Reproductive Health II: Kids or not, it's still important.

Recently a presenter on a UK show advised women to have their babies young as she has so many friends desperate for children and unable to conceive in their late 20s (let alone their 30s and 40s I assume). 

The belief that women’s fertility drops off precipitously after the age of 25 was based on uncontested data rather prehistorically gathered in the 1800s. Why it has taken the scientific community 200 years to pursue a more rigorous update on that accepted data has a lot to do with the fact that women are still rather notably absent from medical study.


While it is true women do have a finite number of eggs, and it is also true that for most women the number of ovular cycles does drop in their 40s, the infertility seen in women in their late 20s and also their 30s today has an awful lot to do with population-wide adherence to food intake restriction and excessive exercise regimes.

Before you undergo fertility treatment or follow advice from medical specialists who have told you that you should increase your activity levels and lower your food intake amounts further, review your current reproductive health status from an energy-balance perspective and then circle back to discuss your observations with those medical specialists.

What follows is a sex-differentiated review of reproductive and sexual health, but I encourage you all to read both sections, as many aspects are common to both men and women.

Additionally, for transgendered individuals who are perhaps in transition but struggling with an eating disorder, both sections will hopefully be of some help to you.

Ladies , Let's Discuss

Reproductive health is pretty indistinguishable from overall health status. In fact, we could say that the absence of reproductive health is often a harbinger of further health deterioration to come. Because reproductive function is not required for the immediate survival of an individual, it tends to be one of the first facets of health that will deteriorate because maintaining its robust function is discretionary (over the short-term).


The image above is from an actual advertisement for Chi-Ches-Ters Pills for period pains, or what they called "blackouts".

If you do not have a regular menstrual cycle (reminder: the monthly bleed associated with taking the Pill (oral contraception) is NOT a menstrual cycle) then, in the absence of a diagnosed and serious medical condition that might be to blame, the most likely reason for your infertility is functional hypothalamic amenorrhea. And I’ll explain what that is in a moment. 

If you have a regular menstrual cycle but have not been able to conceive, then it is possible that your cycle is anovular. Anovular menstruation is also often a sign of functional hypothalamic amenorrhea.

If your absent, irregular or anovular menstruation has been investigated with ultrasound as well as blood screening to identify the levels of your reproductive hormones, and due to that you have been diagnosed with polycystic ovarian syndrome (PCOS), then you a) have a statistically very high likelihood of a misdiagnosis on your hands and b) the commonly advised treatment of exercising more and restricting intake/food groups will further harm your chances of conception.

If you are of average or above-average weight then you are far more likely to be misdiagnosed with PCOS than if you are frankly below-average weight. I’ll get to all the ins and outs of false PCOS diagnoses later on in the post as well. 

One fascinating anomaly to the saga of amenorrhea, is that some patients with an active and enduring case of an eating disorder will experience years of amenorrhea (no period) and suddenly their periods will reappear despite a maintained very low weight (often below BMI 17.5). Many misconstrue this miraculous reappearance of their period as a sign of confirmed health at that weight. I contend that it is much more likely to be a last-ditch maneuver to pass on the genes to a subsequent generation (assuming survival of the baby) as the potential mother’s survival is going to be severely curtailed (due to the eating disorder). 

There is no science to support that theory at present, but there is science to confirm that menstruating women with active eating disorders have no better outcomes than those with amenorrhea. 1

The Pill

If you come off of the Pill (oral contraception) because you and your partner hope to have children and you discover your menstrual cycle remains stubbornly absent, then you may be told that it can “take a while” for your regular period to return.

In fact clinical trial data show that even continuous oral contraception options levonorgestrel and ethinyl do not impact return to fertility 2 and the average time to menses resumption or conception is 90 days following the cessation of oral contraception. 3

If, after three months, your period has not returned, then you may be advised to take various synthetic hormone replacements for a short duration to “kick-start” your menstrual cycle. However that approach will not resolve the underlying reason for the presence of functional hypothalamic amenorrhea in the first place.

