Marasco et al.

J
J Hum Hum
Lact Lact2000Polycys
16(2), 16(2), 2000tic Ovary Syndrome

Insights in Practice

Polycystic Ovary Syndrome: A Connection to Insufficient Milk Supply?

Lisa Marasco, BA, IBCLC, Chele Marmet, MA, IBCLC, and Ellen Shell, MA, IBCLC

Abstract
Despite advances in lactation skills and knowledge, insufficient milk production still contin-
ues to mystify mothers and lactation consultants alike. Based on 3 cases with similar threads, a
connection is proposed between polycystic ovary syndrome (PCOS) and insufficient milk
supply. Described are the etiology and possible symptoms of PCOS such as amenor-
rhea/oligomenorrhea, hirsutism, obesity, infertility, persistent acne, ovarian cysts, elevated tri-
glycerides, and adult-onset diabetes, along with possible pathological interference with mam-
mogenesis, lactogenesis, and galactopoiesis. Clinical suggestions include guidelines for
screening mothers and careful monitoring of babies at risk. Further research is necessary to
confirm the proposed association and to develop therapies with the potential to improve lacta-
tion success. J Hum Lact 2000;16(2):143-148.
Keywords: breastfeeding, lactation, infertility, polycystic ovary syndrome, Stein-Leventhal
syndrome, hyperandrogenic chronic anovulation syndrome, lactogenesis, insufficient milk
supply, insufficient mammary tissue, failure to thrive

Knowledge regarding the influence of various factors
upon the physiology of lactogenesis and galactopoiesis
has progressed rapidly in the past 20 years. Neverthe-
less, breastfeeding professionals continue to be plagued
by enigmatic cases that defy all of our skills and applied
knowledge. Despite animal experts’ reports that lacta-
tion failure in animals is extremely rare, it has been vari-
1
ously estimated that between 2% and 15% of women
are unable to produce enough milk to support their
babies.
Received for review, April 6, 1998; revised manuscript accepted for publica-
tion, October 5, 1999.
Lisa Marasco is a lactation consultant in private practice doing graduate
studies in lactation at the Lactation Institute. Chele Marmet and Ellen Shell
are directors of the Lactation Institute in Encino, California, and are adjunct
faculty in lactation at Pacific Oaks College, Pasadena, California. Address
correspondence to Lisa Marasco, BA, IBCLC, 4452 Village Knoll Drive,
Santa Maria, CA 93455, USA.
The authors would also like to acknowledge Sally Chasman, IBCLC, clinical
instructor for the Lactation Institute, for her case experience.
J Hum Lact 16(2), 2000
 Copyright 2000 International Lactation Consultant Association
Research in the past two decades has identified sev-
eral possible physical causes of primary maternal lacta-
2
tion failure, including breast surgeries (augmenta-
tion/reduction mammoplasties, biopsies), low thyroid
hormone, pituitary problems, excessive hemorrhaging,
and uncontrolled diabetes. Another possible fac-
tor—insufficient mammary tissue—has been noted,1
but the cause is not well understood. However, lactation
and health professionals continue to encounter puzzling
cases that do not respond to methods commonly used to
increase milk supply.
The prevalence of polycys tic ovary syndrome
(PCOS) has been estimated at anywhere from 3% to
3,4
20% of the female population. Originally called
5
Stein-Leventhal syndrome and described as consisting
of amenorrhea, hirsutism, and obesity in association
with large, cystic ovaries, PCOS symptoms typically
develop during adolescence, although some women do
not exhibit clear clinical manifestations until after
puberty.6 As research has progressed, clinical markers
have expanded to include elevated LH/FSH ratios, tes-
tosterone, estrogen, dehydroephiandrosterone sulfate,
and cholesterol; hyperinsulinemia; extremely low lev-

143
144 Marasco et al.
els of progesterone; and persistent acne.6 Some women
with PCOS have high serum prolactin levels that may
7
result in galactorrhea. Infertility problems, including
miscarriages, are common. Many of these women
develop diabetes in their 30s and 40s, and the high cho-
lesterol levels often associated with the syndrome put
8 16,17
them at risk for cardiovascular disease as well. PCOS
also has been correlated with increased risks for
9 10
endometrial and breast cancers.
