytocin and prolactin
are the main lactogenic hormones. Both also influence carbo-
hydrate metabolism.
Prolactin peaks 40–45 min after the onset of suckling
[50,51]. Prolactin acts directly on pancreatic beta-cells and
increases insulin concentration [52–54]. However patients
with T1DM have little or no endogenous insulin production.
In human adipose tissue, prolactin also suppresses lipogene-
sis and decreases GLUT4 mRNA expression, which reduces
glucose uptake [55]. Basal and peak prolactin levels fall in
breastfeeding women, but remain above the normal limit,
within the 3–6 months postpartum despite stable milk pro-
duction [56,57]. Consequently, prolactin is unlikely to induce
changes in glycaemia in women with T1DM at later time
points postpartum (such as was assessed in our study).
Oxytocin mediates the milk ejection reflex. It is also
expressed in insulin-sensitive tissues (e.g. adipocytes, skele-
tal and cardiac muscle and endothelial cells) and can stimu-
late insulin and glucagon secretion [58,59]. In non-diabetic
patients, oxytocin causes a rise in glucose and glucagon fol-
lowed by a rise in insulin and adrenaline (Fig. 1) [60]. In indi-
viduals with T1D, little effect on insulin secretion is expected.
However, in individuals with some preserved hormonal
responses to hypoglycaemia, oxytocin stimulates glucagon
secretion [61]. Oxytocin can also increase glucose uptake into
Oxytocin
glucose uptake
↑ insulin ↑ glucagon
into muscle
Changes with
Type 1 Diabetes
Oxytocin
glucose uptake
↑ insulin ↑ glucagon
into muscle
Lile endogenous Reduced with
insulin producon long-standing T1D
in T1D
Fig. 1 – Effects of oxytocin on carbohydrate metabolism in
non-diabetic individuals.
 diabetes research and clinical practice
skeletal muscle [62] and cardiomyocytes, by a direct action via
the oxytocin receptor [63]. In T1DM glucagon secretion is pro-
gressively lost with longer duration of diabetes [64]. As such,
in long-standing T1D, oxytocin may have a more pronounced
effect on glucose uptake into skeletal muscle.
7.4. Areas for further research
Glycaemia in breastfeeding women with T1DM is poorly
described and many of these studies were conducted before
the advent of contemporary means of glucose monitoring
including continuous glucose monitoring systems [49]. Con-
sequently, there is no standard recommendation regarding
insulin doses during breastfeeding and the risk of hypogly-
caemia during/after suckling. Future research should aim to
address the following areas:
1. The overall glycaemic patterns in breastfeeding women
compared to artificial feeding women. In particular, the
difference in insulin requirements needs to be further
defined.
2. The acute effects of suckling on glycaemia. If acute effects
are present, what dietary recommendations (or changes to
insulin doses) are required to mitigate these effects? Such
future studies should consider the use of CGMS or other
state-of-the-art assessment of glycaemia.
3. The impact of breastfeeding on maternal glycaemia in the
early postpartum period, particularly with respect to
maternal hypoglycaemia.
4. The cellular/physiologic mechanisms underlying the
effect of suckling on glycaemia.
5. The long-term metabolic implications on the offspring of
women with diabetes who were exposed to milk contain-
ing high concentrations of glucose in the immediate
post-partum period.
This paper was written as state-of-the-art review [65]. A
literature search was undertaken using PubMed with the
main search terms being ‘‘type 1 diabetes”, ‘‘insulin depen-
dent”, ‘‘breastfeeding”, ‘‘lactation”, ‘‘lactogenesis”, ‘‘gly-
caemia”, ‘‘insulin”, ‘‘hypoglycaemia”, ‘‘breastmilk”,
‘‘prolactin” and ‘‘oxytocin”. All available studies were
examined. No formal quality assessment of the studies was
performed however randomised controlled studies and com-
parative studies with concurrent controls were prioritised,
particularly if contemporary.
8. Conclusion
T1DM is a common endocrinopathy in women of child-
bearing age. Breastfeeding has well-recognised maternal
and fetal benefits and should be strongly encouraged in this
population, if it is safe to do so. Lactogenesis may be delayed
in women with T1DM, and is adversely affected by poor gly-
caemic control and early mother-baby separation. There is
no clear evidence that breastfeeding increases the maternal
risk of hypoglycaemia at 2–4 months postpartum; however,
monitoring of blood sugar levels should be undertaken to
determine any acute effect of suckling on glycaemia.
1 3 5 ( 2 0 1 8 ) 9 3 –1 0 1 99
However, the impact of breastfeeding on maternal glycaemia
in the early postpartum period is unclear. The optimal man-
agement of women with type 1 diabetes during breastfeeding
needs clarification to enable better support of these women in
undertaking prolonged breast feeding. Further, potential for
long-term metabolic implications in infants who ingest
breastmilk containing high glucose concentrations warrants
further research.
Conflicts of interest
Nil.
Funding sources
NA received a Royal Brisbane and Women’s Hospital Founda-
tion Grant and a NHMRC Research Grant to support this
research.
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