Reproductive Health I: Fertility & Pregnancy

Because the eating disorder spectrum (anorexia nervosa, restriction/reactive eating cycles, bulimia nervosa, orthorexia and anorexia athletica) usually activates in the pre-teen to teen years and persists for at least 50% of all clinically-diagnosed patients well into adulthood and the childbearing years, the issues surrounding fertility and pregnancy become particularly pertinent for women on this spectrum. Of course, it necessarily affects men on this spectrum as well. 

So in this post we’re going to look at recovery specifically through the lens of wanting to have children.

 Elizabeth Cooper: Flickr.com

Elizabeth Cooper: Flickr.com

Fertility and Restrictive Eating Behaviors

No matter what restrictive facets you may have been practicing over the years, and no matter how they may have shifted around, the behaviors negatively impact fertility. 

Prevalence of Infertility in Partially-Recovered and Unrecovered Patients

The onset of this spectrum disorder usually occurs somewhere between the ages of 9-15, just as the body is about to undergo a massive maturation process to the age of 25. The initial bout may be extreme, requiring hospitalization, or may remain at a level that keeps it largely undetected from family and professionals alike.

The average prevalence for clinically diagnosed anorexia nervosa (AN) and bulimia nervosa (BN) is 0.3% and 1% respectively. 1 The prevalence for AN in the population aged 15-24 has increased steadily to reach 2.7% as of 1991. 2 The prevalence of EDNOS (eating disorder not otherwise specified) is estimated at 2.4%. 3 Within these communities most seek medical intervention and 50% recover fully.

As a refresher, EDNOS is a catchall category that exists within the DSM-IV (diagnostic and statistical manual for mental disorders, fourth edition) when patients do not fit within the criteria of either AN or BN.

A far greater community of sub-clinical patients exists who have not sought any medical intervention – the ones who developed restrictive eating behaviors in their early teens wherein their symptoms were largely hidden from and undetected by others.

Looking at the whole eating behaviors iceberg both above and below the waterline, the actual prevalence for the eating disorder spectrum in the entire population is approximately 33%, as 93% of the population diets (restricts calories). 4 Given that 50% of those “above the waterline” are either partially-recovered or actively restricting and 100% of those “below the waterline” are actively restricting in sub-clinical ways, 30% of the total population may have fertility issues directly related to restrictive eating behaviors.

Two Types of Infertility

Fertility in both men and women is directly correlated to serum leptin levels. Leptin is a fat-tissue based hormone that gates the function of reproductive hormones and is also responsible for bone and blood formation, metabolism, appetite and normal neuropeptide function. 5,6

Insufficient body fat percentages result in metabolic suppression states and infertility. For males [l]eptin increments were paralleled by increments of gonadotropins, testosterone, and the free androgen index (FAI).  7 In other words, leptin gates reproductive hormones for both men and women.

“Falling leptin levels in response to starvation result in decreased estradiol levels and amenorrhea in subjects with anorexia nervosa or strenuously exercising athletes. In addition, leptin has a potentially important role during pregnancy and in the physiology of the neonate.” 8

For women actively dealing with this spectrum disorder, the primary issue prohibiting pregnancy is usually oligomenorrhea or amenorrhea (irregular and absent menstrual cycle respectively). Oligomenorrhea or amenorrhea that are due to restrictive behaviors are directly attributable to low body fat percentages.

Anovular infertility in women is a particular state in which there is the presence of a menstrual cycle and the absence of ovulation: no egg is released during the ovulatory phase of the menstrual cycle. 

“Anovular infertility is common in women who have only partially recovered [from eating disorders]. Terming this hypothalamic anovulation is misleading and dangerous, as it leads to medical intervention to induce pregnancy. This is unwise, as the pregnancies of such women are known to have more complications, result in more premature births, and to be associated with poor Apgar scores* and underweight neonates.” 9

*Apgar scores: activity (and muscle tone), pulse (heart rate), grimace (reflex irritability), appearance (skin coloration) and respiration (breathing rate and effort to breathe). These are tests that are done for your newborn to assess whether there is an immediate need for further medical care. The scale is 0 to 2, with 2 being the best.

Intervention to Induce Fertility

Until recently, male infertility due to anorexia athletica or anorexia nervosa could only be treated by weight restoration and cessation of over-exercise. Sadly, in the last decade it has become more feasible to treat these patients with transdermal, oral or injected testosterone preparations. I say sadly, because such pharmaceutical fabrication of fertility overlooks the relative risk implications for a patient being administered synthetic preparations to simulate fertility when the correct treatment of the underlying restrictive behaviors would allow for spontaneous reoccurrence of fertility with no risk.

And of course, pharmaceutical and combined pharmaceutical/in-vitro interventions to induce synthetic fertility in women are the norm, not the exception.