PCOS criteria and terminology are in flux. While
Stein-Leventhal syndrome was diagnosed based on
ovarian morphology, PCOS is now commonly used to
describe the constellation of clinical and hormonal
clues involved. Current research is now leading away
from specific diagnostic criteria, focusing instead on the
larger picture of two dominant characteristics of the
syndrome: chronic anovulation and hyperandrogene-
mia. Thus, the disorder has recently been renamed as the
11
syndrome of hyperandrogenic chronic anovulation.
12
Cresswell et al. described two distinct forms of
PCOS with separate potential gestational origins, postu-
lating that excessive in-utero fetal exposure to andro-
gens may play a role in the development of PCOS
pathology. Choosing subjects according to the criteria
of the presence of multiple ovarian cysts, two groups
emerged. Women with the first form were classically
obese and were born to overweight mothers. They had
higher-than-average birth weights and as adults had ele-
vated testosterone levels, pointing to a possible vertical
transmission and suggesting a genetic component, a
13,14
finding shared by other researchers. Women present-
ing with the second form were of normal stature and did
not have excess testosterone. These women were dis-
covered to have gestated longer than 40 weeks as
infants.
Current literature reveals many variations in diagnos-
tic criteria for PCOS. Each case must be assessed indi-
vidually, and the diagnosis is often one of exclusion for
15
all other causes of the presenting clinical symptoms.
For research purposes, Charles Glueck, MD, of Jewish
Hospital in Cincinnati, Ohio, uses three possible mini-
mum criteria for diagnosis: (1) demonstration of multi-
ple ovarian cysts on pelvic ultrasound, or the combina-
tion of either (2) fasting hyperinsulinemia plus high
serum testosterone or (3) fasting hyperinsulinemia plus
amenorrhea/oligomenorrhea (personal communica-
tion, April 1998).
Treatment has traditionally centered around present-
ing symptoms and complaints: birth control pills to
J Hum Lact 16(2), 2000
regulate cycles, fertility medications to facilitate preg-
nancy, antiandrogen drugs such as spironolactone to
combat hirsutism, and the promotion of weight loss to
control hyperinsulinemia. More recently, oral antidia-
betes drugs have been explored as a new approach to
reversing the endocrinopathy of PCOS, with encourag-
ing results. In many cases, however, symptoms are
treated without the formality of a specific diagnosis.
Case Histories
The following cases illustrate milk supply failures
that remain unexplained after extensive screening and
intervention. While the details and official diagnoses
varied, common threads can be found in the partici-
pants’ health histories that suggest a possible common
pathology.
Case 1. “Shari,” age 26, gravida 2, para 2, was re-
ferred to and saw the lactation consultant at 6 days post-
partum because her baby had suffered a 12.6% weight
loss. Shari reported that with her first baby, now 5 years
old, breastfeeding was not established due to birth com-
plications, introduction of bottles, and lack of knowl-
edgeable help. The new baby, “Ryan,” was born after a
24-hour labor augmented by pitocin and accompanied
with an intrathecal narcotic; Shari reported heavy bleed-
ing afterward, though no transfusion was necessary. A
strong desire to breastfeed Ryan was expressed, and
Shari demonstrated willingness to follow any pre-
scribed management suggestions.
An examination of Shari’s breasts revealed soft, flac-
cid breasts, somewhat asymmetrical but with good
breast growth during pregnancy (48C to 50DD). Her
nipples and areolar tissue were normal, as was the
baby’s digital suck assessment. Observed positioning
was not optimal, and she complained of some nipple
pain, but this was easily rectified. Once latched cor-
rectly, Ryan suckled well. Test weights (pre- and post-
feeding) on an electronic baby scale18 showed an intake
of approximately 22 ccs after 30 minutes of breastfeed-
ing. Shari reported that the baby had been previously
feeding at 3- to 4-hour intervals.
