Should I cut out dairy if I want to get pregnant?

Will dairy negatively affect your fertility? Should you cut it out if you’re trying to get pregnant?

Short answer? No, you should not.

There seems to be a trend lately toward demonizing particular food groups. “Sugar is toxic.” “Gluten is a hormone disruptor.” “Dairy is very bad for fertility.” And the solution is to remove as much as possible of the offensive food from your daily fare. However, when you look at the scientific literature, there is rarely evidence to back up these claims, or if there is, it is MUCH less black and white than what gets spread online. Let’s look at the claims on dairy. “VERY BAD for fertility” according to a recent podcast a member of my Facebook support group listened to. “In this article we will examine the link between milk and infertility and why this beloved, popular food can be so detrimental to your fertility.” from Oh, and how about this gem, “Dairy can actually hurt everyone’s fertility because of the fertility harming toxins it contains, and for people who have lactose intolerance, or a casein (milk) allergy or sensitivity, it can actually cause infertility” from tomakeamommy (emphasis mine).  And you can find a ton more if you google “is dairy bad for fertility?”

What all these sources have in common is an almost complete lack of scientific support for their claims. Or they take studies in mice or that find hormones/chemicals in milk and then make all kinds of assumptions to translate the studies to humans, or hypothesize the downstream effects of the hormones/chemicals – but this gets reported as FACT, not the speculation it actually is (hello, pseudo-science.)

There aren’t actually a lot of studies on the role of dairy in fertility, so let’s take a look at those that are out there. (I searched on Pubmed using “dairy infertility not cow not cattle” because most of the articles that came up initially when I used “dairy infertility” were related to cow physiology and menstrual cycles which is not super relevant.

Dairy intake and IVF outcome – no effect

The most relevant article, IMHO is this one, “Dairy intake in relation to in vitro fertilization outcomes among women from a fertility clinic.” The study population was women attending the Massachusetts General Hospital fertility clinic and enrolling in the Environment and Reproductive Health (EARTH) study, an ongoing prospective cohort started in 2006 to identify environmental and nutritional determinants of fertility among couples. There was no criterion for cause of infertility, meaning that the study group should be a representative cross-section of infertile women in general.

The findings? The researchers divided 232 women into four groups based on amount of dairy products consumed. After adjusting for possible confounding factors there was not a statistically significant difference between the group with the lowest dairy intake and the group with the highest. Of note, prior to adjustment there was a 21% higher live birth rate in those consuming the most diary (significant with a p-value of 0.02), after adjustment, there was a 16% higher live birth rate among those consuming the most dairy, but not significant, with a p-value of 0.10. One can definitely say there is no detrimental effect of dairy consumption in this group.

The researchers looked at other intermediate outcomes during the IVF cycle and found no relationship between dairy intake and uterine lining thickness, estradiol levels at retrieval, or number of eggs retrieved. They also looked at different age groups and found no association between dairy intake and live birth rate in women under 35, but to their surprise, there was a positive association in women older than 35 (meaning higher pregnancy rates in groups with more dairy intake). Again, no evidence for a detriment to fertility – if anything suggestion of a positive effect.

It’s possible that women who are infertile have different characteristics from those who do not have difficulty conceiving, and that in the latter population dairy does cause higher rates of infertility (those women would then likely attend fertility treatment centers like this one and increased dairy would thus show a negative effect…) but I would surmise that women who are having trouble conceiving would be MORE sensitive to dairy than the general population, if in fact dairy was causing infertility/trouble conceiving.