Time is Ticking: Time-Limited Child Bearing Years for Women

“As American society has become increasingly medicalized, biomedically shaped constructions of risk have begun to dominate traditional cultural constructions…Because women's involvement in medical treatment was greater than that of men and because they were more intent on treatment, women assumed the role of final arbiter of what was a risk, and which risks to take. Women perceived more risks than men and were more willing to take risks than men. Notions of risk changed for both women and men, however, as they proceeded through medical treatment. This research suggests that once infertility is medically designated as a disease, both patients and practitioners pursue a ‘cure’ through a well-delineated pattern of medical treatment, despite the risks of such treatment and independent of the likelihood of success. When medical views of risk and responsibility are teamed with women's persistence in the pursuit of a pregnancy, medical treatment may be taken to extremes. Americans consider risk-taking to be their prerogative when personal histories reflect strong cultural mandates about norms, values, rights, and responsibilities, and these in turn are interpreted as health-related by both consumers and health professionals. As a consequence, the forces that trigger medicalization are activated and medical technology is given potentially limitless scope.”  10

As women delay having children more in society today, it is common for obstetricians/gynecologists and endocrinologists to presume that a patient seeking to become pregnant is experiencing age-related infertility.

As 2/3 of all patients with active restrictive eating behaviors are in the average BMI range (18.5-25), it is an astute medical professional indeed who will identify sub-optimal weight as the source of infertility.

Furthermore, women who seek fertility treatment are reluctant to self-identify with their medical professionals as having restrictive eating/over-exercise behaviors for several reasons.

Firstly, the woman may have successfully hidden her behaviors from her spouse and immediate family for years and being forced to make it self-evident at a time when increased commitment is needed in the marital connection feels very risky.

Secondly, the woman may truly be unaware that she has restrictive eating behaviors—many with sub-clinical cases simply assume that they have been health conscious and have “done all the right things”.

Thirdly, significant anxiety about the prospect of having to make a concerted effort to gain weight creates all the impetus necessary to consider an avoidant technique of inducing fertility through pharmaceutical intervention instead.

In the next few sections I am going to look at the dominant drugs used for fertility treatment in women, the pregnancy risks associated with fertility drug treatments, subsequent risks to childhood development linked to fertility treatments and the specific comorbid risks factors associated with a non-weight-restored mother throughout that process.

Assisted Reproductive Technologies (ART) and Assisted Conception: The Drugs and Such

Canadian researcher Anne Rochon Ford quotes one American biologist as saying: ‘The gynaecologist/obstetrician is probably more of a medical empiricist than any other specialist; that is, the gynaecologist administers hormones as a treatment because they work and not because there is a clearly-defined understanding of their action in the body.’” 11

Clomiphene Citrate

The most commonly prescribed drug to induce ovulation is clomiphene citrate (brand names: clomid, milophene and serophene). The drug was initially used for oligomenorrhea in the 1960s and subsequent use was broadened to include anovulation.

It is the first choice largely due to the fact that it is inexpensive, orally administered and used alone does not have the same risks of multiple egg release, although still present, as other pharmaceutical options have.

For an oligomenorrheic or amenorrheic, oral contraceptives may be used in conjunction with clomiphene citrate to stimulate ovulation and simulate a complete menstrual cycle.

Like many drugs, it goes in and out of favor, but has experienced a bit of resurgence in the last decade as the dominant approach of hyper-stimulation of the ovaries (with in-vitro fertilization through the 1990s) declined as a favored approach.

As one country example, from 1973-1993 sales of clomiphene citrate increased 11 fold in Denmark. 12

The two most prominent side effects of clomiphene citrate are visual symptoms (blurring, flashes, spots) and ovarian hyperstimulation syndrome. Ovarian hyperstimulation syndrome can be life threatening.

Worrisomely, the list is long for fetal and neonatal abnormalities associated with the use of clomiphene citrate:

Congenital heart lesions, Down syndrome, club foot, congenital gut lesions, hypospadias, microcephaly, harelip and cleft palate, congenital hip, hemangioma, undescended testicles, polydactyly, conjoined twins and teratomatous malformation, patent ductus arteriosus, amaurosis, arteriovenous fistula, inguinal hernia, umbilical hernia, syndactyly, pectus excavatum, myopathy, dermoid cyst of scalp, omphalocele, spina bifida occulta, ichthyosis, and persistent lingual frenulum. Neonatal death and fetal death/stillbirth in infants with birth defects have also been reported at a rate of <1%.” 13

While some studies suggest that the birth defect rate is the same for spontaneous birth and assisted conception with clomiphene citrate, repeated clomiphene citrate use increases the risk hypospadias and neural tube defects by 1-2% beyond that expected for spontaneous births. 14,15 However, the data are not definitive when it comes to the correlation of clomiphene citrate use and hypospadias. 16

In particular the pharmacokinetics of this drug are poorly understood. What that means is that the way the body breaks down the chemical and excretes it seems to indicate that half-lives will allow for fetal exposure to this drug if conception occurs during the use of this drug. 17

And at the end of considering the risks to the potential mother and her fetus, the published successful therapy rate (resulting in pregnancy) is approximately 30% [ibid.].

