While the title of this post may sound hyperbolic, it nonetheless is grounded in truth. There are a wide variety of dietary and lifestyle factors that affect reproduction. Stress may be one of the greatest of all.
Dozens of studies performed on cynomolgus monkeys, bonobos, chimps, and baboons have demonstrated that having low social status–even while maintaining the exact same diet at high social status individuals–induces impaired fertility in primates. Human models, while approximations, do not differ. In some, a simple progesterone-dampening effect occurs, in others the levels decrease precipitously, in most cortisol levels skyrocket, but in general a wide spectrum of reproductive disorders- from hormone deficiency to full-blown long-term amenorrheic infertility- follow from psychological stress. This is something about which I have written before, and it’s a serious problem, causing not just outright and obvious infertility but also sneakily impaired and sub-optimal fertility all across the country.
Pysychological stress wreaks all sorts of havoc on the body. Most importantly, cortisol levels rise, and the body’s inflammatory and immune responses become impaired. Blood sugar levels rise, and insulin levels rise, too. When these things happen, healing cannot occur, and tissues become progressively damaged with time. This applies to reproductive tissues as much as it does to the rest of them. Hypercortisolemia is good for nobody.
Several hormone responses also occur. Three of the primary ones are as follows:
1) As I mentioned, due to elevated cortisol levels, insulin levels may rise, and testosterone levels rise right alongside it. This is because insulin directly stimulates testosterone production in the ovaries. This is bad for reproduction because a proper balance between testosterone and female balance needs to be maintained in order for proper reproductive signalling and tissue development to occur. One particularly potent way in which this imbalance often hurts women is in the hormone condition Poly Cystic Ovarian Syndrome. It is not the only thing that contributes to PCOS– definitely not– but it can play a big time role in it.
2) Moreover, another effect that may occur as a result of stress is an increase in production of DHEA-S, a hormone produced in the stress glands. DHEA-S is, like all other hormones, an important and very healthful hormone in proper balance. But if the stress glands are in overdrive, they might over-produce everything, including DHEA-S. This is detrimental, because DHEA-S is also a classically male sex hormone, and it plays a role similar to testosterone in PCOS. DHEA-S in excess blocks estrogen signaling, interferes with LH and FSH signaling, and also increases hormonal acne. DHEA-S can play a role in both type I and type II PCOS.
3) Finally, the brain, via the hypothalamus, sometimes turns off pituitary activity in response to stress. This often leads to a cessation of LH and FSH signaling–the two primary pituitary signalling molecules–which in turn decreases levels of estrogen and progesterone in the blood. Recall that reduced progesterone levels are one of the primary markers of reproductive distress in primate studies. Prolactin levels may also decrease. These facts make it impossible both to ovulate and to menstruate.
*Graphic extracted from PCOS Unlocked: The Manual.
These three categories– testosterone elevation, DHEA-S elevation, and pituitary decreases may occur differently in all women. And there are a wide variety of other, more subtle, hormonal responses that also occur, especially when considered in conjunction with all of the other bodily stress that follows from psychological woes.
All that being said, STRESS IS BAD. We know some of the reasons why, as I’ve explained above. Others likely exist. Even if you don’t have infertility problems, you may have hormone imbalances or deficiencies, and those can be just as insidious. Eat right, sleep right, live well, breath deeply. Repeat.
Stress is a significant problem for women’s health, and particularly women’s hormonal health. This is manifested in a wide array of problems, but also most predominantly these days in the condition PCOS, or Poly Cystic Ovarian Syndrome.
You can read more about stress and it’s interplay with cysts, as well as how to overcome it all, in my forthcoming guide, PCOS Unlocked: The Manual. Coming to this website on 10.17.12, ONE WEEK FROM TODAY.
PCOS and Hypothalamic Amenorrhea: what’s wrong with the contemporary understanding, and how women can have both
PCOS is complicated. It’s an easy diagnosis, but the causes of it are rarely understood. This is because cysts crop up under a wide variety of hormonal circumstances. We might think that this would mean that the medical community recognizes the need for diverse treatment among PCOS patients, but actually it does not. Instead of considering the wide variety of PCOS needs, many doctors (especially those who are not endocrinologists) use blanket diagnoses and treatments for all of their PCOS patients. This is not wholly unreasonable. There is a majority PCOS condition, and the biochemistry of this condition is both simple and compelling. However, there remain other causes and problems. Failing to address them means that thousands of women end up falling through the cracks.
