Amenorrhea

Author: Kenneth M Bielak, MD; Chief Editor: Richard Scott Lucidi, MD, FACOG more...
Updated: Mar 02, 2016

Background
Amenorrhea is the absence of menstrual bleeding.[1] Amenorrhea is a normal
feature in prepubertal, pregnant, and postmenopausal females. In females of
reproductive age, diagnosing amenorrhea is a matter of first determining whether
pregnancy is the etiology. In the absence of pregnancy, the challenge is to
determine the exact cause of absent menses.[2]
Primary amenorrhea is the failure of menses to occur by age 16 years, in the
presence of normal growth and secondary sexual characteristics. If by age 13
menses has not occurred and the onset of puberty, such as breast development, is
absent, a workup for primary amenorrhea should start.
Secondary amenorrhea is defined as the cessation of menses sometime after
menarche has occurred. Oligomenorrhea is defined as menses occurring at
intervals longer than 35 days apart.
No consensus has been reached regarding the point at which oligomenorrhea
becomes amenorrhea. Some authors suggest the absence of menses for 6 months
constitutes amenorrhea, but the basis for this recommendation is unclear. For a
post-menarchal girl or a reproductive-aged woman to experience a menstrual cycle
interval of more than 90 days is statistically unusual. Practically speaking, this
should be an indication for an evaluation to seek the cause.

Pathophysiology
The menstrual cycle is an orderly progression of coordinated hormonal events in
the female body that stimulates growth of a follicle to release an egg and prepare a
site for implantation if fertilization should occur. Menstruation occurs when an egg
released by the ovary remains unfertilized; subsequently, the soggy decidua of the
endometrium (which was primed to receive a fertilized egg) is sloughed in a flow of
menses in preparation for another cycle.
The menstrual cycle can be divided into 3 physiologic phases: follicular, ovulatory,
and luteal. Each phase has a distinct hormonal secretory milieu. Consideration of
the target organs of these reproductive hormones (hypothalamus, pituitary, ovary,
uterus) is helpful for identifying the disease process responsible for a patients
amenorrhea.

Follicular phase
In physiologic terms, the first day of menses is considered the first day of the
menstrual cycle. The following 13 days of the cycle are designated the follicular
phase. As levels of progesterone, estradiol, and inhibin decline 2-3 days before
menses, the pituitary begins to release higher levels of follicle-stimulating hormone
(FSH), which recruits oocytes for the next menstrual cycle. The hypothalamus is
the initiator of the follicular phase via gonadotropin-releasing hormone (GnRH).
The GnRH pump in the hypothalamus releases GnRH in a pulsatile fashion into
the portal vessel system surrounding the anterior pituitary gland. GnRH interacts
with the anterior pituitary gland to stimulate release of FSH in the follicular phase.
FSH is secreted into the circulation and communicates with the granulosa cells
surrounding the developing oocytes.
As FSH increases during the early portion of the follicular phase, it meshes with
granulosa cells to stimulate the aromatization of androgens into estradiol. The
increase in estradiol and FSH leads to an increase in FSH-receptor content in the
many developing follicles.
Over the next several days, the steady increase of estradiol (E2) levels exerts a
progressively greater suppressive influence on pituitary FSH release. Only one
selected lead follicle, with the largest reservoir of estrogen, can withstand the
declining FSH environment. The remaining oocytes that were initially recruited with
the lead follicle undergo atresia.
Immediately prior to ovulation, the combination of E2 and FSH leads to the
production of luteinizing-hormone (LH) receptors on the granulosa cells
surrounding the lead follicle.
During the late follicular phase, estrogen has a positive influence on LH secretion,
instead of suppressing pituitary LH secretion as it does early in the follicular phase.
To have this positive effect, the E2 level must achieve a sustained elevation for
several days. The LH surge promotes maturation of the dominant oocyte, the
release of the oocyte and then the luteinization of the granulosa cells and the
surrounding theca cells of the dominant follicle resulting in progesterone
production.
The appropriate level of progesterone arising from the maturing dominant follicle

contributes to the precise timing of the mid cycle surge of LH. E2 promotes uterine
endometrial gland growth, which allows for future implantation.