In the written maternal history, past pituitary prob-
lems were noted. Further questioning revealed that
Shari had been diagnosed with Stein-Leventhal syn-
drome and also had experienced a weight gain of 54.5
kg (120 lbs) since her first baby. She reported difficulty
becoming pregnant and had suffered from irregular
menses since menarche at age 12. Progesterone therapy
J Hum Lact 16(2), 2000 Polycystic Ovary Syndrome
had been initiated when Shari was 20 to help regulate
her cycles, and her first baby, unplanned, was conceived
during this therapy; the second baby was conceived
after discontinuation of clomid treatments for infertility.
The original assessment of the lactation consultant
was delayed lactogenesis of unknown origin, possibly
due to poor latch and infrequent feedings. It was initially
hoped that positional interventions and increasing the
frequency of feeds to 8 to 12 times a day would make a
difference. At age 10 days, however, Ryan’s weight
remained the same and a test weight showed an intake of
only 28 ccs after 30 minutes of breastfeeding. Supple-
mental feeds of pumped milk plus artificial infant milk
were initiated for Ryan, and Shari was taught breast
19
massage and breast compression to maximize Ryan’s
intake while breastfeeding. She was asked to monitor
Ryan for increased urine and stool output and to chart all
feeds. Shari also began pumping with a hospital-grade
electric breast pump after every feeding and added an
herbal galactogogue to her diet. Since she complained
of continued heavy bleeding, Shari was referred back to
her obstetrician to screen out the possibility of a retained
placental fragment.
Two days later, Shari experienced heavy cramping
followed by passage of a large, “golf-ball sized” clot,
then 24 hours later developed appendicitis that ended in
an emergency appendectomy. Ryan did not breastfeed
during hospitalization, but Shari pumped and was feed-
ing him “constantly” at the breast once she was dis-
charged. Test weights at an appointment with the lacta-
tion consultant 5 days postsurgery (age 19 days) showed
an intake of only 10 ccs, and so Shari opted to request
metoclopramide from her physician to help boost milk
supply. Four days later, she called the lactation consult-
ant to excitedly report an increase in milk supply after
starting on metoclopramide (10 mg three times a day).
With metoclopramide therapy and an increase in for-
mula supplementation that stabilized at about 8 oz per
24 hours, Ryan finally began to gain weight at a rate of
approximately an ounce a day. At his fifth follow-up at
age 5 weeks, he took 68 ccs in 30 to 40 minutes while
breastfeeding and appeared satisfied, although he still
displayed some hunger cues. Shari reported that the
most she had ever pumped in one session since her last
visit was 75 ccs combined from both breasts.
Shari continued breastfeeding in this fashion, report-
ing a “small” menstrual period at 4 weeks postpartum,
and monthly thereafter. Interestingly, during the 2 days
of her “mini-period” she noted that her milk supply
145
increased to the point that she hardly needed any supple-
mentation; once the bleeding stopped, however, her
supply returned to the lower level, and supplementation
was required again.
Case 2. “Pam,” a 32-year-old gravida 3, para 3
mother, complained that her 13-day-old baby had had
no bowel movements for the first 10 days of life, was
very sleepy, and “never stops nursing.” Baby “Josh’s”
birth weight was 3722 g (8 lbs 3 oz), but at the lactation
consultant’s office he weighed in at a pound under birth
weight, though he otherwise appeared alert and healthy.
A digital suck exam revealed good sucking mechanics.
Pam shared that she had “studied up on breastfeeding”
and was putting baby to the breast frequently; she dis-
played good latch and positioning technique. Her nip-
ples and areolar tissue were normal, but her breasts were
saggy and soft, with some asymmetry and wideness of
spac ing, suggest ing in sufficient mam mary tis sue
though she reported breast growth from a D to an E cup
during pregnancy. Labor with an intrathecal narcotic
was reportedly normal; postpartum lochia was light.