The current understanding of PCOS is flawed in two major ways. First is what I just described above, the fact that the wide array of different hormonal issues that might cause PCOS has not really been explored or emphasized. Instead, PCOS is broadly regarded as a direct effect of being insulin resistant and overweight. However, this only accounts for between 60-80 percent of PCOS patients. The second flaw is a corollary of that nearsightedness: most members of the medical community (though there is a real debate getting off the ground) believe that it is impossible to have both PCOS and hypothalamic amenorrhea at the same time.
The belief in problem number two, ie, that HA and PCOS are incompatible, derives from the first problem, ie– the lack of a nuanced understanding of PCOS. PCOS is widely regarded as a problem of insulin resistance and being overweight. These are two significant factors that generate cystic ovaries. But they are not the only ones. Only 60 percent of PCOS patients are overweight. Some normal weight PCOS patients are also insulin resistant. Yet others still are not. What causes normal weight women to develop cystic ovaries? And what about insulin-sensitive women?
Recommendations for overcoming PCOS are directed at this insulin-resistant. PCOS patients are advised by the National Institute of Health to “drop 5 percent of their body weight” in order to become fertile. This is, again, great for the majority of PCOS patients, who usually do well and recover reproductive function with the simple implementation of an insulin-sensitized lifestyle. This is why the paleo diet kicks ass for overweight women with PCOS. When they exercise, eat low-ish carbohydrate diets and eliminate refined foods…. these women correct their insulin resistance, reduce their testosterone load, and as such watch their hormone balance fall elegantly in line. It is worth noting that there are different nuances within this population– that some of them have vastly different estrogen and progesterone levels and varying degrees of hormonal imbalance. This is another reason that a nuanced understanding of PCOS is necessary for the health of each women. Nonetheless, however, overweight PCOS patients generally recover well on weight-loss and insulin-sensitizing programs.
This does not really do the trick, however, for the rest of the women out there with PCOS.
Below, I discuss the typical and some atypical causes of PCOS, which will hopefully shed light on a) the variety of ways in which hormones can be disrupted, but also in particular b) how hypothalamic amenorrhea (and hypothyroidism) can play a powerful role in causing cystic ovaries.
There are three characteristics necessary for a PCOS diagnosis for all women:
-Cystic ovaries, as detected via ultrasound
-Elevated androgen (male sex hormone) levels
-Irregular or absent menstruation
Overweight and insulin resistance are two important ways these characteristics can be brought about, yet other ways are equally powerful. The thing is– having cystic ovaries means that the process of menstruation is not completed properly. It does not mean necessarily that one universal step (such as insulin resistance) goes wrong. Instead, it means that at some point along the chain throughout the four menstrual weeks, one or more factors misfires. A signal is missed, one hormone floods the rest of them, or one hormone isn’t properly produced, for example. Androgens usually end up at dominating the reproductive scene, and cysts usually develop. But the mechanisms by which this occurs are not as simple as many PCOS practitioners would have us believe.
The dominant pathway by which women develop poly cystic ovaries is, again, that of the overweight woman. It is a fairly simple process:
1) insulin stimulates testosterone production in the ovary, and
2) testosterone production throws off estrogen levels and inhibits estrogen signalling.
In PCOS, testosterone and estrogen become improperly balanced, and the rest of the menstrual cycle, which takes its cues from the rise and fall of estrogen levels, suffers. LH and FSH, two pituitary hormones that tell the ovaries what to do and when, are of particular concern. LH and FSH levels become dysregulated with dysregulated estrogen because they take their cue from blood estrogen concentrations. This is why the vast majority of PCOS patients have a reversed and high LH and FSH ratio compared to healthy women. The pituitary gland keeps trying to make the body ovulate, but it does not read estrogen signals properly, and the ovaries do not hear the pituitary properly. So these are the markers of the typical PCOS diagnosis: inverted LH and FSH, insulin resistance, overweight, and elevated testosterone levels.
Yet there are other means by which a woman’s hormonal profile can create cysts.