Ovulatory phase
Ovulation occurs approximately 34-36 hours after the onset of the LH surge or 1012 hours after the LH peak and 24-36 hours after peak E2 levels. The rise in
progesterone increases the distensibility of the follicular wall and enhances
proteolytic enzymatic activity, which eventually breaks down the collagenous
follicular wall.
After the ovum is released, the granulosa cells increase in size and take on a
yellowish pigmentation characteristic of lutein. The corpus luteum then produces
estrogen, progesterone, and androgens and becomes increasingly vascularized.

Luteal phase
The lifespan and steroidogenic capacity of the corpus luteum depends on
continued LH secretion from the pituitary gland. The corpus luteum secretes
progesterone that interacts with the endometrium of the uterus to prepare it for
implantation. This process is termed endometrial decidualization.
In the normal ovulatory menstrual cycle, the corpus luteum declines in function 911 days after ovulation. If the corpus luteum is not rescued by human chorionic
gonadotropin (hCG) hormone from the developing placenta, menstruation reliably
occurs 14 days after ovulation. If conception occurs, placental hCG interacts with
the LH receptor to maintain luteal function until placental production of
progesterone is well established.

Puberty
The orderly progression of puberty begins with breast budding (thelarche),
accelerated growth, and menses (menarche). Adrenarche, sexual hair growth, is
independent from GnRH function and typically occurs between breast budding and
accelerated growth but may occur anywhere along the puberty timeline. Secretion
of dehydroepiandrostenedione (DHEA) initiates adrenarche. In the United States,
the average age of girls at menarche is 12.6 years, with a range of 9-15 years.
(Age 15 years is 2 standard deviations above the mean, while age 16 years is 3
standard deviations above.) Progression of puberty requires exposure to
estrogens.
Menses occurring on a predictable cyclic pattern are associated with follicle
development and ovulation. At birth, female infants have a predetermined number
of primordial follicles. During the first trimester of pregnancy, fetal oogonia increase
in number by rapid mitosis. By the 16 to 20th week of pregnancy, up to 6 million
oogonia are present and mitosis halts. After reaching a maximum number of
oogonia cells at 20 weeks, supporting cells envelop the oocyte forming the
primordial follicle. The oocyte within the primordial follicle will enter into meiosis I,
arresting at the diplotene stage of prophase. Over the remaining 20 weeks of
pregnancy, over 4 million oocytes will undergo spontaneous atresia resulting in 2
million oocytes available at birth. Atresia continues such that only 300,000 oocytes
remain at the time of puberty. Up to 500 oocytes will ovulate during a woman
reproductive life with the remainder undergoing apoptosis. The oocytes will remain
arrested at Meiosis I unless the oocyte is chosen to progress to a primary follicle
and eventual the dominant follicle chosen for ovulation. Upon the LH surge
associated with ovulation, the oocyte is stimulated to complete meiosis 1 with
subsequent arrest at metaphase of meiosis 2. Completion of meiosis 2 occurs
after fertilization of a single sperm. At birth, female infants have a predetermined
number of primordial follicles that are arrested during meiosis 1 at the diplotene
stage of prophase until stimulation at puberty. Until puberty, the hypothalamus is in
a quiescent state. At approximately age 8 years, the GnRH pump is reactivated
under the primary control of Kisspeptin {ref 85}.
Menarche and sustained menstrual cycles requires normal function of the
endocrine axis comprising the hypothalamus, pituitary, and ovaries (see the image
below). Any disruption in this axis may result in amenorrhea. Defining the level of
primary dysfunction is critical in determining the pathophysiology of amenorrhea.

Hypothalamus, pituitary and ovaries form a functional endocrine axis, known as HPO axis with
hormonal regulations and feedback loops.