Functional Hypothalamic Amenorrhea

Functional hypothalamic amenorrhea (FHA) is a condition that is a non-organic and reversible. In other words whatever brought the condition on is what must be removed from the patient’s life as a way to reverse the presence of the condition, and there is nothing inherently malfunctioning or failing within the patient’s body at all.

Applying synthetic hormone replacements and/or oral contraceptives to a patient with FHA is somewhat like asking a patient to wear a glove to protect her thumb while she continues to hit the thumb repeatedly with a hammer. It would be best to ask the patient to stop hitting her thumb with the hammer as a way to resolve the damage to her thumb.

I have already provided several clinical trials that indicate oral contraceptives offer no bone-sparing value in other blog posts. 4,5 A meta-analysis review of all forms of hormone replacement and oral contraceptive application for patients with FHA revealed that the most successful and essential strategy for improving bone density mass in these patients is for them to increase their food intake until their periods return. 6

Two things can trigger FHA: energy deficiency and/or extreme stress. By definition, an energy deficiency within the body is extremely stressful. By far the most common cause of FHA in women today is a combination of not taking in enough energy (food) to meet energy requirements and then exacerbating that deficiency by expending energy through exercise and activity.

No Period So What?

Many of you may think, or have even been told by your health care practitioner, that the absence of a menstrual cycle is not such a big deal. It’s a big deal even if you don’t ever want to have children.

Of course you all know about the impact that no period has on your bones: they become porous and eventually prone to fracture. If you are young you might be thinking: “Well it’s a long way off and so it’s not like a few broken bones are going to be the end of the world.” There probably won’t be much I could tell you that will shift your attitude on that because it is hazard of youth to believe yourself immortal.

Many people don’t know that most of the fractures associated with the onset of osteoporosis due to long-term absence of menstruation involve tremendous pain and disability. You cannot set a fractured rib or vertebra (because immobilizing your torso means you would be unable to breathe. Most hairline fractures in the pelvis will involve unending pain and the body also lacks the energy (due to prolonged and sustained restriction of energy intake) to generate osteoblasts (cells that create bone matter) to build and heal the fracture as well.

And that disability and pain doesn’t happen when you are 80. That kind of senior-onset osteoporosis does not occur as a result of years of absent menstruation.  Many women in their 30s and 40s, after a decade spent in their twenties without any regular menstrual cycle, due to restriction, will be disabled to an equivalent level of those women who have a genetic predisposition to develop osteoporosis in their late senior years. But as I said, if you are a teen or young adult, then these realities will hold little sway.

Beyond the impact on your bones, walking around as a post-pubescent woman with no reproductive hormones to your name has broad systemic functional issues in the more immediate time frame.

Alongside the low reproductive hormones of FHA often resides hypercortisolism (the stress hormone – as I said restriction is stressful). Hypercortisolism is not a benign state as cortisol is a potent neurotoxin. 7 That results in marked neuroendocrine anomalies that affect brain function. 8 Keep in mind that this hypercortisolism is not always evident in blood tests as it resides in cerebrospinal fluid. 9

Then there’s the cardiovascular risk too. That’s right, you’re all ‘healthy and active’ and predisposed to the accelerated development of heart disease. In more technical terms, there is decreased endothelium-dependent dilation of the brachial artery in patients with FHA. 10

And I have discussed the risk of sudden and fatal heart failure associated with exercising while restricting energy intake in the blog post Insidious Activity

Polycystic Ovarian Syndrome Misdiagnosis

As I have already addressed the common misdiagnosis of polycystic ovarian syndrome (PCOS) in patients who have eating disorders in the Usual Question section here: But I have PCOS? I will simply point you to that definitive data.

The presence of polycystic ovaries occurs for those with eating disorders because their ovaries have atrophied and they do not have any syndrome. The polycystic ovaries resolve with rest, re-feeding, weight gain and the resumption of regular menses.