First is a simple case, and this one is thankfully recognized by many in the medical community: that of hypothyroidism. Having low T3 (the active form of thyroid hormone) in the blood is strongly correlated with cystic ovaries. When women with subclinical hypothyroidism correct their condition (this is normally done in medical studies by taking T3 pills), the majority of cases begin menstruating again. This is presumably because low T3 levels decrease the activity of cells and hormonal signalling, which means that the menstrual cycle proceeds with fits and starts, rather than powerful, holistic health. Three common causes of lower thyroid function are poor sleep, restricted calorie intake, and a long-term carbohydrate limited diet (since glucose is necessary for the conversion of T4 to T3 in the liver).
Second is the important and powerful case of hypothalamic amneorrhea. HA is known by many to be exactly the opposite of PCOS. In PCOS, hormone levels often skyrocket. High testosterone, high and uneven LH to FSH ratio, high estrogen levels (though not always). In HA, hormone levels plummet. Low LH, low FSH, low estrogen, low testosterone. PCOS is a problem of being overweight; HA is a problem of being underweight. In PCOS, women over-produce hormones. In HA, women under-produce hormones.
Or so the story goes. However, women can present with cystic ovaries and still have low levels of hormones. The problem– the real, truly universal problem that creates cysts–is a hormone imbalance. Absolute levels of the hormones are important, but even more important is the balance between testosterone, estrogen, progesterone, and leptin, even. The other factors– insulin resistance, LH and FSH inversion, and being overweight– they are not the only thing that can create an androgen-dominant cystic profile.
Hypothalamic amenorrhea is a problem of being too stressed, eating too few calories, exercising too much, and having too little body fat. In essence, it is a condition caused by hypothalamic stress and down-regulation. Hence the name.
The ways in which these four problems typically classed under a diagnosis of hypothalamic amenorrhea– the eating, the exercising, the stress, and the body fat– can cause cysts and/or co-occur with more classically PCOS-type symptoms are vast. Here are a couple of examples:
-A woman is really stressed out by work and life. While most of her hormone production plummets, her DHEA-S production (the top-of-the-food-chain hormone produced by the adrenal gland) skyrockets in response to HPA axis dysregulation. DHEA-S is an androgen, and it influences the development of cystic ovaries if estrogen levels are not equally as high.
-A woman is fairly healthy but has slept poorly throughout her entire life. This pushes her towards insulin resistance, but more than that it dys- and up-regulates her cortisol production. Cortisol signals to the HPA axis to decrease pituitary activity, and it does so. Her hormone levels all decrease. This woman’s predisposition to insulin resistance coupled with adrenally-induced fluctuations triggers the development of ovarian cysts.
-A woman is stressed out via the typical HA pathways–caloric restriction, excess exercise, and stress–so her pituitary hormones decrease in potency. Testosterone and estrogen levels are low but okay, and the woman is probably thin but may also be larger, depending on the degree of stress. Nevertheless, this time it is progesterone that takes the largest hit from the stress (taking it’s cue from both estrogen and LH), and menstruation can never occur without sufficient progesterone levels.
-A woman has a tendency towards insulin resistance, and is overweight, and then loses weight. While this corrects the insulin problem, the drop in estrogen levels she experiences from the weight loss (since estrogen is produced in fat cells) causes an imbalance in her predisposed-to-testosterone-production ovaries.
- Or a similar phenomenon occurs with leptin: In this case, a woman may be a bit insulin resistant, and therefore have a predisposition to testosterone production, but she does not test into a “dangerous” testosterone zone. Instead, her problem lies in the fact that she lost weight, and with it, she lost the potency of her leptin stores. During puberty, each woman’s body adapts to whatever levels of estrogen and leptin she has circulating in her blood at the time (creating a bit of a leptin “set point”). Later in life, one of these women loses weight. As she loses weight, and, significantly, if she is restricting calories or exercising excessively, her leptin (and estrogen) levels drop. The hypothalamus perceives this drop as an indication of a time of famine, and initiates a starvation response, primarily by decreasing the production of sex hormones. In this woman’s case, therefore, estrogen is low, and testosterone may be low to high, depending on the degree of insulin resistance and ovarian malfunction, but LH and FSH are both also low. She does not present with typical PCOS. She is not over-producing hormones, but is, instead, under-producing.
All that said, these are some examples of how typical HA problems can cause the cystic condition that is typically associated solely with PCOS. Stress, excess exercise, restricted macronutrient intake, restricted calories, and weight fluctuation can all contribute to cyst development. Many of these situations can co-occur, and that totally depends on a woman’s genetics, epigenetics, lifestyle, and diet.