Gonadotropins, Clomiphene Citrate and In-Vitro Fertilization

Various gonadotropins are the next option in efforts at assisted conception if clomiphene citrate alone has been unsuccessful. Generally, a woman will be exposed to at least three rounds of clomiphene citrate to attempt to stimulate fertility, occasionally up to six rounds, before this next step will be considered.

There are three basic classes of gonadotropins: a mixture of luteinizing hormone and follicular stimulating hormone (brand names: Pergonal, Repronex, Menogon); recombinant follicular stimulating hormone (brand names: Fertinex, Follistim, Gonal F, Puregon); or human chorionic gonadotropin (brand names: Pregnyl, Novarel, Profasi and Ovidrel). 18

These are all injected drugs and can be taken up to three to six times. You are closely monitored throughout this process due to potentially serious side effects appearing. You may additionally be taking oral clomiphene citrate in sequence with gonadotropin injections, depending on whether in-vitro fertilization is the eventual outcome or not. 19

The risk of ovarian hyperstimulation syndrome is slightly higher than when taking clomiphene citrate in isolation. Multiple gestation, ectopic pregnancy, adnexal torsion (twisting of the ovary resulting in cessation of blood flow to itself) have risks of 1-2%, 1-3% and less than 1% respectively.

Actual successful treatment, resulting in pregnancy, either with subsequent intrauterine insemination or not, is about 20%.

The injections can cost in the range of $2000-5000 (USD) per cycle and intrauterine insemination can cost in the range of $300-1000 (USD). If IUI is unsuccessful, then in-vitro insemination is attempted to the tune of between $12,000 and $15,000 (USD). 20

Long Term Risks to You and your Baby

There is a lot of back and forth on whether clomiphene citrate and/or the gonadotropin families increase the risk of breast cancer and/or ovarian cancer.

Generally, infertile women are at a slightly higher risk of ovarian cancer and so the fact that there are higher rates of ovarian cancer in those who have received fertility drugs may be due to prior infertility.

Women have lifetime risks of developing ovarian cancer of between 1-2% in high-incidence countries (Scandinavia, North America). Comparatively, the lifetime risk of breast cancer is 13.2%. 21 The challenge with trying to identify if there are any increased risks of ovarian cancer with fertility drug use is to have a large enough cohort and monitor them over a long enough period of time, wherein it may even be likely to have cases of ovarian cancer within the group.

Specifically, women treated with clomiphene citrate do have a higher risk of breast cancer. 22

An epidemiological study 8,431 U.S. women indicate higher doses of clomiphene citrate may increase uterine cancer risk, specifically for nulliparous women (never having given birth to a child).

From a biological standpoint, the frequency of cell division that occurs in the reproductive organs makes them sensitive to toxicity-induced mutation. That the jury is out on whether or not there is increased risk of ovarian cancer with fertility drug use is not particularly reassuring to me just yet.

Because cells in reproductive organs undergo meiotic cell division, creating 4 daughter cells with chromosomal cross-over instead of 2 daughter cells and no chromosomal cross-over in mitotic cell division, opportunity for spontaneous mutation is increased.

For your baby, there is more agreement on the negative impacts of fertility drugs and assisted reproductive technologies.

As mentioned above, the rate of birth defects with clomiphene citrate use alone is either equivalent to spontaneous birth rates for defects, or perhaps 1-2% higher than that.

Assisted reproductive technologies (IVF and IUI) result in children approximately 2 to 4 times more likely to have birth defects than their spontaneous birth cohort. 23

One of the more significant risks with all fertility treatments is multiple gestation. There are inherent risks associated with bringing multiples to term.

Researcher Jason Min and his colleagues sought to redefine the actual success rates of these various fertility treatments by measuringsingleton (1 baby), term gestation, live birth rate per cycle of fertility treatment. The success rate using these terms is 11.1%.

The Unrecovered or Partially-Recovered Patient

Fertility Treatments and You

Specifically, luteinizing pulse rates for women who are at sub-optimal or partially-recovered weights may actually increase the chance that, while you may initially conceive with clomiphene citrate, there is a subsequent miscarriage. 24,25

In other words, clomiphene citrate does not ‘fix’ hypoleptinemia (low serum leptin levels due to restrictive eating behaviors and/or over-exercise). And it is leptin that is acting on all the reproductive hormones that not only allow for conception but also allow for you to bring a healthy baby to full term.

Miscarriage for any reason is a stressful event for any parent and the event itself could precipitate a relapse or worsening of restrictive eating behaviors.

For all those with oligomenorrhea or amenorrhea on the eating disorder spectrum, the first line of treatment should always be to gain sufficient weight to allow for a spontaneous recovery of fertility and the menstrual cycle.

In conjunction with a concerted effort to become fully weight restored, cognitive behavioral therapy should also be undertaken to help reinforce non-restrictive behaviors in anticipation of getting pregnant.