Hey Guys— I Haven’t Forgotten You.

And for the men with low reproductive hormone function due to energy restriction— all this talk of periods is great and all for when you want to be educated for the women you love who are in your life, but I apologize for dragging you through information that doesn’t help you understand your reproductive health in any useful way.

Reproductive Hormone Impact

There is suppression of serum testosterone levels during and subsequent to more prolonged exercise (and to some extent in the hours following intense short term exercise). Again the mechanisms are not clear: a variety of systems could influence the decrease of testosterone synthesis, including decreased gonadotrophin, increased cortisol, catecholamine or prolactin levels, or perhaps even an accumulation of metabolic waste materials. Endurance training induces changes in the function of the reproductive axis in men in a manner which appears similar to the changes in women. As in women, there is a subclinical inhibition of normal reproductive function…” 11

So, yes you have an equivalent reproductive hormone dump as the females do with restrictive behaviors (keep in mind this includes energy expenditure (exercise) as well as food intake restriction). This equivalent restriction-generated condition in men is best identified as functional hypothalamic pituitary (male) hypogonadism (FHPG). As with FHA, the presence of the condition means nothing is inherently malfunctioning or failing within the patient’s body at all. The reversal of the condition is entirely dependent upon the removal of the external factors associated with its onset: energy restriction relative to physical requirements.

While females with FHA deal with absent sex drive, vaginal dryness, and occasionally symptoms associated with early onset menopause, males deal with absent sex drive, erectile dysfunction and low volume of ejaculate.

Bone Mineral Density

What isn’t so clear, because of the dearth of study on the topic, is the impact on your bone mineral density.  As best as we can assess from the data thus far, bone mineral density is negatively impacted for men as well, but it is more directly correlated with the level of endurance training applied: the higher the endurance applied, the lower the bone mineral density outcomes. 12,13

Additionally, types of training seem more or less conducive to bone density loss for males. Cycling appears to be more strongly associated with lower bone density outcomes. 14 Very small longitudinal trials looking at athletes during their active seasons suggest significant bone mineral density reductions during the season and that occurs despite calcium supplementation. 15

Most certainly fertility is affected by energy restriction in equivalent ways for men and women. There is plenty of data on infertility due to eating disorders and exercise training in men. 16,17

Just an interesting side note here, a solid meta-analysis debunked the misconception that obesity correlates with subfertility in men. There was no correlation found at all. 18

Cardiovascular Impact

And while the bone mineral density costs of FHPG are perhaps equivocal, the cardiovascular impacts are more sinister when compared to female outcomes of enduring FHA.

Because male patients with an active eating disorder disproportionately express the condition through excessive exercise, cardiovascular impacts of energy deficiencies within the body can be both acute and deadly.

The increased risk of atrial fibrillation for those practicing endurance sports is between 2 to 10 times that of controls, when adjusting for other risk factors. 19 Even leisure-time exercise of more than 5 hours per week at age 30 generated an increased risk of atrial fibrillation in later life compared to those who exercised less than 1 hour per week at age 30. 20 Keep in mind these data are arrived at through retrospective self-reports, and we know how unreliable self-reports will be.

Peter Ofman and his colleagues, when performing a meta-analysis on the relative risk of atrial fibrillation in exercisers suggested an overall risk of only 1.08. 21

Drca’s findings did indicate that walking and bicycling for less than 1 hour per day was inversely correlated with the onset of atrial fibrillation. 22

There is also a lot of contention in research communities as to whether acute volume overload of the atria and right ventricle that occurs during endurance exercise is or is not significant. However, its transience (meaning that the heart can repair the damage) will be dependent upon whether the athlete in question rests or not. 23 For a readable and comprehensive review on the cardiovascular impacts:Cardiovascular Damage Resulting from Chronic Excessive Endurance Exercise

Overall exercise has a J-shaped set of outcomes for morbidity and mortality for all of us. It is more like the Nike brand mark “swoosh” than a J-shaped curve really. Some modest risk is attributed to the absence of all activity *; a modest decrease in morbidity and mortality is attributed to very modest activity; and a steep and fast increase in risk of illness and death is attributable to increased activity. 24,25

In that lowest trough point of the curve is where we see an actual increase in bone mineral density and improvements in cardiac function for both men and women. However, there are no improvements realized with very modest activity when the patient is energy-depleted (as are those with eating disorders).