In the written maternal history, the mother indicated
that she was not completely successful in her attempts to
breastfeed her first 2 children, having to supplement
from the beginning and eventually weaning at 4 and 6
months, respectively. At age 24, Pam had conceived her
first baby very easily, but after weaning at 4 months, she
experienced an extended amenorrhea of 18 months. As
her weight increased and ovarian cysts were found, she
was diagnosed with PCOS, with high estrogen levels
noted. A family history of diabetes on the maternal side
was also reported.
The lactation consultant’s initial assumption was
failed lactogenesis potentially due to hormone imbal-
ances. The plan of action included continued frequent
breastfeeds augmented with supplementary feedings;
Pam did not feel that she could cope with the addition of
pumping. In the meantime, she was referred back to her
obstetrician to request a blood panel screening for
androgens and prolactin and also possibly metoclopra-
mide therapy. Blood tests were not conducted, but meto-
clopramide was prescribed at 10 mg three times a day.
After 2 weeks of this therapy and continued frequent
breastfeeding, only a small increase in milk supply was
noted.
Case 3. Nine teen year-old “Ann’s” baby girl,
“Caren,” was born healthy at 3210 g (7lbs 1 oz), but had
lost 455 g (16 oz) in the first 10 days after her birth. With
146 Marasco et al.
the help of the first lactation consultant Ann saw, she be-
gan pumping 8 to 10 times a day to increase her milk
supply, while she also supplemented Caren with for-
mula during breastfeeding, using a supplemental nutri-
tion system (SNS). With these additions, Caren gained
455 g (16 oz) in 1 week; however, when Ann cut back
the supplement at 2 weeks, growth again slowed.
At 2 months, mother was having milk supply prob-
lems, and baby was still having weight gain problems,
so Ann went to a second lactation consultant. Caren now
weighed 3881 g (8 lbs 8.6 oz) and was being breastfed
while receiving 426 cc (15 oz) of formula per day from
the SNS. Breastfeedings with the SNS took 60 to 90
minutes, and she felt like she was breastfeeding the baby
“all the time.” Her pumping had understandably
dropped to 2 times a day between feeds, yielding a mere
15 ccs total at each pumping session. In desperation,
Ann had also started an herbal galactogogue in the
hopes of boosting her milk supply.
Ann’s health history revealed many problems that
appeared at puberty. She developed migraines, and then
at age 18 experienced ovarian pain, facial hair growth,
and a 22.7 kg (50 lb) weight gain in 3 months despite no
alteration in diet or lifestyle, prompting her physician to
give a preliminary diagnosis of PCOS. Ann’s family had
a history of diabetes and heart palpitations, and Ann had
also begun to experience the latter, though she had not
yet notified her doctor. Ann reported that her menstrual
cycles had always been irregular and that her pregnancy
had been unexpected. However, she noticed that her
facial hair growth had slowed for the duration of her
pregnancy.
An examination of Ann’s breasts revealed that they
were somewhat atypical in shape, spaced four fingers’
width apart, and bowing to the outside. She reported
breast growth from AA to B, though the consultant sus-
pected it was less; nipples and areolar tissue appeared
normal. Upon a digital suck exam, it was found that
20,21
Caren had a bubble palate and poor suck mechanics.
Caren appeared to latch well onto the breast, but few
swallows were audible, and she could not maintain a
good latch. The lactation consultant suggested that
Ann’s milk supply deficit most likely had a hormonal
basis and that Caren’s suck problems were peripheral.
Interventions were twofold: to improve milk supply,
pumping frequency was increased to 10 to 12 times a
day, and to help correct sucking behavior, the consultant
switched Ann to finger-feeding. In addition to breast-
feedings, Caren received expressed milk plus artificial
J Hum Lact 16(2), 2000
infant milk to equal 568 cc (20 oz) per 24 hours; breast-
feedings were mainly for comfort. Ann was also
referred back to her physician for her heart palpitations
and to check her prolactin and thyroid levels. The doctor
ruled out any heart abnormalities but did not pursue the
blood tests.