Changes in reproductive hormones with dairy consumption

The  next study, Dairy Food Intake Is Associated with Reproductive Hormones and Sporadic Anovulation among Healthy Premenopausal Women” tested hormone levels at four times during two menstrual cycles (eight tests in total) in 259 healthy, regularly menstruating women and assessed correlation with overall dairy intake, high fat, low fat, different individual types of dairy (e.g. milk, butter, cream, yogurt, ice cream), as well as looking at ovulatory versus anovulatory cycles (assessment based on hormone measurements in the luteal phase). In this study, a ~5% decrease in estradiol was found for each serving of dairy consumed, but also a 3% increase in luteinizing hormone (LH). I’m not in the least convinced that either of these changes is meaningful given the wide range in inter-woman hormone variability as in the figure below (from, and also the very wide ranges given. I looked at the supplementary data where hormonal changes were broken down by menstrual cycle change, and the only time when the range of decrease in estradiol did not include “no change” was during late luteal phase and menses. (and then the range was from  -10 to -3.2% during late luteal phase, to -8.3 to -1.2% during menses). Of note the decreases were larger with low-fat dairy than full fat.

The researchers also assessed whether there was an association between consumption of different types of dairy and anovulatory cycles. Their model which adjusted for various factors found that cream and yogurt were both associated with an increased likelihood of anovulatory cycles, but… with cream (7.5% anovulatory cycles with no cream consumption versus 9.8% with cream), the 95% confidence interval includes 1.0 which means the statistical significance is marginal (i.e. if they were to do another study, they could very well get a different outcome). With yogurt, there does seem to be a difference (6.1% anovulatory cycles with no yogurt consumption, 13.2% with).

Also, they only followed women for two cycles and do not report the number of women with 0, 1, or 2 anovulatory cycles, nor did they confirm ovulatory cycles before the study commenced. So… grain or two of salt on this one. Regardless, given a (non-significant) decrease in anovulation upon consumption of cheese (11.6% in those consuming no cheese versus 7.9% in those who did eat cheese), butter (9.3% vs. 6.8%), and only a miniscule increase in those consuming ice cream (8% versus 9%), and no difference in ovulation based on overall dairy consumption, low-fat or high-fat dairy consumption, one cannot say unequivocally that “dairy causes infertility” or “dairy is bad for fertility.”

Dairy products and anovulation – high fat dairy seems to be protective

Since the previous study brought up anovulation, the next study I want to look at is the one we refer to in No Period. Now What?, “A prospective study of dairy foods intake and anovulatory infertility.” Researchers evaluated questionnaires from participants in the Nurses Health Study II, and found 18,555 women who were attempting to get pregnant. Within the eight years the subjects were followed, 3,430 women reported infertility of more than a year’s duration, with 438 of those reporting “ovulatory disorder.” Unfortunately the authors do not report an analysis of dairy intake with general infertility. The researchers do examine correlations between dairy intake and ovulatory disorders, and overall find no association.

They go on to further examine association of low-fat (skim/low-fat milk, sherbet, yogurt and cottage cheese) or high-fat (whole milk, cream, ice cream, cream cheese and other cheese) dairy with ovulatory disorders. In this case, they find an 11% increased risk of anovulation per serving of low-fat diary, and an almost 50% decreased risk with one serving of full fat dairy per day versus <1 per week. Interestingly, they also find a strong correlation between yogurt and anovulation (as well as sherbert and frozen yogurt), with a 30-60% higher risk (depending on the statistical model) with an increase of 1 serving yogurt per day. I assume that they put yogurt into the low fat category as most of what is available in stores is fat-reduced. I would suspect that full fat yogurt would not show the same association. I do find, after looking at the data, that their assertions of effect might be a little strong… with low fat diary ovulatory disorder occurs in 1.1% of women consuming <1 serving per week, 1.6% of those consuming 2-4 servings per week, 2.3% of those consuming 5-6 servings, 1.9% of those consuming LF dairy once per day, and 1.4% of those consuming more than one serving low-fat dairy per day. Adjustment for confounding factors makes the differences more significant… but in general you can see that the percentages are quite low.

Once again, one cannot draw the conclusion that “dairy is bad for fertility.” As far as anovulatory infertility goes, it seems that there might be a correlation between consumption of low-fat dairy products and ovulatory disorders, but high fat dairy seems to be protective (and why we encourage women with HA to consume high fat dairy products!!)

additional studies

Phew! Time is getting short here, so I’m going to throw out a few other things I’ve come across without going into quite so much detail.