*Keep in mind that an active eating disorder involves distinct anomalies such that exercise is contraindicated for this subpopulation. Read Insidious Activity for more information.

While the depletion of testosterone associated with FHPG may even have some heart-protective benefits, when the progressive muscle atrophy associated with energy depletion in the body (the heart is a muscle) is combined with any kind of endurance athletic endeavor, then sudden death is a real risk.

A Word On Ergogenic Substances 

Ergogenic substances are those use to enhance athletic performance. Many young males use these same substances to improve appearance (non-athletic use).

The prevalence of non-medical anabolic steroid use is estimated at between 4 to 11% of high school-aged males. 26 There are suggestions that the incidence is declining, however that may be due to the increased popularity of what are called steroid precursors or prohormones that still have the same metabolic pathways and therefore carry the same overall adverse effect. 27 Additionally, many studies suggest the presumed decrease in use failed to include even younger males (ages 9-13) where prevalence is increasing. 28

Here is a simplistic explanation of the perfect storm that is chronic exercise, chronic deficiencies in energy intake, and the application of ergogenic substances at the same time: all the worst outcomes associated with hypercortisolism on steroids.

A close analogy to FHPG + ergogenic substances would be rabbit starvation, or mal de caribou. Rabbit starvation, or mal de caribou, is the consumption of lean meat alongside the lack of other nutrients in your diet. It causes proteinuria (protein toxicity) in humans. Equivalently, the lack of testosterone and other reproductive hormones in your system due to energy deficiencies combined with the application of synthetic replenishment of testosterone or a prohormone testosterone substance, et voilà toxicity— severe organ damage ensues.

Everyone Can Now Return From Their Breakout Group

But enough with all the dire warnings as a way to get you to consider that FHA and FHPG are really big health issues.

What if you are just feeling good except for that sex drive thing? Maybe your reproductive hormone levels have your medical team piqued, but you are living your life and it’s just fine thank you very much. Sex drive is part of reproductive health.

Bottom line is that either you will see the absence of your reproductive health in your life as a harbinger of overall failing health or you won’t.

Sometimes the absence of reproductive health in a patient’s life is a welcome omission. Let’s look at this a bit more…


We cannot discuss reproductive health without considering the implications of sexuality as human beings.

You all know by now that the appearance of an active eating disorder in anyone’s life has a genetic base. But a myriad complex environmental stimuli will play a role in both the activation as well as the perseveration of the condition.

Sexual abuse does not cause an eating disorder. But sexual abuse may function as an activator for a genetically predisposed individual, and it can also act as reinforcement of food-avoidant behaviors (the perseveration of the condition). I’ll get to this in a moment, but first let’s look at how sexual attribution & orientation may be important for those who deem their reproductive function is best left dormant.

Sexual Attribution & Orientation

Despite our still dominant cultural belief systems, sexual preference is neither a genetic inevitability nor a choice. Part of the reason that its genetic foundation is given emphasis in our society is because we lack enough social sophistication to allow for the actual reality of the overall fluidity of sexual preference across an entire spectrum and also within an individual’s lifetime. To admit to that reality tends to provide fodder for those who still believe that the presence of choice means sexual preference is morally right or wrong.

Yes there is a genetic foundation, but not 100% heritability factor. Even eye color is 98%, not 100%. My great aunt was born with dark brown eyes. At some unrecalled point in her life, her eyes turned blue. Illness? Perhaps. But she’s a great example of that 2% application of environmental outcome for eye color.