The problem with having a poorly-nuanced understanding of PCOS lies in the way in which blanket recommendations are made for women with PCOS or HA. As a result of this mindset, I have been criticized for recommending that thin women with PCOS eat carbohdyrates. This is because those who are criticizing me believe that PCOS is solely a result of insulin resistance. I do not believe so. I believe that many women with PCOS do not necessarily have a problem with insulin resistance, and even if they do, it can be compounded by factors that lie outside of that typical diagnosis.
I would, then, tentatively recommend that women who are overweight and insulin resistant follow the typical PCOS protocol and under-take insulin sensitizing steps. On the other hand, I would tentatively recommend that potentially under-weight and overly-stressed women with PCOS consider eating more, possibly upping their carbohydrate intake, and exercising less. Women with low thyroid would do well to correct that problem however they see fit. This is, however, particular to the individual, so please do not take my musings about PCOS etiology and treatment as prescriptions. At all.
The real recommendation, therefore, is to get a blood test (!), and to have discussions with your doctor about all of the possibilities that could be affecting your hormone levels. With PCOS it is crucial to order blood tests. While it is a near certainty that androgen levels are elevated relative to the rest of the hormones, that is not the case 100 percent of the time. All of the hormone levels– testosterone, estrogen, progesterone, LH, FSH, and T3 levels may be all over the map and still cause a woman to present with PCOS. An adequate picture of what is happening in the body is crucial for moving forward. This then enables women to undertake dietary and lifestyle changes appropriate to their own holistic health and well-being needs.
For more information on PCOS, why you have it, and how to overcome it, check out PCOS Unlocked: The Manual, the multi-media resource I created in order to share all the PCOS information and experience I’ve amassed in my brain, and apply it to solving the unique case of your PCOS.
I spend a disproportionate amount of my time telling women to eat carbohydrates (read: “safe starches”–see below). The thing is, a low carbohydrate diet (<50g/day) can do wonderful things for people. This we all know well. It’s a quick way to lose weight, to sharpen insulin sensitivity, and to reduce appetite in the short term, and it can be hugely therapeutic for people with cancer, migraines,and chronic infections or psychological disorders.
On the other hand, low carbohydrate diets can be a significant tax on people, women especially.
Because low carbohydrate diets are so popular for weight loss, it is common for women trying to lose weight and to “look good” to exercise often, eat very few carbohydrates, fast, and restrict food intake. The more of these restrictions a woman undertakes at once, the more and more her body reads this as living in a starved, stressed state. The results are significant. Her adrenals fire heavily, her liver gets tired from performing so much gluconeogenesis, her insulin sensitivity drops, her body fat levels fluctuate, her leptin signalling gets off, she stops sleeping soundly, and she stops menstruating regularly.
I cannot say that this applies to everyone. Many women undertake low-carb diets–Peggy the Primal Parent comes to mind as a fierce advocate (recently, however, she has, in her own words “scrutinized” and weighed evidence against the diet)–and feel great energy, life, and liberation from symptoms of their previous lifestyles. But women who are experiencing low-thyroid symptoms, menstrual dysregulation, sleep and or mood and mental health related issues may find significant relief from adding carbohydrates back into their diets.
-Glucose is necessary for the conversion of T4 to T3 in the liver. Certainly, the liver is capable of producing its own glucose with gluconeogenesis, but that process can become taxed over time, particularly if the woman’s liver is already taxed from poor eating habits in the past, mineral deficiencies, stress, or caloric restriction. Instead, when a woman ingests glucose, she assures that her liver does not have to work overtime. She provides the glucose that her brain needs, rather than forcing her body to make its on its own. This helps the body function more efficiently and with less stress in general, but it also specifically optimizes thyroid activity. Hypothyroidism is implicated in mood disorders, reproductive irregularities such as PCOS and amenorrhea, in skin conditions, and in weight gain, among other things. Many women, contrary to popular paleo belief, in fact lose weight once they add carbohydrates back into their diets.
This is true of clinical hypothyroidism, as well as sub-clinical hypothyroidism. Note that in many studies, women with cystic ovaries and sublicinical hypothyroidism see the resumption of regular ovulation when they correct their thyroid issues.