In 1994 a study was published ostensibly looking at correlation between dairy intake and fertility on a global scale, “Adult hypolactasia, milk consumption, and age-specific fertility.” The authors compare rates across countries of hypolactasia (lacking the enzyme lactase that digests the sugar galactose in milk), amount of milk consumed per person in each country, and number of births across age groups, using that as a proxy for fertility. They state that “decline in fertility with aging is steeper in populations with high per capita consumption of milk” and suggest that might be due to the effect of galactose on ovarian function. There are so many reaches in this paper I don’t even know where to start (for example using number of live births per age group as a proxy for fertility). I will point out that when they restricted their analysis to European and North American countries where economic development is similar, “the correlation between milk consumption and decline in fertility is not present.”

Just to throw in a little something on the male side, this study, “Impact of men’s dairy intake on assisted reproductive technology outcomes among couples attending a fertility clinic” likewise found no effect of dairy intake on live birth rates in couples based on the males’ dairy intake.

Finally, this study, “Low Starch/Low Dairy Diet Results in Successful Treatment of Obesity and Co-Morbidities Linked to Polycystic Ovary Syndrome (PCOS)found improvement in some hormonal measures of PCOS when women diagnosed with PCOS were put on a low starch/low dairy diet… but A) hello, you obviously can’t assign that improvement solely to low starch or low dairy, that would require another study where the two factors are separated, B) there is no evidence in the paper that this leads to improvement in fertility and C) even if it is the case for women with PCOS, no reason on earth to then go and say that dairy is “very bad” for *everyone*. PCOS is a specific hormonal condition, so in the absence of a similar study in women without PCOS showing that dairy harms fertility (which in fact we have the opposite of, see above), one simply cannot make that claim.


In conclusion, if you like dairy, eat/drink dairy without fears of it affecting your chances of getting pregnant. If you do want to consume dairy, it seems that the full fat versions are probably better for you, especially if you are already missing periods. If you don’t like dairy, or are allergic, don’t have lactase, then don’t consume them (although Shanta in my facebook support group says, “I eat LOADS of lactose free dairy and full fat yogurt and cheese, in fact i go through more than a liter of yogurt a day, and it REALLY helped my recovery, so you can always go the lactose-free route.)

If there are others studies you’re aware of that support diary as detrimental, please let me know, I’d love to take a look.



Can Maca help restore periods?

Can maca help restore a missing period?

A little while back I did a survey of women in my “No Period. Now What?” facebook support group and found that among 53 women 63 supplements were being taken with the idea of helping to restore missing periods. Maca was taken by 10 of these women, so I thought we’d investigate it next. Thanks to Eryn for digging up some references!

Overview of Maca

Maca, aka Lepidium meyenii, is grown in the central Andes. The part that is eaten is the “hypocotyl”, a tuberous root-like structure that is a storage organ for nutrients. Maca has been cultivated and used for food and medicinal  purposes for hundreds of years.

From Creative Commons License 4.0

Maca and period restoration

Our question is whether maca can be useful in a woman trying to restore menstrual cycles. I was rather surprised after reading some abstracts to find that there were hints of potential usefulness of this supplement – but after reading the full studies, my conclusion is that while maca is not going to hurt recovery, it is unlikely to help either.

In the first study, rats were fed dried maca powder as 5%, 25%, or 50% of their diet. Seven weeks later, during the “pro-estrus” phase (like the follicular phase in humans) hormones were measured, and in the rats consuming 50% maca, a 4.5-fold elevation in LH levels and 19-fold elevation in FSH levels were seen. This elevation was dose dependent (meaning elevations were seen at lower amounts consumed as well, in proportion to the amount of maca). However, there are two key points missing from the abstract, which is where that info comes from. One is that there was essentially no elevation at the lowest dose, 5% of feed, which is about 3g/kg/day.  The second point was that these elevations were very transient, seen only at the time of the pre-ovulatory surge. There was not an overall increase in LH levels.