Types of amenorrhea based on HPO axis etiology

Hypothalamic amenorrhea

Hypothalamic dysfunction results in decreased or inhibited GnRH secretion, which

affects the pulsatile release of pituitary gonadotropins, LH and FSH, causing
anovulation. A common cause of amenorrhea is functional hypothalamic
amenorrhea.[3] It is characterized by abnormal hypothalamic GnRH secretion,
decreased gonadotropin pulsations, low or normal LH concentrations, absent LH
surges, abnormal follicular development, and low serum estradiol. Serum FSH
concentrations are usually in the normal range, with high FSH-to-LH ratio.[4]
Functional hypothalamic amenorrhea can be caused by eating disorders, exercise,
or high levels of prolonged physical or mental stress. This can also include major
psychiatric disorders such as depression. Hypothyroidism, hyperthyroidism,
sarcoidosis, galactosemia or any severe chronic medical condition may result in
amenorrhea.[5]
Idiopathic hypogonadotropic hypogonadism leads to low gonadotropin (FSH/LH)
levels. When this occurs with anosmia, it is diagnosed as Kallmann syndrome, the
signs of which include midline facial defects, renal agenesis, and neurologic
deficiencies. Kallmann syndrome results from a failure of GnRH cells to migrate to
the forebrain, a phenomenon associated with mutations in the genes KAL1,
FGFR1, FGF8, PROKR2, and PROK2. Kallmann syndrome most commonly
occurs as an X-linked recessive disorder caused by a KAL1 defect. Autosomal
dominant and autosomal recessive inheritances are less common.[6, 7] For detailed
information, see Gonadotropin-Releasing Hormone Deficiency in Adults.
Evidence suggests a negative correlation between body fat levels and menstrual
abnormalities. A critical body fat level must be present for the reproductive system
to function normally.
In some female athletes, the synergistic effects of excessive exercise and
disordered eating cause severe suppression of GnRH, leading to low estradiol
levels. The female athletic triad, as defined by the American College of Sports
Medicine, is characterized by low energy availability with or without disordered
eating, amenorrhea, and osteoporosis.[3] A 2009 study by DeSouza et al found that
about half of exercising women could be amenorrheic.[8]
Anorexia nervosa is a serious psychiatric disease with severe medical
complications including primary amenorrhea (15%), osteopenia (52%), and
osteoporosis (35%).[9]
Functional causes of amenorrhea include severe chronic disease, rapid weight
loss, malnutrition, depression or other psychiatric disorders, recreational drug
abuse, and psychotropic drug use.
Pituitary amenorrhea
A deficiency in FSH and LH may result from GnRH receptor gene mutations,
although such mutations are rare. Mutations in the FSH beta gene have also been
associated with amenorrhea; women with these mutations have low FSH and
estradiol levels and high LH levels.
Primary amenorrhea caused by hyperprolactinemia is a rare condition
characterized by the onset of thelarche and pubarche at appropriate ages but
arrest of pubertal development before menarche.[10] Hyperprolactinemia is
associated with suppression of the GnRH from the hypothalamus and subsequent
inhibition of LH and FSH, suppressed gonadal function and galactorrhea.
Prolactinomas are the most common cause of persistent hyperprolactinemia,
accounting for 40-50% of pituitary tumors.[11] Prolactinomas are more commonly
noted in secondary amenorrhea.
Pituitary tumors may suppress gonadotropin secretion, such as in Cushing disease
or hypothalamic tumors, craniopharyngioma, or germinoma. Brain injury or cranial
irradiation may also result in amenorrhea. Other pituitary causes include empty
sella syndrome, pituitary infarct, hemochromatoses, and sarcoidosis.
Ovarian causes of primary amenorrhea
Gonadal dysgenesis is characterized by the congenital loss or underdevelopment
of germ cells within the gonad during organogenesis. The gonads usually contain
only fibrous tissue and are called streak gonads. In females, the most common
form of gonadal dysgenesis is Turner syndrome (45,X), in which gonadotropin
levels, especially the FSH levels, are high during early childhood and after age 910 years.
Additional anomalies associated with Turner syndrome include short stature,
webbed neck, coarctation of the aorta (10%), renal abnormalities (50%),
hypertension, pigmented nevi, short forth metacarpal and metatarsals, Hashimoto
thyroiditis, obesity, and osteoporosis.[3] Depletion of ovarian follicles causes
amenorrhea.
Spontaneous 46,XX primary ovarian insufficiency (POI), (also known as premature
ovarian failure [POF] and premature menopause) affects 1 in 10,000 women by
age 20 years, 1 in 1000 women by age 30 years, 1 in 250 women by age 35 years,
and 1 in 100 women by age 40 years.[12] POI is hypergonadotropic hypogonadism,
characterized by oligomenorrhea/amenorrhea, estrogen deficiency, and its
associated symptoms such as hot flashes, vaginal dryness, dyspareunia, and
insomnia. For more detailed information, see Spontaneous Primary Ovarian
Insufficiency and Premature Ovarian Failure.
The fragile X permutation accounts for approximately 6% of cases of overt POI. It
is caused by an increased number of CGG repeats in the FMR1 gene located on
the long arm of the X chromosome. In the permutation, the number of CGG
repeats ranges from 55-200. Approximately 21% of permutation carriers have