-Glucose elicits an insulin response, which in turn spikes leptin levels in the blood. This is a short-term spike, so eating carbohydrates should not be used as a replacement for body fat, which is the primary long-term secretor of leptin. However, moderate, regular consumption of carbohydrate spikes leptin frequently enough to help signal to the hypothalamus that the body is being fed. Recall that leptin is absolutely crucial for reproductive function. Without leptin, the hypothalamus does not tell the pituitary to produce sex hormones. At all.
-Moderate carbohydrate intake is associated with better mood, stress-reduction, and sleep, pretty well across the board. I see this in my work and in anecdotes, as well as in many controlled studies. The carbohydrate-well-being connection also plays out decently in biochemical theory. Carbohydrate intake (via insulin and albumin) boosts tryptophan levels in the brain, and tryptophan is the protein precursor to serotonin. Presumably, then, carbohydrate intake helps with the vast array of issues associated with serotonin deficiency which include moodiness, stress, and insomnia. For a look at the details and complexities of the issue, see Emily Deans here and here. The primary takeaway of this point being that while the exact mechanism of carbohydrates boosting mood and sleep quality is unknown, carbohydrates still appear to be a healthy, and in many cases necessary, macronutrient.
The whole point being that carbohydrates are not just okay but important. For women who have appetite control problems, sugar addictions, and a lot of weight to lose, absolutely I believe a low-carbohydrate diet can do them wonders. For women who struggle with menstruation, fertility, stress, exercise performance, or stress, along with any other hormonal oddities, carbohydrates help assure the woman’s body that she is healthy and fed. This is crucial for reproductive health.
In all cases, diet is a matter of personal physiology and experimentation. If a woman’s body works better on carbs, she should eat them, and delight in those joys rather than worry needlessly. At the very least, they are not harmful, and at their best, they are life saving.
Carbohydrates to eat:
I recommend glucose-containing carbohydrates rather than fructose for a wide variety of reasons, least of which are appetite control, liver function, and the prevention of metabolic syndrome. Many studies seem to be indicating that fructose is the real culprit in all of these problems. Glucose, on the other hand, when eaten absent of fructose has real satiating power.
I also recommend starchy glucose, since it is a “complex carbohydrate” and is broken down more slowly during digestion, which prevents blood sugar from rising or dropping too sharply.
Of course, grain-based carbohydrates are a no.
Finally, I recommend carbohydrates that contain nutrients over empty carbohydrates.
This means that I recommend eating:
Starchy tubers such as sweet potatoes, batata, jerusalem artichoke, cassava, tarot, and bamboo. Regular potatoes are fine, too, but they contain fewer vitamins than their sweet counterparts. Of the sweet potatoes, Japanese sweet potatoes are the most delicious, in my opinion, followed by white sweet potatoes and then yams and regular orange sweet potatoes.
For fruits, I recommend berries and cherries, which contain more glucose than fructose, and also bananas, which are pure 100 calorie glucose bombs.
Both white and brown rice are fine, but are fairly nutrient-poor. Brown rice contains anti-nutrients in it’s shell, so white rice is more innocuous in terms of nutrient absorption.
Vegetables of course are great, but they do not count for carbohydrate consumption. I know that much of carbohydrate content is indeed processed as glucose, but much of it is also tied up in fiber, which is broken down and turned into short-chain fatty acids by gut bacteria. For this reason, vegetables alone cannot make up a woman’s carbohydrate consumption. Instead, starchy tubers and low-fructose fruits work the best.
How much to eat:
For a woman recovering from stress, metabolic distress, and hypothalamic amenorrhea, I recommend eating between 100-200 g/day. That goes for athletes as well. And for pregnant women. At least 100 g/day.
Moreover, carbohydrates taken later in the day help with insulin sensitivity (since that gives the body the longest amount of time throughout a 24 hour period to operate at low insulin and leptin levels). They also, anecdotally, help put people to sleep.
Carbohydrates elsewhere in the paleo blogosphere:
Chris Kresser and Chris Masterjohn: Cholesterol, mostly, also: Telltale signs you need more carbs
Jimmy Moore: Is there any such thing as a safe starch?
Jamie Scott: A Week of It
Paul Jaminet: Higher Carb Dieting Pros and Cons (includes a discussion of the “longevity trade-off”)
Cheeseslave: Why I ditched low carb
Beth Mazur: Why I don’t eat low carb
Julianne Taylor: Okay, People, Carb’s Don’t Kill
Melissa McEwen (always a badass on women and fertility): What the bleep do we know about carbs
While you’re at it, go read Melissa’s post on Why Women Need Fat. Now.Read More
The volume of emails I receive from women who start having menstrual problems on a paleo diet is staggering. It is not an enormous volume, no. But it is enough to give a woman pause. What gives? Aren’t we supposed to be healthier on a paleo diet?