The huge elevations in LH are clearly not reproducible in humans, because 50% of our diet as maca powder is not feasible. Even 3 grams per kilogram, i.e., 180 grams per day in someone weighing 60kg (about 130 lb) doesn’t jibe with the dosages normally prescribed. A website selling maca powder indicates that a serving is about 9 grams. In the Andes, people will often eat 100-200g of the root 2-3 times a week, a much higher amount than what is realistically available to those of us outside Peru.

There are a few other studies in rodents, but unfortunately not much in humans to support or refute these results. A study performed in men (due to positive effects on sperm parameters) showed no change in FSH, LH, estradiol, prolactin, or testosterone while taking 1.5 or 3g of maca for up to 12 weeks.

These two results, an elevation in the levels of LH and FSH *only* during the pre-ovulatory surge in mice, and no change in reproductive hormones in males in response to maca suggest that maca is not going to help with no periods based on a hormonal mechanism.


As I was researching the toxicity of maca (which seems to be zero), I came across an article where they did a double-blind, placebo-controlled study looking at a number of health outcomes after consuming maca (3g/day) for 12 weeks (197 subjects across all groups). The health outcomes were assessed on a weekly basis, giving a really nice data set. There were no adverse events reported which is great, and they reference another study that found no toxicity in rats at up to 17g/kg, which is an enormous amount, so maca seems to be very safe to eat.


Some of the health outcomes that were measured in the study I just mentioned and found to be significantly different from placebo (on top of a placebo effect!) may be of interest to readers – improved libido, energy, mood, and “Health Related Quality of Life” score. The “HRQL” is a 36-question survey that contains “five items related to general health, five items related to physical activities associated with current health status, two items related to limitations on work or other regular daily activities as a consequence of reduced physical health, two items on bodily pain, one item about vitality, and five items on mental health [].”

This study suggests that there may be other reasons to take maca than period restoration per se… it may help with overall quality of life while you are working to recover. And in someone who is at a “fertile BMI,” not doing high intensity exercise, but still stressed and anxious… maybe something like maca could help with the mental stress part.

MACA for Missing periods?

My ultimate conclusion is if you like maca, go ahead and have some (after checking the sourcing, see below), but don’t feel like this is something that you need to go out and get to help you restore your missing period. It may have some mood boosting effects that could be helpful during recovery in other ways though.

I will leave you with a quote from a recent review of maca,

To date, the health claims of maca cannot be fully supported from a scientific standpoint and more research is needed. It appears that the indigenous local knowledge about the health benefits of maca has been dragged out of context to fit the demands of a growing market for herbal remedies. This globalisation (or hype esp. in China) also has had serious consequences for the local producers in Peru. The lack of protocols to regulate the production and marketing of maca during this rapid expansion, poses a threat to both the safety of consumers and the sustainability of supply.



Acetyl-L-Carnitine and Restoring Missing Periods

Continuing my series of posts on supplements and recovery of mising periods… overview here, and post on Vitex here 🙂 I am going to review acetyl-l-carnitine next as it is a supplement for which there is evidence for effectiveness in restoring missing menstrual periods from controlled clinical studies. Thanks to Addie for helping with the research!

Here’s a table of contents for this post, as it ended up being super long!!

Alright, let’s get started. First, acetyl-L-carnitine, also known as L-acetylcarnitine, ALC, or ALCAR, is a derivative of the amino acid L-carnitine (aka levocarnitine). L-carnitine acts as a recipient of an acetyl group in a reaction that releases CoA for use in the Krebs cycle that generates energy (ATP) in the mitochondria. ALC is naturally synthesized in our bodies on an ongoing basis, and crosses the blood/brain barrier, therefore potentially affecting brain hormones, chemistry, or brain function. Studies have been performed examining the effectiveness of ALC in a number of indications, ranging from diabetic neuropathy to Alzheimer’s disease.