POF/POI compared with 1% in the general population.[13] Autoimmune oophoritis

occurs in 3-4% of POI cases.[14]
Amenorrhea is also seen in pure 46, XX gonadal dysgenesis and in 46,XY gonadal
dysgenesis. These women have significantly elevated FSH levels due to the
absence of ovarian follicles and reduction in negative feedback on FSH from
estradiol and inhibin A and B.
The early stages of testicular formation require the action of several genes, of
which one of the earliest and most important is the sex-determining region of the Y
chromosome (SRY). In Swyer syndrome, a testicular regression syndrome that
occurs very early in embryogenesis, the fetus has a 46,XY karyotype but with
mutations of the SRY gene such that the testes never form and anti-mllerian
hormone is not produced, thereby resulting in a female phenotype.
These individuals have a vagina, uterus, and fallopian tubes. Germ cells in the
gonads are lost before birth. The streak gonads must be surgically removed
because of the increased risk for developing germ cell tumor. Pure gonadal
dysgenesis occurs when the syndrome affects the gonads only and no other
dysmorphic features are noted.
Polycystic ovarian syndrome (PCOS) usually presents as secondary amenorrhea,
but in some cases may present as primary amenorrhea. See Polycystic Ovarian
Syndrome for more information.

Congenital and anatomical abnormalities

A uterus and patent vaginal tract are needed for normal menstrual flow to occur.
Female reproductive tract abnormalities account for about one fifth of primary
amenorrhea cases. Cyclic pelvic pain is common in girls with disorders of the
reproductive tract involving outflow obstruction. Imperforate hymen causes an
outflow obstruction. These patients can have blood in the vagina that collects and
can result in a perirectal mass. Transverse vaginal septum can be anywhere along
the tract between the hymenal ring and cervix.
Vaginal agenesis, or mllerian dysgenesis (also known as Mayer-RokitanskyKuster-Hauser [MRKH] syndrome) is caused by agenesis or partial agenesis of the
mllerian duct system. It is characterized by congenital aplasia of the uterus and
upper two thirds of the vagina in women showing normal development of the
secondary sexual characteristics and a normal 46,XX karyotype.[15] The first sign is
primary amenorrhea. It affects 1 of 4500 women. It can be associated with renal,
vertebral, and, to a lesser extent, auditory and cardiac defects.[15]

Receptor and enzyme defects

Congenital adrenal hyperplasia as a result of 17 alpha-hydroxylase deficiency
(CYP17) causes an excess of deoxycortisone to be produced and deficiency of
cortisol and adrenal and gonadal sex steroids. Patients with this disorder who
experience primary amenorrhea can be either genotypic males (XY) or females
(XX).[3]
Complete androgen insensitivity syndrome is caused by a defective androgen
receptor. Although patients with this syndrome have a 46,XY karyotype and
produce testicularly derived testosterone, the testosterone cannot activate cellular
transcription; therefore, the patient has female external genitalia. In most cases the
disorder is X-linked. The testes, located internally and sometimes in the labia or
inguinal area, also produce mllerian-inhibiting hormone, so all mllerian-derived
structures (ie, the fallopian tubes, uterus, upper third of the vagina) are absent.[15,
16]

Gonadotropin resistance is rare, but inactivating mutations of the receptors for LH

and FSH can cause anovulatory amenorrhea.[17]
Aromatase deficiency is also a rare disorder. Aromatase catalyzes the conversion
of androgen to estrogen. When estrogen synthesis cannot occur, increased levels
of testosterone result and virilization of the female occurs. Often, girls have cystic
ovaries and resultant amenorrhea.[18]

Etiology
Amenorrhea after puberty can be divided into 2 groups: (1) amenorrhea without
evidence of associated androgen excess and (2) amenorrhea with evidence of
androgen excess (eg, hirsutism, virilization, sexual ambiguity). For a review of the
causes of amenorrhea associated with androgen excess, see Polycystic Ovarian
Syndrome.

