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Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853 and
Mary Imogene Bassett Hospital and Research Institute, Cooperstown, NY 13326
*
2To whom correspondence should be addressed. E-mail: kmr5{at}cornell.edu
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ABSTRACT |
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 TOP ABSTRACT LITERATURE CITED |
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KEY WORDS: • obesity • lactogenesis • breastfeeding • rats • fat cow syndrome
Although much is known about the physiological and metabolic control of lactogenesis in livestock and experimental species, little attention has been given to how obesity might affect this important process. Some insight is provided by the fat cow syndrome as well as from studies of rodents fed diets high in fat. These are reviewed along with studies in women in which an association between high body mass index (BMI)3 before conception has been associated with shortened duration of lactation and with impaired initiation of lactation. Finally, more recent data will be considered that establish a specific link between high BMI before conception and delayed lactogenesis.
It has long been known that overfed and over fat dairy species do
poorly in the early postpartum period. This phenomenon, fat cow
syndrome, refers to "a combination of metabolic, digestive,
infectious, and reproductive conditions" that affects the obese
periparturient cow (1
). The metabolic conditions include
milk fever and ketosis, the digestive disorders include displaced
abomasum, the infections diseases include mastitis, and the
reproductive conditions include retained fetal membranes and metritis
(1
). Despite treatment, affected cows are likely to die,
so prevention is the preferred management strategy (2
).
The primary causal agent in fat cow syndrome is "the excessive intake
of an unbalanced diet" (1
). This results in extensive
fatty metamorphosis of the liver, which is responsible for most of the
manifestations of this condition (1
, 2
). Despite the clear
association of fat cow syndrome with early lactation failure,
lactogenesis has not been studied specifically in affected animals.
The characteristics of lactation have been studied in rats made obese
by various kinds of high fat feeding [reviewed in (3
)].
Briefly, two types of dietary treatments have been used; both produce
rats with excessive body fat when fed over a period. With cafeteria
feeding, rats are offered a selection of high fat, highly palatable
foods in addition to their usual closed formula diet. With high fat
feeding, rats are offered an open formula diet with some of the
carbohydrates replaced by additional fat.
When either of these dietary regimens is begun several weeks before
mating, rats will be heavier at conception than control animals. Such
rats may suffer from estrus cycle abnormalities, may not conceive as
readily or may implant fewer embryos than controls [reviewed in
(3
)]. In addition, rats fed these high fat diets may
deliver fewer and lighter pups than controls, are more likely to have
difficulty delivering, and their pups are much more likely to die in
the first few days after birth (4
–7
; Table 1
);T1>. In many of the litters born to obese dams, we have
observed that pups die without having any milk in their stomachs
(Rasmussen K.M., unpublished results). This observation
suggests that primary lactation failure is the cause of death in these
pups. It is possible that inappropriate maternal behavior in the
immediate postpartum period also contributes to pup death, but we have
been unable to document that this is a significant contributing cause
(Rasmussen, K. M. and McGuire, M. K., unpublished results).
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) fed rats a high fat diet
beginning at 27 d of age and, after mating beginning at 65 d
of age, killed them in either late pregnancy (d 18) or early lactation
(d 3). The metabolic transition from pregnancy to lactation was
abnormal in obese rats. As expected, plasma insulin values were higher
at d 18 of pregnancy than at d 3 of lactation in control animals.
However, this was not the case in the obese rats; plasma insulin values
at the end of pregnancy did not differ from those early in lactation.
Also as expected, plasma glucose values did not differ at these two
times in the control rats, but they were significantly higher in late
pregnancy than in early lactation in the obese rats. Plasma prolactin
concentrations also did not respond appropriately to lactation in obese
rats: they rose significantly from d 18 of pregnancy to d 3 of
lactation in control rats but not in obese rats. These unique findings
suggest inappropriate regulation of the primary substrate for
successful lactation, namely glucose, and point to impaired
lactogenesis as a possible cause of the lactation failure and high
mortality observed among the pups of obese dams.
It is more complicated to study a possible association between obesity
and lactational performance in women because the decision about whether
to breastfeed at all is determined by a mix of psychosocial and
sociodemographic factors. If one studies only those women who have
chosen to give their infant a chance to suckle, some of these factors
are eliminated or at least minimized. A woman’s ability to act on her
intention to breastfeed may be affected by the medical consequences of
her obesity. For example, women who are obese before pregnancy are at
higher risk of Cesarean delivery (8
) and of having a
macrosomic fetus (9
). Cesarean delivery may result in a
delay in giving the infant his or her first chance to suckle after
delivery; it may also result in discomfort or illness
(10
). Macrosomic infants may suffer birth trauma and often
have unstable plasma glucose values immediately after birth
(11
). In many hospitals this condition is treated by
giving the infant formula regardless of the mother’s desire to
breastfeed (Kjolhede, C. L., personal communication). If this is
successful, the total amount of formula given to the infant may be
small, but it delays early and frequent suckling, which is known to
enhance the eventual success of breastfeeding (12
).