Chemical structure of Acetyl-L-Carnitine:

By Ed (Edgar181) - Own work, Public Domain,

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Does Vitex Help Restore Missing Periods?

why would I use vitex, and WHAT IS it?

To determine what supplements women might use to try and restore missing periods, I did a quick survey of women in my “No Period. Now What?” facebook support group. The most common herb/supplement mentioned  was Vitex, taken by over a third of those who responded to my survey (21/53). Vitex is a shortened name for Vitex Agnus Castus also known as Chasteberry.  Most women reported taking “vitex’, but some said “agnus castus” or “chasteberry” – as far as I can tell they are synonyms. It’s a small, bushy plant, with pretty purple flowers and small brown berries.



I did a search of the medical literature using the following queries in pubmed to find research relevant to understanding whether vitex can help restore a missing period.

Vitex fertility
Vitex amenorrhea
Vitex oligomenorrhea
Vitex luteal phase
Vitex follicular phase
Vitex progesterone
Vitex estrogen
Vitex osteoporosis


The searches came up with between 5-25 results, many overlapping between searches. I read through abstracts where available (a few articles were in languages I don’t speak, or had no abstract available) and the full article if the abstract seemed relevant and I wanted to learn more.

My conclusion is that Vitex Agnus Castus does NOT lead to restoration of cycles in someone experiencing hypothalamic amenorrhea (unless that amenorrhea is due to elevated levels of prolactin), and may in fact be hindering the return of a missing period.

Continue reading

Supplements to Recover Missing Periods?

I recently asked in my Facebook support group what supplements women had used while trying to recover from hypothalamic amenorrhea / no period as I wanted to look further into the science behind each of them. I was astounded at the range of answers – 53 women used one or more of 65 different supplements!

Can pills help recover missing periods?

By Root66 (Own work) [GFDL ( or CC BY-SA 3.0 (], via Wikimedia Commons

How do I restore missing periods?

Unfortunately, many women are prescribed supplements instead of what we all know works – eating more, exercising less (particularly less high intensity exercise), and reducing stress. A common refrain was captured well by one poster:

Ellen: Oooh, I’ve tried so many supplements in hopes of sidestepping real lifestyle change! I’ve dabbled with vitex, maca, soy, estroven, bulletproof diet recipes, acupuncture…while some (acupuncture) really benefited me in other aspects like stress level, none served as proxies for eating bravely and resting bravely- which I am finally giving a go.

It is really important to take heed of what Ellen says – there is no way around making lifestyle changes. If you have no period due to HA, while you might (possibly – success is not guaranteed!) be able to get pregnant using injectable gonadotropins or IVF, those are not going to restore your system to balance or bring back that missing period / cycle. In the words of another wise woman: Continue reading

Menstrual Cycle Hormones

Whenever someone asks me about levels of menstrual cycle-related hormones during their cycle and the answer isn’t obvious I go to the figure below from Wikimedia (this article). What I love about it is that it shows the average (bold blue line) and then the biological variability around that average (dark blue shaded area)… and then also how much this can vary between cycles and between women.The figure is based on a study performed in 2006 that measured hormone levels in 20 ‘normally cycling women’ not on birth control pills. The data were reanalyzed in 2014 and these figures created.

One example of when I might refer to these figures is if someone tells me that they’ve just had blood drawn, they don’t know what cycle day they’re on (e.g. have not yet had their first post-HA or first postpartum period), and LH was measured at 17 and estradiol at 215 pg/mL. I can check these figures and see that that most likely corresponds to just before ovulation. If LH is 17 and e2 is 85 pg/mL that might mean that ovulation has just occurred. If LH is 17 and estradiol is 30 pg/mL then I might suggest inducing a bleed and testing a hormone panel to determine if PCOS might be in play.

I think what is unique and particularly helpful in these figures is the inclusion of variability so one has an idea of the typical range for these hormones. Let me know if you have any questions!