Sexual orientation appears to have a heritability factor of anywhere between 31% to 74%. 29 Gender attribution (I loathe the fact that it is still often identified as “gender identification disorder”) has a heritability factor estimated at 62%. 30 Just so we’re clear, this kind of heritability does not mean something so simplistic (and wrong) as “Dad has blue eyes and is gay, and so am I”!

Do not misconstrue the less-than 100% heritability factor with the scientifically unfounded idea that sexual preference or attribution is “re-trainable” or “correctible”.  The heritability of athletic endeavor is 66% but I can tell you right now that despite the fact I have world-renowned arctic explorers among my fairly recent ancestors, you will not be able to train me to survive an equivalent endeavor.

Evolution’s Rainbow is a truly inspired book to consider if you would like to understand all the biological and environmental complexities that shape both gender and sexual orientation throughout the animal kingdom.

The point I am making is that orientation and attribution of sexuality are both heritable and environmental in their expression, but messing with it is like trying to make my great aunt’s blue eyes brown. You are what you are: nature and environment all enmeshed in a wondrous and unique outcome. You need “retrain” or “correct” absolutely nothing in your lived experience.

The heritability estimates for eating disorders range from 18% to 56%. 31,32,33 And yes you also do not need to retrain or correct the presence of an eating disorder in your lived experience as well. But let’s look at this concept in a bit more depth…

Heritability Gets You Only So Far

Heritable human attributes that are shaped by environmental inputs are not interchangeable: eye color is not sexual orientation is not the onset of deadly chronic neurobiological conditions.

The entire sweep of the bell curve of sexual orientation and attribution is full of health-neutral human attributes, whereas the onset of celiac disease, asthma or eating disorders is not. Accepting the gender attribution or orientation in yourself or others has no distinct negative health outcomes*.

High-risk sexual behaviors that are linked to poor health outcomes are not correlated with sexual orientation and attribution; however the victimization suffered by those of the LGBT communities is correlated with poor health outcomes. 34 Victimization is an external environmental input and not an inherent facet of sexual orientation or attribution.

*We can therefore confirm that someone who abuses those with LGBT sexual orientation or attribution is actively harming the health of those individuals.

Seeking “remission” from having blue eyes or "trying to correct" knowing you are the opposite sex of what your sexual morphology suggests, is clearly a silly concept. But if we argue that health-negative heritable attributes require a proactive effort to mitigate their presence in one’s life, we might be entering a space where we are actively harming the health of others.

Abuse, Sexual Identity and Ambivalence

Now I have to wend my way back around to the point at the beginning of this particular section: consider investigating whether your dismissal of the importance of your failing reproductive health (due to restriction) might be present due to an underlying breach of intimate trust and/or severe anxiety associated with sexual preference or gender identification.

In the absence of any sexual drive whatsoever, then issues surrounding past sexual abuse or ambivalence regarding your inherent sexual preferences and/or gender identification are mercifully dulled as well.

Yet another boring old reminder from me: engage counseling or psychological therapeutic services if you are embarking on a recovery effort from an eating disorder.


The nature of sexual trauma is so monstrously complex and, somewhat worryingly, its presence in your life might be completely obscured from your understanding of self.

There was great controversy surrounding false memory syndrome in the 1990s: patients who believed they were retrieving repressed memories of abuse were actually unwittingly victim to false memories being implanted by eager, and often very genuine but misguided, psychologists and psychiatrists. A leader in the field of uncovering this absolutely devastating and destructive psychology-induced mess was Elizabeth F. Loftus.