Pregnancy and You

Whether you choose to undergo fertility treatments, or you decide to gain enough weight to allow for spontaneous fertility and the resumption of a normal menstrual cycle, without a careful self-assessment prior to conception as to whether you are truly in a phase of complete remission or not, pregnancy is a stressor known to cause relapse in restrictive eating patterns. 26

Particularly stressful is the final trimester where you are meant to be at your heaviest weight, as is the baby. Women with no history of restrictive eating behaviors can find the discomfort of the weight, the position of the baby and the activity of the baby all negatively impact sleep and restfulness generally. On top of all that you are likely going to struggle with efforts to continue providing sufficient energy for both you and baby because your body shape is completely outside of your usual experience and sense of self.

Because the eating disorder spectrum hinges on anxieties over food intake, body image and weight gain, pregnancy requires an ability to accept increased food intake, significant weight gain and a body image that is unrecognizable to your sense of self.

Even for fully recovered former anorexics, bulimics and ED-NOS patients, 22% suffer a relapse of their eating disorders during pregnancy. 27

Pregnancy and Your Baby

The result of relapse, or being partially-recovered at the outset of conception, carries with it a much higher risk of having pre-term babies with lower birth weights, smaller head circumference, microcephaly and being small for their gestational age.

Women who showed symptoms of either anorexia nervosa or bulimia nervosa during pregnancy had a higher frequency of birth by cesarean section and postpartum depression than did nonsymptomatic women.” 28

I will get into the issues of postpartum anxieties and depression later on in this post.

In a longitudinal study with bulimic patients, researchers found that short-term episodes of bulimic-free behaviors are associated with pregnancy and breastfeeding.

The prevalence of miscarriage, hyperemesis gravidarum (extreme morning sickness essentially), and postnatal depression was greater among women who had not recovered from their eating disorder at the time of their pregnancy. Recovery from eating disorder behavior before attempting conception reduces the prevalence of the gynecologic, obstetric, and psychiatric problems associated with eating disorder behavior.” 29

Low birth weight, whether for singleton or multiple births, is associated with learning disabilities.

While the autism spectrum disorder has both genetic underpinnings and unclear environmental triggers, sufficient epidemiological evidence suggest that low birth weight may be one of several independent pre and perinatal risk factors in the development of autism. 30

Ultrasound and Your Baby

While routine ultrasounds are performed on all pregnancies these days, the application of ultrasound on a growing fetus and the increase of its use correlates strongly with the increase in autism in our communities. 31

Animal studies show fetal ultrasound impairs subsequent brain function. 32 Human studies indicate increased sinistrality (left-handedness) suggesting ultrasound affects the fetal brain. 33 And sinistrality and ambiguous handedness are more common in certain sub-types of the autistic spectrum. 34

“The risk of inducing thermal effects is greater in the second and third trimesters, when fetal bone is intercepted by the ultrasound beam and significant temperature increase can occur in the fetal brain. Non-thermal bioeffects may be more significant in early gestation, when the relatively loosely tethered embryonic tissues are exposed to an ultrasound beam in a liquid path. The likelihood of producing cavitation-type non-thermal effects is enhanced by the presence in the sound-field of gas-encapsulated echo-contrast media.”  35

And while it is clear that routine ultrasound scanning of the developing fetus is not questioned, it is equally clear that this practice does not improve perinatal outcome when compared with a more selective use based on clinical judgment of the risks inherent in a particular pregnancy. 36

Problematically an assisted conception pregnancy would be deemed somewhat higher risk; a pregnant patient with a history of restrictive eating behaviors would also be deemed high risk; and it is likely arguable that in recent years the dependency on ultrasound for obstetric evaluations would also necessarily suggest clinicians may be less skilled in detection of anomalies without its use.

Other Well-Known Negative Impacts

I am going to mention these simply because they should not be overlooked in preparation for having a family. Smoking, drinking, marijuana and prescription opiates all have negative impacts on fetal development. Importantly, smoking is often used as a way to maintain a low weight in those on the eating disorder spectrum. More commonly alcohol is used to self-medicate aspects of anxieties underlying the eating disorder, although some may use alcohol directly to maintain a too-low weight as well. Both marijuana and prescription opiates are often favored by untreated patients who have anxiety disorders.

Obviously if these substances are somehow interwoven in the expression of the eating disorder that you have, then you cannot assume that they will magically disappear as a necessity in your life were you to get pregnant. Cognitive behavioral therapy is suitable for addressing the entire suite of behaviors you may have been reinforcing as a result of anxieties around body image, weight gain and food intake.

Despite the list of depressing statistics when it comes to relapse during pregnancy and undernourishment of both mother and fetus as a result, the majority of women manage to lower the intensity and frequency of restriction such that none of the above negative outcomes are ever realized in the baby at all.

You And Your New Baby

And for most of you, you will arrive at this point and you and your baby will be doing just fine.