Do you really ovulate “late”?

Some women, as they recover from hypothalamic amenorrhea (missing periods), will be worried that they are ovulating “late” in their cycle, maybe Cycle Day 21, 22… but then they get their period around the normal time, maybe CD 28-30.

In some cases, and this was true for me, the issue is the short luteal phase (the time between ovulation and when your period arrives) leading to a seemingly long follicular phase (time between period and ovulation).

When I tracked my ovulations and periods carefully I noticed that my ovulations were routinely 28-30 days apart, as expected. So it wasn’t that the ovulation was messed up, it was more that my period wasn’t aligning with the ovulation as in a normal cycle. A similar phenomenon was observed in a research study where women with short luteal phases were observed to have longer follicular phases (this was not the main focus of the study, but my observation from data reported in Table 2).

My theory is that to some degree, our period and then subsequent ovulation are actually hormonally separate events. The period comes because of a drop in progesterone, that is unrelated to the decrease in estrogen that primes the small increase in FSH to start the new follicle growing. So in a woman with a short luteal phase, the drop in progesterone occurs early, leading to an early period – but that does NOT drive the start of follicular growth, which waits for a few days and then begins, on its regular 28 day cycle.

I know this is confusing, so check out these diagrams. Here’s a normal cycle…the small increase in FSH at the beginning leads to growth of the egg-containing follicle. In the middle of the cycle, around CD12-13, LH spikes leading to ovulation around CD14. After ovulation, the follicular structure collapses into the “corpus luteum” which starts secreting progesterone by around CD16. When progesterone levels fall approximately 12 days later, the period starts, FSH increases, and the whole cycle begins again – with ovulation around CD14 and period around CD28.

Here’s my view of what is happening when one has a short luteal phase. Let’s imagine that the first period in this diagram was induced by Provera and then Clomid is used to start the follicular growth. So the follicular phase proceeds just as above – a small increase in FSH leads to growth of the egg-containing follicle, LH spikes around CD12-13, and ovulation happens on CD14. This is where things aren’t working quite right – the corpus luteum forms, but isn’t making enough progesterone. So the increase in progesterone is lower, and for a shorter amount of time. This leads to an early period – in this diagram, about a week early, for a 6 to 7 day luteal phase.

This leads to what I’m terming the “apparent cycle day” in the figure – menses have started, so ostensibly it’s CD1 again. However. The OTHER hormones involved in the cycle are not at CD1 levels yet. They are still at CD22, 23, 24 levels. The estrogen needs to drop further to instigate the increase in FSH to start the follicular growth… and THOSE hormones are not affected by the lack of proesterone. They continue along their merry way as if it’s CD 22-28, not caring that you’re bleeding already and *think* it’s CD1. So then you get to CD14 and think that ovulation should be happening… but it doesn’t. So you get frustrated (trust me, I know!!) But in reality, your other hormones are on their normal 28-30 day cycle, when when you get to where CD14 would have been if your period had come on time at CD28, that’s when you ovulate. Does that make sense? If not, feel free to drop a question in the comments!

To further illustrate this, here’s a table with my cycle data (this was after my second son was born in September 2008… my first postpartum ovulation was 7/29/2009 while I was still breastfeeding morning and night. I got my period just five days later on 8/3/09, for a four day luteal phase. This cycle isn’t a great example as the cycle is long as is common in initial postpartum or recovery cycles. However the next one (cycle #2) is a perfect example. After only a six-day luteal phase, I got my peiod on 9/15/09 – had it been a normal length LP (e.g., CD14 ovulation, CD28 period start), my period would have come on 9/21/09 instead. I then ovulated on 10/6/09, which based on when my period actually started was apparently CD22… but had my period come when it “should have”… the ovulation would have been CD15.