Caren gained well as long as her supplement was kept
at 568 cc (20 oz); if she had less, her gain was less. Her
suck was also improving with the finger-feeding. On the
new schedule, Ann reached a plateau of approximately
23 ccs total per pumping session. Additional galacto-
gogue herbs were discussed and chosen by Ann, but
after 2 weeks of no improvement, Ann decided to try
22
domperidone therapy. Much to her delight, her milk
supply improved to the point that Caren was willing to
feed at the breast again; a test weight showed an intake
of 75 ccs. While supplementation was reduced to 398 g
(14 oz) a day, a full supply still was not established.
Each of the mothers in these 3 cases had an independent
medical diagnosis of PCOS. They also had the help and
advice of expert board-certified lactation consultants
who applied a majority of the therapies currently used:
good breastfeeding management, good positioning,
pumping with hospital-grade electric breast pumps,
suck evaluation and training, and medications and
herbs. In spite of their hard work and care, these mothers
produced very little milk.
Discussion
The endocrinopathy of PCOS is not well understood.
However, the existence of high levels of androgens (tes-
tosterone and adrostenedione) certainly may present
problems for the endocrinology of lactation, as might
the elevated estrogen levels found in obese women with
PCOS, the insulin resistance common to the syndrome,
and the frequently low progesterone levels. In addition,
according to infertility expert Randall Craig, MD, of the
Fertility Treatment Center in Chandler, Arizona, andro-
gens may have the unto ward effect of “down-
regulating” both estrogen and prolactin receptors (per-
sonal communication, April 1997).
The possible ramifications of such hormonal aberra-
tions raise many intriguing questions. Estrogen is
important for breast development both during puberty
2
and during pregnancy ; if the receptors for estrogen are
limited, might pathogenesis for poor breast develop-
ment exist? And conversely, if levels of estrogen remain
high after parturition due to PCOS pathology and ade-
quate receptors do exist, might this inhibit lactogenesis II?
J Hum Lact 16(2), 2000 Polycystic Ovary Syndrome
While estrogen is reputed to develop the ductile sys-
tem of mammary tissue, progesterone plays a strong
23
role in lobuloalveolar development. Progesterone is
normally secreted by the corpus luteum after ovulation.
In the case of PCOS, however, the frequent anovulatory
status of these women results in erratic release of pro-
gesterone and thus overall low levels. Since PCOS onset
occurs most often during puberty, what might be the
overall potential for disruption of both the ductile and
lobuloalveolar development of mammogenesis?
Prolactin, which is important both for mammary
23
growth during pregnancy and the endocrine phase of
lactation, has the potential under PCOS of being limited
in effect if the prolactin receptors are down-regulated. It
is unknown whether a successful pregnancy temporar-
ily negates the hormonal imbalances of PCOS, but it is
considered probable that any endocrinopathy regression
can return after parturition. This may explain why case
mothers experienced only modest responses to meto-
clopramide and domperidone, which reputedly work by
boosting prolactin.
One additional potential pathology involves insulin
2
resistance. According to Lawrence, prolactin, insulin,
and hydrocortisone are essential for lactogenesis to
occur. The role of insulin is to help stimulate the stem
cells of the mammary gland to proliferate and then to
mediate cell division during induction of milk synthe-
sis. Is it possible that insulin resistance might restrict
prolactin efficacy and thus reduce milk production?
Clinical Application
The apparent endocrinopathies involved with PCOS
may offer a potential explanation for the etiology of
some insufficient milk cases. Lactation consultants
have long noted that infertile mothers have a higher-
than-average rate of breastfeeding failure. Considering
the wide variation of possible presentations of PCOS
and recently identified dual forms, it is no wonder that a
connection between PCOS and breastfeeding failure
has not previously been made, as the medical commu-
nity itself has struggled in its definition of and approach
24
to PCOS. In addition, anecdotal reports show that
many women with PCOS do breastfeed successfully,
obscuring the possible relationship even further.