There are only two more areas to maintain a watchful eye on.

The first is postpartum anxiety and/or depression and the second is inadvertent underfeeding of your child.

Postpartum Anxiety and Depression

Postpartum generalized anxiety (PPA) is more prevalent than postpartum depression (PPD).  37

For women, a previous history of an anxiety disorder appears to be a greater risk factor for a postnatal mood disorder (i.e. depression or anxiety) than a history of a depressive disorder.” 38

There has been much symptom confusion in the medical community thanks to the domination of the serotonin-re-uptake inhibitors (SSRIs) as a first line of treatment for major depressive disorder. The extremely effective marketing of these drugs is such that anxiety disorders, although much more common than major depressive disorders, are misdiagnosed and subsequently treated with SSRIs.

The fact that postpartum anxiety is common for women who have experienced an anxiety disorder prior to pregnancy is critically important for those on the eating disorder spectrum. The eating disorder spectrum spans both anxiety and obsessive compulsive traits.

In addition to a predisposition to both PPA and PPD for women on the eating disorder spectrum, there is evidence that if the mother’s thyroid levels late in the pregnancy are low this also predicts the chance of PPA or PPD after the baby’s birth. 39 Given that hypothyroidism is often present in clinically and sub-clinically restricting patients, it is yet another reason to consider full recovery prior to conception.

Assisted reproductive technologies (IVF and IUI) also inherently generate higher levels of anxiety in the mother prior to birth and that is in turn a great predictor for PPD. 40

If the mother experiences PPD then a 13-year longitudinal study indicates that anxiety disorders in the adolescents of the PPD mothers is higher than for those children whose mothers had not experienced PPD. 41

Taking anti-depressants during pregnancy, questionably protective in any case when it comes to the development of PPD and obviously not protective for PPA, is definitely not advised for the fetus. In one study, rate of pre-term birth for women taking high-dose and low to medium dose was 20% and 9% respectively; it was zero for those not taking anti-depressants.

Admissions to the special care nursery occurred at the rate 26.7% in the high-dose group, 17.1% in the low-to-medium-dose group, and 7.1% in the no-antidepressant group.” 42

Many women struggling with PPD and/or PPA are diagnosed by a psychiatrist and, if not breast feeding, often placed on multiple anti-depressants and anxiolytics at once. Of those who experience PPD or PPA, 46% will still have appreciable symptoms one year beyond the birth of their child. 43

Because there is evidence that women prone to PPD and PPA are more impacted by the drop in progesterone and estrogen postpartum, estradiol has been used in several trials with a strong and immediate positive response (placebo controlled). 44

Generally, the persistence of PPD and PPA followed by a high incidence of subsequent bouts of depression or anxiety is tough to treat with chemical intervention because the mother is often faced with life stressors that are endemic to her overall circumstances.

Financial stressors, unequal sharing of responsibility associated with caring for the child, persistent health issues (backaches, headaches, lack of sexual desire, painful intercourse, vaginal infections, lack of sleep), marital issues, lack of day care options, coping styles that are not expressive…all these factors, and more, are facets that play into the persistence of PPD and PPA at the 12, 14 and 19 month marks beyond birth. 45 Interestingly, in this longitudinal study of French and Italian mothers, returning to work and working were not associated with either the presence or continuation of physical or mental issues.

Partner or marital counseling ahead of deciding to start a family is likely of value even when the marriage appears strong. Guided discussion with a neutral third-party on the sharing of responsibilities of caring for the child; consideration of what might need to happen should you or your partner develop postpartum depression and/or anxieties (and these are conditions that also affect fathers); the level of child care, family support and general care giving relief you will have available when the child is born; and the financial planning for the increased costs of the baby as well as any drop in income that may be associated with maternity leave and/or reduced work beyond the baby’s arrival.

If you are planning to become a single parent, then solo counseling will still be valuable as you will want to identify your support options (family, friends, day care services) and take stock of life stressors and financial stressors that may negatively impact you when the baby arrives.

All of the challenges of adjusting to life with baby are made much more difficult if the restrictive eating behaviors were not adequately addressed prior to conception, as they will worsen after the arrival of your baby.

Underfeeding Your Child

When mothers have unrelenting anxieties around body image, food intake and weight gain, it understandably impacts how the entire family interacts with food and nourishment. The same can be said if it is the father dealing with the eating disorder spectrum.

However, in the early postpartum period, the mother is usually exclusively responsible for the feeding of her baby with breastfeeding.

Before I wade further into this topic, I want to reinforce the concept that underfeeding your child when you have restrictive eating behaviors is never, never done in any conscious fashion and does not constitute child abuse in my estimation at all.

All of us, whether on the eating disorder spectrum or not, are inadvertently passing on our anxieties, worries, insecurities and approaches to life to our children through our actions and behaviors.