One anomalous cycle happens on cycle 10 – I had gotten pregnant the cycle before, but unfortunately had a miscarriage that was resolved after two D&Cs. After that I started to use progesterone suppositories to support my luteal phase, which leads to close to normal LPs and pretty close to CD14 ovulation. I did NOT use progesterone on cycles 15 or 16… leading to shorter luteal phase and apparent later ovulation!

You can see from this data set that there’s a fair bit of variability between cycles – compare the days between ovulation and you see that mostly they’re around ~28-30 days, but there are a few that are shorter, and a few that ar longer. I know that some women are like clockwork, but that is certainly not true for me!!

I hope this helps explain why a short luteal phase and longer apparently follicular phase are associated – again, feel free to ask any questions you may have – or please share if this has been your experience as well – or not!

xox Nico

P.S. Check out Chapter 19 in No Period. Now What? for a LOT more information on luteal phases, why they might be short, and what you can do about it!!

Femara or Clomid for Ovulation Induction?

Summary: If you are not ovulating naturally even after working on recovery, and want to use medication to induce ovulation for pregnancy, Femara (letrozole) is preferable to Clomid (clomiphene)*.




Letrozole, By MindZiper – Own work, CC0,


In No Period. Now What? (NPNW), our book on hypothalamic amenorrhea recovery, Chapter 21 covers the oral medications that can be used to encourage ovulation. We discuss how soy isoflavones, Femara, Clomid, and tamoxifen reduce estrogen levels to encourage an increase in follicle-stimulating hormone (FSH) that in turn leads to growth and maturation of eggs. These medications can be used when pregnancy is desired, but also to “jump-start” menstrual cycles*. It is really important to note that these meds are unlikely to work without progress having made toward recovery in the form of increased eating, reduced exercise, and reduced psychological stress – all of which you can read about in earlier sections in our book.




Clomiphene, by MarinaVladivostok (Own work) [CC0], via Wikimedia Commons



We also cover research comparing pregnancy rates, likelihood of a multiple-gestation pregnancy, uterine lining thickness, and other metrics between Femara (letrozole) and Clomid (clomiphene citrate) to help women decide which choice is optimal for them. (Tamoxifen is an alternate that is rarely used, so there is not a large body of research to reference, although in many ways it is preferable to Clomid based on fewer effects on the uterine lining.) We also discuss dosing recommendations, what to do if the first cycle doesn’t work, and much more. 🙂

Our conclusion in NPNW is that if one is trying to get pregnant, Continue reading

What to do if you’re a competitive athlete with a missing period?

Our hypothalamic amenorrhea / female athlete triad recovery book No Period. Now What? describes the causes of HA, many of the short- and long-term effects, and offers a Recovery Plan that has worked for hundreds of women. We also offer support throughout in the form of our own experiences, anecdotes from other women in similar situations, and advice we have gleaned over our years working with women to restore menstrual cycles.

There are two major components to recovery, both of which are covered in great detail in our book, but simply put, they are to eat more and cut out high intensity exercise.

Easy, right? Except, really, not at all. It is incredibly difficult for most of us to relinquish the food myths that we have been taught over the years, to let go of the rules that we have placed on ourselves, and particularly, to gain weight. For many it’s even more difficult to stop our cardiovascular exercise, whether it be running, biking, classes, or being a ‘gym rat.’ That’s why we spend more than a hundred pages on the rationale for the recommendations, ideas to implement them, and support for all the mental work that needs to happen.

While it’s hard enough for a recreational athlete to cut out high intensity exercise, for a competitive athlete this might truly be impossible. If you’re in high school and hoping for a college scholarship, or already in college being provided funds to attend, or a professional athlete – you might not be able to just quit for a few months. There is so much riding on your ability to perform.

relay Pole_vaulter Division’s_own_earns_Camp_Pendleton_Female_Athlete_of_the_Year,_runner_up_in_Marine_Corps_award_140313-M-PC317-003 Women 60 m final during Doha 2010 World Indoor Championships, by Erik van Leeuwen

(Photo credits, L to R: Erik van Leeuwen, Atitaya Kongkaew, Sgt. Timothy Lenzo (, Erik van Leeuwen, all via Wikimedia Commons)

And yet.