For the lactation consultant in clinical practice, it
may be wise to ask questions about menstrual problems,
infertility, miscarriages, ovarian cysts, hirsutism, adult
acne, and glucose and cholesterol metabolism imbal-
147
ances. Inquiries may also be made regarding the
maternal family history of adult-onset diabetes, obesity,
elevated blood triglycerides, high blood pressure, infer-
tility, hirsutism, menstrual problems, and/or breastfeed-
ing problems. In-hospital lactation consultants might
consider referring mothers with such histories to an out-
patient lactation consultant for follow-up breastfeeding
care.
One other factor that lactation consultants may wish
to consider is the overall appearance and growth history
of the mother’s breasts. Due to the unusual hormonal
interplays, PCOS may also have a relationship with the
diagnosis of insufficient mammary tissue, which has
25
been described by Neifert et al. and Marmet and
20
Shell.
Women who present with apparent delayed or failed
lactogenesis should be followed carefully to ensure that
their infants receive adequate nourishment while ruling
out other possibilities. When all else fails and milk sup-
ply problems continue unresolved, mothers with suspi-
cious histories who do not respond to normal supply-
boosting protocols may be relieved to know that their
problem may have a physiological basis. Unfortunately,
many suffer shame and self-doubt when all of their
efforts still do not produce a full milk supply. Further
research is needed to establish the certainty of the pro-
posed correlation between PCOS and milk supply prob-
lems. In addition, possible therapies based on proposed
etiologies need to be explored.
APPENDIX
Diagnostic Parameters for Polycystic Ovary
Syndrome26
• Se vere men strual ab nor mali ties such as
oligomenorrhea or amenorrhea
• Multiple ovarian subcapsular follicles by pelvic
ultrasound obtained during first 3 days of sponta-
neous menstruation
• LH/FSH ratio > 2.5 during days 4 to 6 of men -
strual cycle or during amenorrhea
• Serum total testosterone > 80 mg/dl
• Clinical manifestations of hyperandrogenism
such as hirsutism or resistant acne
• Hyperinsulinemia: fasting serum insulin > 20
uu/ml
148 Marasco et al.
References
1. Neifert M, Seacat J, Jobe W. The influence of breast surgery, breast ap-
pearance, and pregnancy induced changes on lactation sufficiency as
measured by weight gain. Birth. 1990;17:31-38.
2. Lawrence R. Breastfeeding: A Guide for the Medical Profession. 5th
ed. St. Louis, Mo: Mosby; 1999.
3. Solomon CG. The epidemiology of PCOS prevalence and associated
disease risks. Endocrinol Metab Clin North Am. 1999;28:247-263.
4. Knochenhauer E, Key T, Kahsar-Miller M, Waggoner W, Boots LR,
Azziz R. Prevalence of the polycystic ovary syndrome in unselected
black and white women of the southeastern United States: A prospec-
tive study. J Clin Endocrinol Metab. 1998;83:3078-3082.
5. Stein IF, Leven thal ML. Ame norrhea as so ci ated with bi lat eral
polycystic ovaries. Am J Obstet Gynecol. 1935;29:181-191.
6. Chang RJ, Katz SE. Diagnosis of polycystic ovary syndrome. Endocri-
nol Metab Clin North Am. 1999;28:397-408.
7. Isik AZ, Gulekli B, Zorlu CG, Ergin T, Gokmen O. Endocrinological
and clinical analysis of hyperprolactinemic patients with and without
ultrasonically diagnosed polycystic ovarian changes. Gynecol Obstet
Invest. 1997;43:183-185.
8. Talbott E, Guzick D, Clerici A, et al. Coronary heart disease risk fac-
tors in women with polycystic ovary syndrome. Arterioscler Thromb
Vasc Biol. 1995;15:821-826.
9. Meirow D, Schenker JG. The link between female infertility and can-
cer: Epidemiology and possible aetiologies. Human Reproduction Up-
date. 1996;2:63-75.