Yes, we are, and really, we are. In the vast majority of women who eat a Standard American Diet, specifically those who are overweight, a paleo diet does wonders for balancing hormone levels. It is usually only when a paleo/whole-foods diet is coupled with restrictive norms that women start running into problems. Too little food, too much exercise, and too much stress are really what it all boils down to. The whole foods are not to blame– not in the slightest. What are to blame, instead, are the obsessive ways in which people interact with these foods.
There are several mechanisms that may be at play in the physiology, depending on each woman’s genetics and how each woman undertakes her paleo diet and lifestyle.
What happens in the body when it stops menstruating
The female reproductive system runs off of a sensitive fleet of circulating hormones. When one or several of them is disrupted, many of the others fail at their jobs, too.
During the menstrual cycle, hormone levels in the blood signal to the hypothalamus to signal to the pituitary to release FSH and LH, two hormones that in turn tell the ovaries what to do. FSH–follicle-stimulating hormone– is released in the first part of the menstrual cycle to incite egg development. LH–luteinizing hormone–is released in the second part of the cycle and prepares the endometrium to be shed. Without proper FSH and LH levels, the female body can never convince the ovaries to do their job. FSH and LH are crucial, and they rely on proper functioning of the HPA axis.
This job of the ovaries is to produce the follicles and the eggs, but in doing so it also produces estrogen and progesterone. This fact is important for signalling menstruation, because it is partly the rise and fall of estrogen and progesterone levels throughout the month that signal to the hypothalamus to release FSH and LH at different times. This is, in essence, a circle of signalling. LH and FSH from the hypothalamus to the ovaries, estrogen and progesterone back to the hypothalamus, and so forth.
Hormone malfunctions that cause amenorrhea
-Decreasing estrogen levels stop the pituitary from being able to send out FSH and LH.
-Decreasing leptin levels stop the pituitary from being able to send out FSH and LH. This is because decreased leptin levels signal to the hypothalamus that the woman is lacking energy stores and is, in essence, starving. When the hypothalamus thinks the woman is starving, it puts a halt to normal reproductive functioning. Leptin levels decrease proportionally with fat mass decreases. On the other hand, leptin can also go undetected when an individual is leptin insensitive. Insensitivity is in general a larger problem for overweight women, and low absolute leptin levels are in general a greater problem for thin women.
-Increased testosterone production interferes with estrogen levels.
-Increased stress and cortisol levels put a halt to hypothalamic and pituitary function.
Cause 1: Weight loss
Both estrogen and leptin are produced in fat cells. These are the two blood serum hormone levels necessary to signal to the hypothalamus that a woman is fed and happy, and that it should go ahead with normal reproduction. Without these two hormones, reproduction ceases. It is well known in the medical literature that the low body fat of anorexic women, models and athletes is what accounts for their amenorrhea. Without fat, a woman simply cannot menstruate.
What is discussed less often in the literature, but is still true (see Wenda Trevathan’s Ancient Bodies Modern Lives) is the fact that a woman’s reproductive system is set up to run on the nutrient basis she has as a young girl. Throughout puberty, if a girl has a higher-than-average or higher-than-healthy body fat percentage, her ovary to hypothalamus signalling may develop as ‘handicapped’ by these fat stores. Because fat cell estrogen is so high, the ovaries do not have to produce as much. For example: If the body’s estrogen set point is 100 units, and fat cells produce 80 units, then the ovaries only need to produce 20 units. Then, if the woman loses weight, the set point remains around 100 or falls a bit to a healthier level (unique to each circumstance), and the fat cells production falls to around 30 units, such that estrogen from the ovaries is then expected to make up for the rest of the estrogen deficit. Many women have no problem with this. Their ovaries jump into higher gear. Many others, on the other hand, do struggle. Their ovaries never end up rising to fill that gap. The thing is– the set point is not stuck precisely at 100. It will decrease to a healthy level. But it might not decrease as far as a woman bent on meeting social expectations of body image is hoping.