The mechanisms underlying the privation of the children stem from the anorexic mother's abnormal concerns with body size extending to her children. The children may become unduly accepting of the underfeeding. 46

Alan Stein, a neurologist who has investigated the eating disturbances related to children of parents with eating disorders, states “Parents spend much time during the first months and years feeding their young infants, and feeding is one of the ways in which much communication occurs between parents and their children. The attitudes, preoccupations, and behaviours manifested by people with eating disorders may interfere with their ability to sit patiently feeding their infants, while responding appropriately to their hunger needs and cues.”

Stein’s research indicates women with eating disorders struggle with over-control, lack of playfulness, anxiety, rigidity, obsessional tidiness, lack of respect for the child’s independence and over and under feeding, when feeding their children.

However, Stein has also found that videotape feedback for mothers feeding their infants is particularly successful in moderating these eating-disorder-generated behaviors related to successfully feeding their children. 48

The challenges are not just limited to the responsibilities associated with directly nourishing your child. In a study focused on bulimic mothers pressures to participate in social activities with their children were generally experienced as stressful, largely due to the fact that most social events involved food. 49

Despite all these challenges, most women and men with eating disorders work very consciously and hard to model healthy eating behaviors to their children and studies indicate that when parents and children undergo counseling to remediate any inadvertent underfeeding, there is tremendous improvement in eating behaviors for both the child and parent. 50

Focused Recovery First

Well, after pulling all that together I wonder why any of us ever have children at all! :-)

The best course of action, and most protective one for you and your baby, is always to seek full recovery first and then attempt to have a family.

However, life doesn’t always work out like that, and all is not lost when life has other plans. First of all, even with recovery long behind you, the process of having a child can cause relapse. Secondly, you may determine that the raised, but still small, risks of assisted conception are ones you are willing to take, given other life-based determinants (age, partner’s desire for a family, or full recovery eludes you). Thirdly, accidents happen! That baby may be on the way because it just is.

The good news is that with some additional care and attention, having a child can be a tremendous force for pursuing full recovery and your experience with the eating disorder spectrum can provide your child with amazing environmental protective benefits, given that he or she is likely genetically predisposed to develop an eating disorder at some point in his or her life.

Marital or partner counseling in preparation for a baby’s arrival is an excellent way to pre-plan the nuts and bolts of having sufficient sharing of responsibilities in child-rearing as well as taking into consideration an extended support group (family, friends, day care etc.) to ensure you are not overwhelmed and at risk of relapse.

Something as simple as videotaping feeding sessions can help you identify issues with adequately feeding your child that may crop up without your awareness or knowledge.

Undergoing cognitive behavioral therapy from time to time as you address possible increased anxieties that appear as your child develops and begins socializing, will allow you to create behaviors that reinforce your desire to develop in your child a healthy relationship with his or her own hunger and nourishment needs.


1. Hoek, Hans Wijbrand. "Incidence, prevalence and mortality of anorexia nervosa and other eating disorders." Current opinion in psychiatry 19, no. 4 (2006): 389-394.

 2. Lucas, Alexander R., C. Mary Beard, W. Michael O’fallon, and Leonard T. Kurland. "50-year trends in the incidence of anorexia nervosa in Rochester, Minn.: a population-based study." Am J Psychiatry 148, no. 7 (1991): 917-922.

3. Machado, Paulo PP, Barbara C. Machado, Sónia Gonçalves, and Hans W. Hoek. "The prevalence of eating disorders not otherwise specified." International Journal of Eating Disorders 40, no. 3 (2007): 212-217.

4. Shisslak, Catherine M., Marjorie Crago, and Linda S. Estes. "The spectrum of eating disturbances." International Journal of Eating Disorders 18, no. 3 (1995): 209-219.

5. Wabitsch, Martin, Anne Ballauff, Reinhard Holl, Werner F. Blum, Eberhard Heinze, Helmut Remschmidt, and Johannes Hebebrand. "Serum leptin, gonadotropin, and testosterone concentrations in male patients with anorexia nervosa during weight gain." The Journal of clinical Endocrinology & Metabolism 86, no. 7 (2001): 2982-2988.

6.  Chan, Jean L., and Christos S. Mantzoros. "Role of leptin in energy-deprivation states: normal human physiology and clinical implications for hypothalamic amenorrhoea and anorexia nervosa." The Lancet 366, no. 9479 (2005): 74-85.

7. Wabitsch, Martin, Anne Ballauff, Reinhard Holl, Werner F. Blum, Eberhard Heinze, Helmut Remschmidt, and Johannes Hebebrand. "Serum leptin, gonadotropin, and testosterone concentrations in male patients with anorexia nervosa during weight gain." The Journal of clinical Endocrinology & Metabolism 86, no. 7 (2001): 2982-2988.

8. Mantzoros, Christos S. "Role of leptin in reproduction." Annals of the New York Academy of Sciences 900, no. 1 (2000): 174-183.