10. Secreto G, Zumoff B. Abnormal production of androgens in women
with breast cancer. Anticancer Res. 1994;14:2113-2117.
11. Lobo R. Therapy of polycystic ovary syndrome. In: Mishell D, Bremer P,
eds. Management of Common Problems in Obstetrics and Gynecology.
Cambridge, Mass: Blackwell Publishers; 1994:637.
12. Cresswell JL, Barker DJP, Osmond C, Egger P, Phillips DIW, Fraser
RB. Fetal growth, length of gestation, and polycystic ovaries in adult
life. Lancet. 1997;350:9085, 1131-1135.
13. Kashar-Miller M, Azziz R. Heritability and the risk of developing an-
drogen excess. J Steroid Biochem Mol Biol. 1999;69:261-268.
14. Legro R. Polycystic ovary syndrome: Phenotype to genotype. Endo-
crinol Metab Clin North Am. 1999;28:379-396.
15. Marantides D. Management of polycystic ovary syndrome. Nurse
Pract. 1997;22:34-41.
16. Velazquez EM, Mendosa S, Hamer T, Sosa F, Glueck CJ. Metformin
therapy in women with polycystic ovary syndrome reduces hyperinsu-
linemia, insulin resistance, hyperandrogenemia, and systolic blood
pressure, while facilitating menstrual regularity and pregnancy. Me-
tabolism. 1994;43:647-655.
J Hum Lact 16(2), 2000
17. Franks S, Gilling-Smith, et al. Insulin action in the normal and
polycystic ovary. Endocrinol Metab Clin North Am. 1999;28:361-378.
18. Meier P, Engstrom J, Crichton C, Clark D, Williams M, Mangurten H.
A new scale for in-home test-weighing for mothers of preterm and high
risk infants. J Hum Lact. 1994;10:163-168.
19. Newman, J. Handout No. 15: Breast compression. Available at:
http://users.erols.com/cindyrn/15.htm. 1998.
20. Marmet C, Shell E. Lactation Charts and Forms: A Guide to Lactation
Consultant Charting. Encino, Calif: Lactation Institute; 1993.
21. Snyder J. Bubble palate and failure to thrive: A case report. J Hum
Lact. 1997;13:139-143.
22. Hale T. Medications and Mothers’ Milk. Amarillo, Tex: Pharmasoft
Medical Publishing; 1999:220.
23. Neville M, Neifert M. Lactation Physiology, Nutrition, and Breast-
feeding. New York, NY: Plenum Press; 1983:155.
24. Polycys tic ova ries: Dis or der or sign? [Edi to rial]. Lan cet.
1990;336:1099-1100.
25. Neifert M, Seacat J, Jobe W. Lactation failure due to insufficient glan-
dular development of the breast. Pediatrics. 1985;76:823-828.
26. Glueck, C. The Diagnosis, Etiology and Therapy with Metformin or
Troglitazone of Polycystic Ovary Syndrome [videotape]. Cincinnati,
Ohio: Cholesterol Center, the Jewish Hospitals; 1997.
Resumen
A pesar de los avances en el conocimiento y habilidades
de la lactancia materna, la producción insuficiente de
leche continúa siendo un mito tanto para las madres
como para las consultoras en lactancia. Tres casos simi-
lares se estudiaron para demostrar la conexión entre el
Síndrome de Ovario Poliquístico y la producción insufi-
ciente de leche. Se describen la etiología y posibles sín-
tomas del Síndrome de Ovario Poliquístico como son la
amenorrea/oligomenorrea, hirsutismo, obesidad, infer-
tilidad, acné persistente, quiste de ovario, triglicéridos
elevados y diabetes del adulto, y al mismo tiempo inter-
ferencias patológicas con la mamogénesis, lactogénesis
y galactopoyesis. Se sugieren guías clínicas para identi-
ficar madres y controlar cuidadosamente a los niños en
riesgo. Futuras investigaciones son necesarias para con-
firmar esta asociación y desarrollar terapias para mejo-
rar la lactancia.