Whether maternal fatness might be associated with any measure of
lactational performance has been examined in prospective studies in a
number of different countries. In the United States, investigators
(13
) noted in passing that there was a tendency for women
who were heavy before becoming pregnant to have ceased breastfeeding by
10 wk postpartum. In the Copenhagen Infant Feeding Study, researchers
(14
) noted that there was no association between
prepregnant BMI and duration of breastfeeding. In this population, the
196 mothers were lean (mean BMI, 21 kg/m2) and
99.5% of them attempted to breastfeed (i.e., gave their infant a
chance to suckle). Investigators in Australia (15
) limited
their subjects to 739 women who had successfully breastfed for at least
14 d. Among these women, those with a BMI > 26
kg/m2 were at a significantly increased risk of
early cessation of breastfeeding. In a more recent study in of 1350
women in Italy, prepregnant BMI (mean, 23 kg/m2)
was significantly negatively associated with the duration of exclusive
breastfeeding (16
).
Perhaps the most dramatic findings are those from a review of medical
records in a rural population of white women in the United States who
attempted to breastfeed (17
). We not only observed that
obesity (BMI > 29.0 kg/m2) was
significantly negatively associated with the duration of exclusive or
any breastfeeding, but that this also was true for overweight (BMI
= 26–29 kg/m2) women. In addition, and more
importantly for evaluating the association between obesity and
lactogenesis, we observed that both overweight and obese women were at
significant excess risk of failing to initiate breastfeeding
successfully [odds ratio, 2.54 (P < 0.05) and 3.65
(P < 0.0008), respectively]. In this study, women who
failed to initiate breastfeeding successfully were those who were no
longer breastfeeding at the time of hospital discharge at 
2 d
postpartum.
In their comprehensive investigation of risk factors for delayed onset
of lactogenesis, Chapman and Perez-Escamilla (18
)
conducted a prospective study among 192 primiparous women from
Connecticut. They reported that among other characteristics, those with
a "heavy/obese build" were significantly more likely to experience
delayed onset of lactogenesis II than those with a "slim/average
build." In a subsequent article that included 60 women from this
population who had undergone Cesarean deliveries, they
(19
) classified subjects as obese if at least two of the
following three indicators were positive: BMI 
30
kg/m2 or subscapular skinfold thickness > 85th percentile of their study population at 72 h postpartum or
heavy/obese body build on d 1 postpartum. Obese women were
significantly (P < 0.05) more likely to have low milk
transfer at 60 h postpartum, an indicator for delayed
lactogenesis. In contrast to the results of most of the studies
described above, they (19
) found that their obese subjects
were marginally more likely to breastfeed longer than their nonobese
counterparts. These results are from regression models that included
many variables not available the other studies. Because this
investigation was conducted in the context of an intervention to
stimulate milk production, their findings suggest that in-depth
breastfeeding support may be important in counteracting the expected
negative effect of maternal obesity on the duration of breastfeeding.
To investigate whether high prepregnant BMI was actually associated
with delayed lactogenesis, we (20
) conducted a prospective
investigation in a population of white women from upstate New York. The
subjects’ psychosocial characteristics related to intention to
breastfeed and intended duration of breastfeeding were assessed during
pregnancy. Breastfeeding behavior was observed and recorded in a
systematic way [using the Mother-Baby Assessment score
(21
)] by trained obstetric nurses while the women were in
the hospital. The onset of lactogenesis II was documented by daily
telephone interview in the first 5 d postpartum (18
).
Women with later (72 h postpartum) onset of lactogenesis II had a
significantly higher prepregnant BMI than did those with an earlier
onset of lactogenesis II. In addition, they were more likely to be
primiparous and, not surprisingly, less likely to have had previous
experience breastfeeding. They also had infants with a lower rating for
breastfeeding behavior in the hospital than did those with earlier
onset of lactogenesis II. There were no differences between these two
groups in psychosocial or sociodemographic characteristics, however. In
regression analysis, maternal parity was an important mediator of the
association between prepregnant BMI and the timing of lactogenesis II.
This is not unexpected because it has long been known that multiparous
women produce more milk in early lactation than primiparous women
(21
).
The results of these studies in women point to the same conclusion: high BMI values before conception are negatively associated with initiation and duration of breastfeeding. Taken together with the data from rats, the results suggest that lactogenesis II is likely to be delayed in obese individuals. In populations in which alternative methods of infant feeding are available, women may choose to offer infant formula rather than wait longer for the development of a copious milk supply, thus, terminating breastfeeding or at least shortening its duration.