The alignment of a woman’s sex hormone levels with the amount of nourishment she has during puberty accounts for why women who live their whole lives on the edge of starvation can still have babies, but women whose body fat percentage decrease from 28 to 21 cannot.
This is not to say that an overweight woman will stop menstruating when she loses weight. Each body is capable of menstruating within the healthiest range of body fat percentages, from around 20 percent to 30 percent. But a woman who has always erred on the side of heavier might find that she cannot dip below 23 or 24 percent body fat without losing her period. 23 or 24 percent body fat is healthy, so this is fine. It might not fly is the woman is trying to meet ridiculous standards of Western body image, but it is optimal for her to have the appropriate serum hormone levels.
Other factors that can hurt estrogen and leptin signalling may also play a role. If a woman can correct those, then she may be able to decrease her body fat levels without hurting her reproductive system. For example, chronic stress hurts hypothalamic signalling. So a stressed out overweight woman is going to have a harder time with reproductive fitness while losing weight than a totally relaxed overweight woman. This is a fact. For menstruation to take place, estrogen and leptin levels must be high enough. Body fat plays a significant role. There are some other factors that can be addresssed and help as well.
Cause 2: Exercise
Weight loss can cause decreased leptin signalling, but exercise can, too. Body fat is the major player in leptin levels, but energy deficiency in general hinders leptin. When a woman is burning more calories than she is consuming–or when she is burning a high quantity of calories while under emotional and physical stress–her body calls it quits. Instead of directing energy towards reproduction, it conserves it for other functions.
Cause 3: Low Calorie Diet
A low calorie diet performs the same function as both weight loss and exercise. It stresses the body and puts the woman in a state of energy deficit. The hypothalamus does not like being in energy deficit, so it tells the ovaries to stop working until it can get itself out of the energy deficit.
A low calorie diet is more of a problem for thin women than it is for women trying to lose weight. Leptin levels first and foremost are reliant on fat stores. The body can eat it’s own fat. That is in fact how weight loss occurs. So if a woman is eating her own fat, she is not starving. Once her body fat levels dip too low, however, and if she is maintaining a low-calorie, starvation-type diet, then she may stop menstruating.
Cause 4: Low Carbohydrate Diet
Many, if not most, women have a real need for carbohydrates. This cause is the most common cause of amenorrhea in the paleo world next to weight loss, in my experience.
Carbohydrates are necessary for the conversion of T4 into T3 (the active form of thyroid hormone) in the liver. The liver is capable of producing its own glycogen when it’s not being fed sugar, but this process can become fatigued over time, especially if the woman is under any kind of stress, or restricting calories, too.
Hypothyroidism, or sub-clinical hypothyroidism, is one of the primary causes of ovarian malfunction. Without sufficient levels of T3, organs shut down, and the reproductive organs are the first ones hit. Without T3, estrogen cannot be produced, and follicles cannot develop. Without T3, a woman cannot menstruate.
For this reason, many paleo women supplement their diets with iodine and find that their amenorrheic symptoms ease. However, many others do not. Instead, they have to add carbohydrates back in to their diets.
Another role that carbohydrates play is spiking leptin levels. Whenever insulin spikes in response to blood glucose, leptin levels rise, too. This means that carbohdyrates help signal to the hypothalamus that the woman is fed. However, this is a short-term elevation. It only spikes in bursts and with meals, so it cannot be used as a long-term solution to health. It is important to note, however, that a high fat, low carbohydrate diet is consistently associated with the lowest leptin levels possible.
Cause 5: High-Dairy Diet (an influence, at least)
Dairy is full of hormones. Even cows raised on pasture cannot help but produce certain hormones that influence a woman’s reproductive system. Dairy is the most androgenic food. It contains a protein that inhibits normal inhibition of testosterone in an individual’s body, such that when someone ingests dairy their testosterone levels can rise unchecked. This is in fact why so many people experience acne when they eat dairy. Even men. It really can increase testosterone levels that much.
Moreover, much of the dairy consumed in today’s world is not organic and grass-fed but is instead choc-full of unnaturally injected hormones. Farms and the US government are touchy about telling the public what goes into their animals, and they claim that these hormone profiles are insignificant. However, anecdotally, myself and with some other women, it seems as though these hormones really can influence women who already have compromised reproductive function. Conventionally raised animals can cause real problems. This goes for dairy, and this goes for eggs and meat products as well.