Since that time, a combination of further clinical trials and much enhanced training for counselors and therapists working in the fields of trauma and abuse, has allowed for scientific confirmation that the absence of any memory of childhood sexual abuse is not absolute confirmation no sexual abuse occurred. However, the recollection of such abuse is spontaneous (not retrieved through hypnosis or guided imagery exercises of any kind) and it can occur several decades after the event. It is best described as discontinuous memory of childhood sexual abuse. 35

The way in which the researchers confirmed discontinuous memory of childhood sexual abuse was they sourced hospital-confirmed cases and interviewed the women many years later. 38% of the women, surveyed 17 years beyond the instances of childhood sexual abuse, had no recollection that the abuse that had occurred. 36 Problematically, self-reports of recollection or memory retrieval are going to be suspect. Gail Goodman and her colleagues in 2003 found that less than 20% did not report their own confirmed cases of childhood sexual abuse. 37 Older age at the time of the abuse, maternal support after disclosure and more severe abuse were correlated with an increased likelihood of recollection and reporting. 38

Rather than the false memory proponents on the one hand, or repressed memory proponents on the other, Elke Geraerts and her colleagues suggest the presence of a spontaneous recollection of childhood sexual abuse after years of ostensibly not remembering the event(s), occurs because [t]hese people did not experience their CSA [childhood sexual abuse] as traumatic; they either failed to think about their abuse for years or forgot their previous recollections, and they recalled their CSA spontaneously after encountering reminders outside of psychotherapy.” 39

Now that quote can be monstrously misconstrued. It does not mean that the sexual abuse was not traumatic; it means that the child was likely encouraged at the time to frame the distressing events as unremarkable and/or actually the result of the child's behaviors. In order for the child to survive such profound negation of their experience (and their worth and value as a human being), detaching from the memories is the only viable option.

And if we look back to the absence of maternal support after disclosure alongside a younger age at the time of the abuse being markers for reduced levels of recollection (38), then if Mommy tells her little boy or girl that Uncle Gorp was just being loving because he likes ‘hugs’ then framing the truly disturbing experience as “not traumatic” has been guided by the trust the child places in Mommy’s understanding of the world at the time. With the benefit of adult reassessment, the recollection that Uncle Gorp’s hug was most certainly a) not a hug and b) actual sexual abuse is what discontinuous memory of CSA is all about.

If you have continuous memory of childhood sexual abuse, then obviously your attempts at recovery from an eating disorder will necessarily unpack whether connections exist for you in persevering with restriction as a way to poorly address the trauma of intimate trust betrayal by negating your own sexual maturation and identity.

If you have no current recollection of childhood sexual abuse, then be suspicious of any counselor or therapist you have hired for your process of recovery from an eating disorder if he or she seems to guide discussions towards the misguided and outdated attitude that eating disorders are caused by childhood sexual abuse.

Childhood sexual abuse does not cause eating disorders. It may or may not be one of many environmental influences in your particular case that either functioned as an activating trigger for restrictive behaviors or it has resulted in the perseveration of restrictive eating behaviors as maladaptive emotional modulation.

Counselors and therapists who create open-ended, safe and gentle spaces in which a patient can explore his or her own framing of environmental influences will greatly reduce the possibility of developing falsely retrieved memories of abuse all while ensuring that instances of childhood abuse are incorporated in the psychological work the patient is undertaking to replace maladaptive behaviors with adaptive ones.

Sexuality and Sexual Identity

Ah what a veritable hornet’s nest of socially-contrived chaos is the development of sexuality and sexual identity for almost all children in all cultures!

For a really fabulous read on sexual identity, consider reading Gender Delusions by Cordelia Fine. 

If you’re an adult and you like sex, your sexual orientation and preferences, and you like your gender, well then count yourself in a charmed minority. And if beyond that you actually feel well matched to your current sexual partner(s), then doubly-charmed indeed!

Not liking sex, your sexual orientation and preferences, your gender, or your current sexual partner(s) does not cause an eating disorder. But applying restrictive behaviors as a salve on all that unpleasantness will mean that these issues in your life will not go away with rest and re-feeding alone. Yes, counseling yet again is the answer.