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FOOTNOTES |
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3 Abbreviation used: BMI, body mass index.
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LITERATURE CITED |
|---|
|
TOPABSTRACTLITERATURE CITED |
|---|
1. Morrow, D. A. (1976) Fat cow syndrome. J. Dairy Sci. 59:1625-1629.
2. McCormack, J. (1978) Fat-cow syndrome and its complications. Vet. Med. Small Anim. Clin. 73:1057-1060.[Medline]
3. Rasmussen, K. M. (1998) Effects of under- and overnutrition on lactation in laboratory rats. J. Nutr. 128:390S-393S.
4. Wehmer, F., Bertino, M. & Jen, K.-L.C. (1979) The effects of high fat diet on reproduction in female rats. Behav. Neural Biol. 27:120-124.[Medline]
5. Rolls, B. J., Rowe, E. A., Fahrbach, S. E., Agius, L. & Williamson, D. F. (1980) Obesity and high energy diets reduce survival and growth rates of rat pups. Proc. Nutr. Soc. 39:51A(abs.).[Medline]
6. Rolls, B. J. & Rowe, E. A. (1982) Pregnancy and lactation in the obese rat: effects on maternal and pup weights. Physiol. Behav. 28:393-400.[Medline]
7. Shaw, M. A., Rasmussen, K. M. & Myers, T. R. (1997) Consumption of a high-fat diet impairs reproductive performance in Sprague-Dawley rats. J. Nutr. 127:64-69.
8. Crane, S. S., Wojtowycz, M. A., Dye, T. D., Aubry, R. H. & Artal, R. (1997) Association between pre-pregnancy obesity and the risk of cesarean delivery. Obstet. Gynecol. 89:213-216.[Abstract]
9. Baeten, J. M., Bukusi, E. A. & Lambe, M. (2001) Pregnancy complications and outcomes among overweight and obese nulliparous women. Am. J. Public Health 91:436-440.
10. Edwards, L. E., Dickes, W. F., Alton, I. R. & Hakanson, E. Y. (1978) Pregnancy in the massively obese: course, outcome, and obesity prognosis of the infant. Am. J. Obstet. Gynecol. 131:479-483.[Medline]
11. Kliegman, R., Gross, T., Morton, S. & Dunnington, R. (1984) Intrauterine growth and postnatal fasting metabolism in infants of obese mothers. J. Pediatr. 104:601-607.[Medline]
12. Salariya, E. M., Easton, P. M. & Cater, J. I. (1978) Duration of breast-feeding after early initiation and frequent feeding. Lancet ii:1141-1143.
13. Ferris, A. M., McCabe, L. T., Allen, L. H. & Pelto, G. H. (1987) Biological and sociocultural determinants of successful lactation among women in eastern Connecticut. J. Am. Diet. Assoc. 87:316-321.[Medline]
14. Michaelsen, K. F., Larsen, P. S., Thomsen, B. L. & Samuelsen, G. (1994) The Copenhagen corhort study on infant nutrition and growth: duration of breast feeding and influencing factors. Acta Paediatr 83:565-571.[Medline]
15. Rutishauser, I.H.E. & Carlin, J. B. (1992) Body mass index and duration of breast feeding: a survival analysis during the first six months of life. J. Epidemol. Commun. Health 46:559-565.
16. Riva, E., Banderali, G., Agostini, C., Silano, M., Radaelli, G. & Giovannini, M. (1999) Factors associated with initiation and duration of breastfeeding in Italy. Acta Paediatr 88:411-415.[Medline]
17. Hilson, J. A., Rasmussen, K. M. & Kjolhede, C. L. (1997) Maternal obesity and breastfeeding success in a rural population of Caucasian women. Am. J. Clin. Nutr. 66:1371-1378.
18. Chapman, D. J. & Perez-Escamilla, R. (1999) Identification of risk factors for delayed onset of lactation. J. Am. Diet. Assoc. 99:450-454.[Medline]
19. Chapman, D. J. & Perez-Escamilla, R. (2000) Maternal perception of the onset of lactation is a valid, public health indicator of lactogenesis stage II. J. Nutr. 130:2972-2980.
20. Hilson, J. A. (2000) Maternal Obesity and Breastfeeding Success. PhD thesis 2000:162 Cornell University , Ithaca, NY .
21. Mulford, C. (1992) The mother-baby assessment (MBA): an Apgar score for breastfeeding. J. Hum. Lact. 8:79-82.
22. Hytten, F. E. (1959) Differences in yield and composition between first and second lactations. Proc. Nutr. Soc. 18:xxi-xxii.
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