Causes of primary amenorrhea

First and foremost, it is imperative to rule out pregnancy. Additional diagnoses of
primary amenorrhea usually result from a genetic or anatomic abnormality. The
relative prevalence of primary amenorrhea (percentages rounded to the nearest
tenth) includes hypergonadotropic hypogonadism (48.5% of cases),
hypogonadotropic hypogonadism (27.8%), and eugonadism (pubertal delay with
normal gonadotropins; 23.7%).[19]
The hypergonadotropic hypogonadism category includes patients with abnormal
sex chromosomes (ie, Turner syndrome), who make up 29.7% of all primary
amenorrhea cases, and those with normal sex chromosomes. The latter group
includes both patients who are 46,XX (15.4%) and those who are 46,XY (3.4%).
Hypogonadotropic hypogonadism includes the following:

Congenital abnormalities
Endocrine disorders
Tumor
Systemic illness (2.6%)
Eating disorder (2.3%)
Congenital abnormalities that can cause hypogonadotropic hypogonadism include
the following:
Isolated GnRH deficiency (8.3%)
Forms of hypopituitarism (2.3%)
Congenital central nervous system (CNS) defects (0.8%)
Constitutional delay (6%)
Endocrine disorders that can cause hypogonadotropic hypogonadism include the
following:
Congenital adrenal hyperplasia (CAH) (0.8%)
Cushing syndrome (0.4%)
Pseudohypoparathyroidism (0.4%)
Hyperprolactinemia (1.9%)
Tumors that can cause hypogonadotropic hypogonadism include the following:
Unclassified pituitary adenoma (0.8%)
Craniopharyngioma (1.1%)
Unclassified malignant tumor (0.4%)
Eugonadism may result from anatomic abnormalities or intersex disorders.
Anatomic abnormalities include congenital absence of the uterus and vagina
(CAUV; 16.2%) and cervical atresia (0.4%). Intersex disorders include androgen
insensitivity (1.5%), 17-ketoreductase deficiency (0.4%), and inappropriate
feedback (5.3%).

Causes of secondary amenorrhea

Disorders associated with a low or normal FSH, which account for 66% of cases of
secondary amenorrhea, include the following:[20]
Weight loss/anorexia
Nonspecific hypothalamic
Chronic anovulation including PCOS
Hypothyroidism
Cushing syndrome
Pituitary tumor, empty sella, Sheehan syndrome
Disorders in which the FSH is high (12%) include the following:
46,XX spontaneous POI
Premature ovarian failure due to abnormal karyotype (45,X mosaic/ring
chromosome)
Pure gonadal dysgenesis
Disorders associated with a high prolactin level make up 13% of cases. Anatomic
disorders (ie, Asherman syndrome) account for 7%.
Hyperandrogenic states as a cause of secondary amenorrhea (2%) include the
following:
Polycystic ovarian syndrome (PCOS)
Ovarian tumor
Non-classic CAH
Undiagnosed

Epidemiology
The incidence of primary amenorrhea in the United States is less than 1%.[21] Each
year, approximately 5-7% of menstruating women in the US experience 3 months
of secondary amenorrhea
No evidence indicates that the prevalence of amenorrhea varies according to
national origin or ethnic group. However, local environmental factors related to
nutrition and the prevalence of chronic disease undoubtedly have an effect. For
instance, the age of the first menses varies by geographic location, as
demonstrated by a World Health Organization study comparing 11 countries, which
reported a median age of menarche of 13-16 years across centers.
Recent increases in the rates of childhood obesity around the world may also
contribute to earlier onset of menarche and increased prevalence of obesityrelated menstrual disorders, especially in areas where obesity is more prevalent.
[22]
Exposure to environmental toxins, namely hormonally active endocrine
disruptors, may also result in increased rates of menstrual and reproductive
disorders in endemic areas.[23]

Prognosis
Loss of menstrual regularity has been associated with an increased risk of wrist
and hip fractures related to reduced bone density, even without the development of
amenorrhea. A later menarche and menstrual cycle intervals longer than 32 days
have both been associated with increased fracture rates in later years. Young
women with ovarian insufficiency that is unresponsive to therapy require hormone

replacement to maintain bone density.