Does everyone have to like sex? No, of course not. Sex drive and interest sit on a bell curve of intensity just like all other human attributes. And of course sex drive is going to naturally vary significantly for each of us throughout our lifetimes as well.

It is not that the outcome must be that we reach some doubly-charmed sexual perfection, but rather that we feel confident we are not actively sabotaging our natural expression as sexual beings. The end goal is that you are okay with how you define your sexuality and sexual identity— that is an intensely personal journey and you call all the shots on what “okay” means to you.

Reproductive Health Is Very Important

It doesn’t help that many reproductive health specialists: gynecologists, obstetricians, urologists, endocrinologists and fertility specialists are generally unfamiliar with the pernicious symptoms associated with an underlying eating disorder.

All while being able to identify functional hypothalamic amenorrhea or functional hypothalamic pituitary hypogonadism, they will still lean towards synthetic hormone interventions and misdiagnoses, such as PCOS, despite the fact that such interventions have very poor clinical outcomes for both men and women.

Reproductive health is the first to go with the progression of an active eating disorder and it is often the last to return during a recovery attempt. Because reproduction is not required for an individual’s immediate and short-term survival, the body will shut it down often with just a soupçon of an energy deficiency appearing.

Remember that the presence of a regular menstrual cycle is not a definitive marker of reproductive health for women with eating disorders. It’s a one-way marker— its absence most definitely suggests the presence of FHA for those with a history of restrictive eating behaviors and/or chronic exercise issues.

Because reproductive hormones don’t just hang out in the sex organs, the impact of low reproductive hormone levels, or skewed balance of those hormones, doesn’t just impact bone mineral density over time. It has more immediate impacts to brain function and cardiac health for both men and women.

I didn’t really touch on it earlier, but the relationship that reproductive hormones have with adipocyte hormones (hormones produced by your fat organ) alongside the impacts of hypercortisolism (often present with the stress of chronic restriction and/or exercise) leads to hypoinsulinemia among a host of other metabolic anomalies and problems. 40,41

Hypoinsulinemia is just one of the many reasons why medically-supervised re-feeding is a non-negotiable necessity.

Sexuality, sexual orientation and sexual attribution are all indelibly linked to overall reproductive health in humans. These important facets of your humanity may or may not be linked to the onset or the perseveration of an active eating disorder. Therefore rest and re-feeding in the absence of careful psychological therapeutic support can be unintentionally de-stabilizing and unnecessarily painful. The same is also true for the presence of childhood sexual abuse in a patient’s history as well.

While it is not easy to find suitable counseling therapeutic support, you can increase your chance of a good match by taking some time to research how you might interview a prospective counselor and how best to prepare yourself so that you are guided by the specific outcomes you want to achieve in therapy.

As a result of discussing the heritability and environmental fluidity of sexual orientation and attribution I also touched on the basic tenet of this entire website (which coincidentally was the motto of one of my universities):

Tuum est— sometimes is translated as “It’s Yours.” or alternately “It’s Up to You.”

1. Roberto, Christina A., Joanna Steinglass, Laurel ES Mayer, Evelyn Attia, and B. Timothy Walsh. "The clinical significance of amenorrhea as a diagnostic criterion for anorexia nervosa." International Journal of Eating Disorders 41, no. 6 (2008): 559-563.

2. Barnhart, Kurt T., and Courtney A. Schreiber. "Return to fertility following discontinuation of oral contraceptives." Fertility and sterility 91, no. 3 (2009): 659-663.

3. Davis, Anne R., Robin Kroll, Barbara Soltes, Vincent Haudiquet, Ginger Constantine, and Gary Grubb. "Return to menses after continuous use of a low-dose oral contraceptive." Obstetrics & Gynecology 107, no. 4 (2006): 3S.