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Update on Birth Control Pills / Oral Contraceptive Pills and Bone Density

I started working on No Period. Now What? August 6 2012. The first year or so I worked on putting together the survey, getting it out to respondents. The second year consisted of research and writing, the third was editing, and the last six months doing book design and copy editing. That means the research we refer to was mostly published in 2014 or earlier. Additional information has become available since then and I plan to check in on different topics to ensure that our recommendations remain valid.

We put together an information sheet on birth control pills, periods, and what to expect; enter your email address to download the guide.



One question I wanted to reexamine as I put together the info sheet was whether there is additional evidence on the effects of birth control pills/oral contraceptive pills (OCP) on bone density. When I was researching for the book, the consensus I found was that OCP seemed to prevent further bone loss in a woman with hypothalamic amenorrhea, but increases in bone density and strength were unlikely. The best way to increase bone density was through weight gain and period restoration.

There are quite a few articles that have been published in the last two years, generally agreeing with my conclusions. As these are recent papers the full texts tend not to be freely available but I feel comfortable using the abstracts for this overview as it was simply to confirm the recommendations and research from the book. If there are any other articles you think we should be aware of or you’d like us to review, please let us know!

I investigated five recent articles, listed below (as well as reading through other abstracts). The first was one of the larger studies I’ve seen, looking at bone density in 826 normally cycling teenagers. Those not using birth control pills had an average 2.5% increase in bone density over the course of a year, versus a 1.45% increase in those on the pill. This illustrates that this formulation of the pill was actually interfering with normal bone growth. A similar but small study found an increase of 2.0% in bone density in teenagers on birth control pills versus 12.2% in non-users.

Agreeing with our assertions in No Period. Now What? a study in 91 women in the armed forces found that the pill essentially had no impact on bone density; weight loss decreased density, whereas weight gain, normal menstrual cycles, and a normal Eating Disorder Inventory score were associated with increased bone density.

A couple of the studies were reviews, similarly agreeing with our conclusions. The major finding by Lebow et al. was that the majority of studies found no benefit of estrogen therapies on bone density. Finally, Bergstrom et al. go even further, arguing that given the limited benefit, those suffering from missing periods should NOT be prescribed birth control as it provides a false sense of security about the state of one’s bones, and may discourage from attempting to recover normal cycles through eating, exercise, and stress changes.

Were you ever prescribed birth control pills to “protect your bones”?


Gersten J, et al. Impact of Extended 30 mcg EE With Continuous Low-Dose EE and Cyclic 20 mcg EE Oral Contraception on Adolescent Bone Density: A Randomized Trial. J Pediatr Adolesc Gynecol. 2016 Jun 7. pii: S1083-3188(16)30058-4. doi: 10.1016/j.jpag.2016.05.012

Biason TP, et al. Low-dose combined oral contraceptive use is associated with lower bone mineral content variation in adolescents over a 1-year period. BMC Endocr Disord. 2015 Apr 3;15:15. doi: 10.1186/s12902-015-0012-7.

Nieves JW, et al. Eating disorders, menstrual dysfunction, weight change and DMPA use predict bone density change in college-aged women. Bone. 2016 Mar;84:113-9. doi: 10.1016/j.bone.2015.12.054. Epub 2015 Dec 30.

Bergstrom I, et al. Women with anorexia nervosa should not be treated with estrogen or birth control pills in a bone-sparing effect. Acta Obstet Gynecol Scand. 2013 Aug;92(8):877-80. doi: 10.1111/aogs.12178. Epub 2013 Jun 15.

Lebow J, and Sim L. The influence of estrogen therapies on bone mineral density in premenopausal women with anorexia nervosa and amenorrhea. Vitam Horm. 2013;92:243-57. doi: 10.1016/B978-0-12-410473-0.00009-X.