9. D. Gaskill & F. Sanders [eds.], The Encultured Body: Policy implications for healthy body image and disordered eating behaviours, Queensland University of Technology, Brisbane, 2000, p. 81

10. Becker, Gay, and Robert D. Nachtigall. "‘Born to be a mother’: the cultural construction of risk in infertility treatment in the US." Social science & medicine 39, no. 4 (1994): 507IN1-518IN2.

11. Klein, Renate, and Robyn Rowland. "Women as test-sites for fertility drugs: clomiphene citrate and hormonal cocktails." Reproductive and Genetic Engineering 1, no. 3 (1988): 251-273.

12. Mosgaard, Berit, øjvind Lidegaard, and Anders Nyboe Andersen. "Use of fertility drugs in Denmark 1973–1993: an analysis based on sale statistics." Acta obstetricia et gynecologica Scandinavica 74, no. 8 (1995): 614-618.

13. Clomiphene citrate tablet contraindications, National Institutes of Health, 2011

14. Elizur, Shai E., and Togas Tulandi. "Drugs in infertility and fetal safety." Fertility and sterility 89, no. 6 (2008): 1595-1602.

15. Greenland, Sander, and Deborah L. Ackerman. "Clomiphene citrate and neural tube defects: a pooled analysis of controlled epidemiologic studies and recommendations for future studies." Fertility and sterility 64, no. 5 (1995): 936-941.

16. Carmichael, Suzan L., Gary M. Shaw, and Edward J. Lammer. "Environmental and genetic contributors to hypospadias: a review of the epidemiologic evidence." Birth Defects Research Part A: Clinical and Molecular Teratology 94, no. 7 (2012): 499-510.

17. Reefhuis, J., M. A. Honein, L. A. Schieve, and S. A. Rasmussen. "Use of clomiphene citrate and birth defects, National Birth Defects Prevention Study, 1997–2005." Human reproduction 26, no. 2 (2011): 451-457.

18. http://www.babycenter.com/0_fertility-drug-gonadotropins_6188.bc

19. Williams, Shaun C., William E. Gibbons, Suheil J. Muasher, and Sergio Oehninger. "Minimal ovarian hyperstimulation for in vitro fertilization using sequential clomiphene citrate and gonadotropin with or without the addition of a gonadotropin-releasing hormone antagonist." Fertility and sterility 78, no. 5 (2002): 1068-1072.

20. http://www.advancedfertility.com/fertility-treatment-costs.htm

21. http://www.worldwidebreastcancer.com/learn/breast-cancer-statistics-worldwide/

22. Lerner-Geva, L., L. Keinan-Boker, T. Blumstein, V. Boyko, L. Olmar, S. Mashiach, J. Rabinovici et al. "Infertility, ovulation induction treatments and the incidence of breast cancer—a historical prospective cohort of Israeli women." Breast cancer research and treatment 100, no. 2 (2006): 201-212.

23. http://www.cdc.gov/art/index.html

24. Loucks, A. B., and E. M. Heath. "Dietary restriction reduces luteinizing hormone (LH) pulse frequency during waking hours and increases LH pulse amplitude during sleep in young menstruating women." The Journal of Clinical Endocrinology & Metabolism 78, no. 4 (1994): 910-915.

25. Milsom, Stella R., Gillian Gibson, Karen Buckingham, and Alistair J. Gunn. "Factors associated with pregnancy or miscarriage after clomiphene therapy in WHO Group II anovulatory women: a study conducted at Fertility Plus, National Women's Hospital, Auckland." Australian and New Zealand journal of obstetrics and gynaecology 42, no. 2 (2002): 170-175.

26. Micali, Nadia, Emily Simonoff, and Janet Treasure. "Risk of major adverse perinatal outcomes in women with eating disorders." The British Journal of Psychiatry 190, no. 3 (2007): 255-259.

27. Kouba, Saloua, Tore Hällström, Caroline Lindholm, and Angelica Lindén Hirschberg. "Pregnancy and neonatal outcomes in women with eating disorders." Obstetrics & Gynecology 105, no. 2 (2005): 255-260.

28. Franko, Debra L., Mark A. Blais, Anne E. Becker, Sherrie Selwyn Delinsky, Dara N. Greenwood, Andrea T. Flores, Elizabeth R. Ekeblad, Kamryn T. Eddy, and David B. Herzog. "Pregnancy complications and neonatal outcomes in women with eating disorders." American Journal of Psychiatry 158, no. 9 (2001): 1461-1466.

29. Conti, Janet, Suzanne Abraham, and Alan Taylor. "Eating behavior and pregnancy outcome." Journal of psychosomatic research 44, no. 3 (1998): 465-477.

30. Kolevzon, Alexander, Raz Gross, and Abraham Reichenberg. "Prenatal and perinatal risk factors for autism: a review and integration of findings." Archives of pediatrics & adolescent medicine 161, no. 4 (2007): 326-333.

31. Devi, P. Uma, R. Suresh, and M. P. Hande. "Effect of fetal exposure to ultrasound on the behavior of the adult mouse." Radiation research 141, no. 3 (1995): 314-317.