Adolescence is a critical period for bone accretion as over half of peak bone mass
is achieved during the teenage years.[24] Regular menses is a sign that the ovaries
are producing normal amounts of estrogen, androgens, and progesterone, all of
which play an important role in building and maintaining bone mass. Late
menarche has been associated with a 3-fold increase in the risk of wrist fracture.
[25]

In some cases, loss of menstrual regularity is an early sign of declining fertility and
impending premature ovarian failure. Also in some cases, follicle depletion
progresses to cause irreversible infertility. Approximately 10% of women evaluated
for amenorrhea in a tertiary center are found to have premature ovarian failure.
Women with PCOS have many long-term health issues, including higher risk of
diabetes and cardiovascular disease, that should be monitored and treated.[26, 27]

Patient Education
For patients with ovarian insufficiency that persists despite appropriate evaluation
and treatment, careful counseling is warranted to stress the need for ongoing
attention to the factors that help maintain bone density. Hormone replacement
therapy is important for these patients. Other factors to consider are the need for
adequate calcium and vitamin D intake (1200-1500 mg/d of elemental calcium and
1000 IU/d of vitamin D) and the need for 20-30 minutes of weight-bearing exercise
each day.
For patient education information, see the Women's Health Center, Eating
Disorders Center, and Pregnancy and Reproduction Center, as well as
Amenorrhea, Anorexia Nervosa, Birth Control Overview, and Birth Control FAQs.
Clinical Presentation

Contributor Information and Disclosures

Author
Kenneth M Bielak, MD Professor, Department of Family Medicine, University of Tennessee Health Science
Center College of Medicine
Kenneth M Bielak, MD is a member of the following medical societies: American Academy of Family Physicians,
American Society for Colposcopy and Cervical Pathology, American College of Sports Medicine, American
Medical Society for Sports Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Gayla S Harris, MD Associate Professor, Department of Obstetrics and Gynecology, University of Tennessee
Health Science Center Graduate School of Medicine
Gayla S Harris, MD is a member of the following medical societies: American Society for Reproductive Medicine
Disclosure: Nothing to disclose.
Chief Editor
Richard Scott Lucidi, MD, FACOG Associate Professor of Reproductive Endocrinology and Infertility,
Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine
Richard Scott Lucidi, MD, FACOG is a member of the following medical societies: American College of
Obstetricians and Gynecologists, American Society for Reproductive Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Elizabeth Alderman, MD Director of Fellowship Training Program, Director of Adolescent Ambulatory Service,
Professor of Clinical Pediatrics, Department of Pediatrics, Division of Adolescent Medicine, Albert Einstein
College of Medicine and Children's Hospital at Montefiore
Elizabeth Alderman, MD is a member of the following medical societies: American Academy of Pediatrics,
American Pediatric Society, North American Society for Pediatric and Adolescent Gynecology, and Society for
Adolescent Medicine
Disclosure: Merck Honoraria Speaking and teaching
A David Barnes, MD, PhD, MPH, FACOG Consulting Staff, Department of Obstetrics and Gynecology,
Mammoth Hospital (Mammoth Lakes, California), Pioneer Valley Hospital (Salt Lake City, Utah), Warren
General Hospital (Warren, Pennsylvania), and Mountain West Hospital (Tooele, Utah)
A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of
Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association,
Association of Military Surgeons of the US, and Utah Medical Association
Disclosure: Nothing to disclose.
Karim Anton Calis, PharmD, MPH, FASHP, FCCP Adjunct Clinical Investigator, Program in Developmental
Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health; Clinical Professor, Medical College of Virginia, Virginia
Commonwealth University School of Pharmacy; Clinical Professor, University of Maryland School of Pharmacy
Karim Anton Calis, PharmD, MPH, FASHP, FCCP is a member of the following medical societies: American
College of Clinical Pharmacy, American Society of Health-System Pharmacists, and Endocrine Society
Disclosure: Nothing to disclose.
Sharon N Covington, LCSW-C, BCD Clinical Assistant Professor, Department of Obstetrics and Gynecology,