4. Bergström, Ingrid, Milita Crisby, AnneMay Engström, Mats Hölcke, Monika Fored, Pia Jakobsson Kruse, and AnnMarie Sandberg. "Women with anorexia nervosa should not be treated with estrogen or birth control pills in a bonesparing effect." Acta obstetricia et gynecologica Scandinavica 92, no. 8 (2013): 877-880.

5. Miller, Karen K., Ellen E. Lee, Elizabeth A. Lawson, Madhusmita Misra, Jennifer Minihan, Steven K. Grinspoon, Suzanne Gleysteen, Diane Mickley, David Herzog, and Anne Klibanski. "Determinants of skeletal loss and recovery in anorexia nervosa." The Journal of Clinical Endocrinology & Metabolism 91, no. 8 (2006): 2931-2937.

6. Vescovi, Jason D., Jaci L. VanHeest, and Mary Jane De Souza. "Short-term response of bone turnover to low-dose oral contraceptives in exercising women with hypothalamic amenorrhea." Contraception 77, no. 2 (2008): 97-104.

7. Marcus, Marsha D., Tammy L. Loucks, and Sarah L. Berga. "Psychological correlates of functional hypothalamic amenorrhea." Fertility and sterility 76, no. 2 (2001): 310-316.

8. ibid.

9. Brundu, Benedetta, Tammy L. Loucks, Lauri J. Adler, Judy L. Cameron, and Sarah L. Berga. "Increased cortisol in the cerebrospinal fluid of women with functional hypothalamic amenorrhea." The Journal of Clinical Endocrinology & Metabolism 91, no. 4 (2006): 1561-1565.

10. Hoch, A. Zeni, RANIA L. Dempsey, GUILLERMO F. Carrera, CHARLES R. Wilson, ELLEN H. Chen, VANESSA M. Barnabei, PAUL R. Sandford, TRACEY A. Ryan, and DAVID D. Gutterman. "Is there an association between athletic amenorrhea and endothelial cell dysfunction?." Medicine and science in sports and exercise 35, no. 3 (2003): 377-383.

11. Cumming, David C., Garry D. Wheeler, and Ewen M. McColl. "The effects of exercise on reproductive function in men." Sports Medicine 7, no. 1 (1989): 1-17.

12. Nichols, Jeanne F., and Mitchell J. Rauh. "Longitudinal changes in bone mineral density in male master cyclists and nonathletes." The Journal of Strength & Conditioning Research 25, no. 3 (2011): 727-734.

13. Hackney, Anthony C. "Endurance exercise training and reproductive endocrine dysfunction in men alterations in the hypothalamic-pituitary-testicular axis." Current pharmaceutical design 7, no. 4 (2001): 261-273.

14. Rector, R. Scott, Robert Rogers, Meghan Ruebel, and Pamela S. Hinton. "Participation in road cycling vs running is associated with lower bone mineral density in men." Metabolism 57, no. 2 (2008): 226-232.

15. Kiesges, R. C., K. D. Ward, M. L. Shelton, W. B. Applegate, E. D. Cantler, G. M. A. Palmieri, K. Harmon, and J. Davis. "Changes in bone mineral content in male athletes." J Amer Med Assoc 276 (1996): 226-230.

16. Arce, Joan Carles, and Mary Jane De Souza. "Exercise and male factor infertility." Sports Medicine 15, no. 3 (1993): 146-169.

17. Jensen, Carl Edward, Klaus Wiswedel, Jennifer McLoughlin, and Zephne van der Spuy. "Prospective study of hormonal and semen profiles in marathon runners." Fertility and sterility 64, no. 6 (1995): 1189-1196.

18. MacDonald, A. A., G. P. Herbison, M. Showell, and C. M. Farquhar. "The impact of body mass index on semen parameters and reproductive hormones in human males: a systematic review with meta-analysis." Human reproduction update 16, no. 3 (2010): 293-311.

19. Mont, Lluís, Roberto Elosua, and Josep Brugada. "Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter." Europace 11, no. 1 (2009): 11-17.

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