32. Kieler, Helle, Sven Cnattingius, Bengt Haglund, Juni Palmgren, and Ove Axelsson. "Sinistrality—a side-effect of prenatal sonography: A comparative study of young men." Epidemiology 12, no. 6 (2001): 618-623.

33. Williams, Emily L., and Manuel F. Casanova. "Autism and dyslexia: a spectrum of cognitive styles as defined by minicolumnar morphometry." Medical hypotheses 74, no. 1 (2010): 59-62.

34.Soper, Henry V., Paul Satz, Donna L. Orsini, Rolando R. Henry, Jennifer C. Zvi, and Marion Schulman. "Handedness patterns in autism suggest subtypes." Journal of autism and developmental disorders 16, no. 2 (1986): 155-167.

35. Barnett, S. B., and D. Maulik. "Guidelines and recommendations for safe use of Doppler ultrasound in perinatal applications." Journal of Maternal-Fetal Medicine 10, no. 2 (2001): 75-84.

36. Ewigman, Bernard G., James P. Crane, Fredric D. Frigoletto, Michael L. LeFevre, Raymond P. Bain, and Donald McNellis. "Effect of prenatal ultrasound screening on perinatal outcome." New England Journal of Medicine 329, no. 12 (1993): 821-827.

37. Wenzel, Amy, E. N. Haugen, L. C. Jackson, and K. Robinson. "Prevalence of generalized anxiety at eight weeks postpartum." Archives of women's mental health 6, no. 1 (2003): 43-49.

38.  Matthey, Stephen, Bryanne Barnett, Pauline Howie, and David J. Kavanagh. "Diagnosing postpartum depression in mothers and fathers: whatever happened to anxiety?." Journal of affective disorders 74, no. 2 (2003): 139-147.

39. Bunevicius, Robertas, Laima Kusminskas, Narseta Mickuviene, Adomas Bunevicius, Cort A. Pedersen, and Victor JM Pop. "Depressive disorder and thyroid axis functioning during pregnancy." The World Journal of Biological Psychiatry 10, no. 4 (2009): 324-329.

40. Monti, Fiorella, Francesca Agostini, Gianfranco Marano, and Francesca Lupi. "The course of maternal depressive symptomatology during the first 18 months postpartum in an Italian sample." Archives of women's mental health 11, no. 3 (2008): 231-238.

41. Halligan, Sarah L., Lynne Murray, Carla Martins, and Peter J. Cooper. "Maternal depression and psychiatric outcomes in adolescent offspring: a 13-year longitudinal study." Journal of affective disorders 97, no. 1 (2007): 145-154.

42. Suri, Rita, Lori Altshuler, Gerhard Hellemann, Vivien K. Burt, Ana Aquino, and Jim Mintz. "Effects of antenatal depression and antidepressant treatment on gestational age at birth and risk of preterm birth." American Journal of Psychiatry (2007).

43. McCue Horwitz, Sarah, Margaret J. Briggs-Gowan, Amy Storfer-Isser, and Alice S. Carter. "Prevalence, correlates, and persistence of maternal depression." Journal of Women's Health 16, no. 5 (2007): 678-691.

44. Gregoire, A. J. P., R. Kumar, B. Everitt, and J. W. W. Studd. "Transdermal oestrogen for treatment of severe postnatal depression." The Lancet 347, no. 9006 (1996): 930-933.

45. SaurelCubizolles, MarieJosèphe, Patrizia Romito, Nathalie Lelong, and PierreYves Ancel. "Women's health after childbirth: a longitudinal study in France and Italy." BJOG: An International Journal of Obstetrics & Gynaecology 107, no. 10 (2000): 1202-1209.

46. Russell, G. F. M., J. Treasure, and I. Eisler. "Mothers with anorexia nervosa who underfeed their children: their recognition and management." Psychological Medicine 28, no. 01 (1998): 93-108.

47. Patel, Priti, Rebecca Wheatcroft, Rebecca J. Park, and Alan Stein. "The children of mothers with eating disorders." Clinical child and family psychology review 5, no. 1 (2002): 1-19.

48. Stein, Alan, Helen Woolley, Robert Senior, Leezah Hertzmann, Mary Lovel, Joanna Lee, Sandra Cooper et al. "Treating disturbances in the relationship between mothers with bulimic eating disorders and their infants: a randomized, controlled trial of video feedback." American Journal of Psychiatry 163, no. 5 (2006): 899-906.

49. Stapleton, Helen, Anna Fielder, and Mavis Kirkham. "Managing infant feeding practices: The competing needs of bulimic mothers and their children." Journal of clinical nursing 18, no. 6 (2009): 874-883.

50. Russell, G. F. M., J. Treasure, and I. Eisler. "Mothers with anorexia nervosa who underfeed their children: their recognition and management." Psychological Medicine 28, no. 01 (1998): 93-108.