Georgetown University School of Medicine; Associate Investigator, Integrative Reproductive Medicine Unit,
Reproductive Biology and Medicine Branch, National Institutes of Child Health and Human Development,
National Institutes of Health; Private Practice, Covington and Hafkin and Associates; Director of Psychological
Support Services, Shady Grove Fertility Reproductive Science Center
Sharon N Covington, LCSW-C, BCD is a member of the following medical societies: Academy of Certified
Social Workers, American Orthopsychiatric Association, American Society for Reproductive Medicine, National
Association of Social Workers, and Society for Assisted Reproductive Technologies
Disclosure: Nothing to disclose.
Lawrence M Nelson, MD, MBA Head of Integrative Reproductive Medicine Group, Intramural Research
Program on Reproductive and Adult Endocrinology, National Institutes of Child Health and Human
Development, National Institutes of Health
Lawrence M Nelson, MD, MBA is a member of the following medical societies: American College of
Obstetricians and Gynecologists, American Society for Reproductive Medicine, Association of Professors of
Gynecology and Obstetrics, Endocrine Society, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.
Vaishali Popat, MD, MPH Clinical Investigator, Intramural Research Program on Reproductive and Adult
Endocrinology, National Institutes of Child Health and Human Development, National Institutes of Health
Vaishali Popat, MD, MPH is a member of the following medical societies: American College of Physicians and
Endocrine Society
Disclosure: Nothing to disclose.
Thomas Michael Price, MD Associate Professor, Division of Reproductive Endocrinology and Infertility,
Department of Obstetrics and Gynecology, Director of Reproductive Endocrinology and Infertility Fellowship
Program, Duke University Medical Center
Thomas Michael Price, MD is a member of the following medical societies: Alpha Omega Alpha, American
College of Obstetricians and Gynecologists, American Medical Association, American Society for Reproductive
Medicine, Association of Professors of Gynecology and Obstetrics, Endocrine Society, Phi Beta Kappa, Society
for Gynecologic Investigation, Society for Reproductive Endocrinology and Infertility, and South Carolina
Medical Association
Disclosure: Clinical Advisors Group Consulting fee Consulting; MEDA Corp Consulting Consulting fee
Consulting; Gerson Lehrman Group Advisor Consulting fee Consulting; Adiana Grant/research funds PI
Tamara Prodanov, MD Research Assistant, National Institutes of Child Health and Human Development,
National Institutes of Health
Disclosure: Nothing to disclose.
Shannon D Sullivan, MD, PhD Staff Physician, Department of Endocrinology, Washington Hospital Center
Shannon D Sullivan, MD, PhD is a member of the following medical societies: American Association of Clinical
Endocrinologists, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of
Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Suzanne R Trupin, MD, FACOG Clinical Professor, Department of Obstetrics and Gynecology, University of
Illinois College of Medicine at Urbana-Champaign; CEO and Owner, Women's Health Practice; CEO and
Owner, Hada Cosmetic Medicine and Midwest Surgical Center
Suzanne R Trupin, MD, FACOG is a member of the following medical societies: American Association of
Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American Institute of
Ultrasound in Medicine, American Medical Association, Association of Reproductive Health Professionals,
International Society for Clinical Densitometry, and North American Menopause Society
Disclosure: Nothing to disclose.
Somya Verma, MD, Fellow in Pediatric Endocrinology, National Institutes of Child Health and Human
Development; Officer of United States Public Health Service Commissioned Corps
Disclosure: Nothing to disclose.
Wayne Wolfram, MD, MPH Associate Professor, Department of Emergency Medicine, Mercy St Vincent
Medical Center
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency
Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Andrea L Zuckerman, MD Assistant Professor of Obstetrics/Gynecology and Pediatrics, Tufts University
School of Medicine; Division Director, Pediatric and Adolescent Gynecology, Tufts Medical Center
Andrea L Zuckerman, MD is a member of the following medical societies: American College of Obstetricians
and Gynecologists, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society,
North American Society for Pediatric and Adolescent Gynecology, and Society for Adolescent Medicine
Disclosure: Nothing to disclose.

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