Cause 6: Altered Phytoestrogen and Hormone-Ingestion Profile
This cause is related to the cause above. We ingest hormones on a regular basis. With a healthy reproductive system, this is not a problem. Hormones from food are far less potent than hormones from the ovaries. Please keep that fact in mind. A healthy reproductive system has very little problem with phytoestrogens in foods. But some women have struggling reproductive systems for one reason or another, and they need to be aware of what hormones they have been and what they are now consuming.
Phytoestrogens are plant estrogens. They look a lot like estrogen, but are not identical. This is why phytoestrogens should never be consumed as a replacement for estrogen. Sometimes they relieve certain symptoms of estrogen-deficiency such as hot flashes, but they also fail to act exactly like estrogen does in the body. This means that other signals and connections are not being made, potentially crucial ones. Hot flashes may cease, but acne may continue to run on unchecked. And other problems can ensue. For example, breast cancer.
Phytoestrogens are primarily in legumes, nuts, and seeds. Soy is the most potent phytoestrogen, and should be avoided at all costs.
There are other sneaky ways in which hormones can infiltrate a woman’s diet, especially if a woman undertakes a paleo diet with compromised reproductive function and inattention to the quality of her food. For example, if a woman goes on an egg-heavy diet when starting paleo, but the chickens are fed a soy rich diet, she is actually eating a soy-rich diet. This is not normally a danger, but with a compromised reproductive system and a soy- or hormonal- influence from poorly treated animal products, it is worth taking into consideration.
These effects, I need to emphasize again, are not usually relevant for women with healthy reproductive systems, and should only be considered in severe cases. Only when hormone levels have dipped so low or have skyrocketed so high that the body becomes sensitive to these normally tolerable and easily managed fluctuations from food. Certainly, conventionally-raised cows are not optimal, but I would not discourage anyone from eating them (in terms of their health) at all if they have no other options. Sincerely. Far, far more important is the quality of hormones being sent through leptin and estrogen signalling within the body.
Cause 7: Stress
The final cause should come as no surprise to anyone. Stress halts reproduction: stress from toxic foods, stress from eating disorders, stress from social life, stress from exercise, stress from work, stress from existential despair… the list is vast. The physiological result of all of the possible stressors is roughly the same, however. Cortisol levels rise and these levels prevent the hypothalamus from sending the appropriate reproductive signals to the ovaries. This may, in fact, be the most important of all the factors I’ve discussed. There is no way to quantify it, and it burns ubiquitously throughout the Western world. What if all of us calmed down? What if we all lived in harmony, and peace, and did not fret? Stress is significant, and stress is real. Hundreds of thousands of American women do not menstruate because they are stressed. How many more experience hindered reproductive function because of stress? I suspect the number lies in tens of millions.Read More
Hypocretin Neurons: The Link Between Fasting, Stress, and Arousal, or, Why Fasting Breeds Insomniacs
There is a hell of a dichotomy occurring in the Paleo blogosphere this month. 99 percent of the time I am pleased as Pooh stuck up a honey tree, nestled in my esoteric corner of paleo-feminist rage, but every once in a while I wish more people could hear what I have to say. Today is one of those days.
The split I am talking about is not all that nefarious. In most cases, it’s benign and can be ignored. But in general I would like to draw attention to it, because I think there’s a lot going on beneath the surface (and here, the depths are not just Nemo and Dory but are instead people’s lives), and that depth requires speaking to. Immediately.
Mark’s Daily Apple has recently done a beautiful series on the benefits of fasting. I loved it. I learned plenty, as I always do on MDA. The series was well-written and -organized, and in fact I ended up directing people who are unfamiliar with fasting to the site in hopes of swaying their opinions. (So let it be clear: I am not against fasting per se.) Yet Chris Kresser has also done an April “Best your Stress” challenge. Serendipitously enough, it concludes today. And it is exactly what it sounds like: an endeavor to spend 30 days taking practical steps to counteract stress. Chris’s idea was that people often spend 30 days trying to get their diets in line. But what about their stress, and their lives? I couldn’t agree more. This man is a gale of fresh, important ideas.
The reason I say these two Big Themes are at odds is because they are. Fasting is a stressor. Period. Mark Sisson would agree. All people who advocate fasting would agree. But all they ever do is put an asterisk at the end of their posts: *people who are stressed should probably not fast, they say. But why? Who is affected, and how? What can fasting and other forms of restriction do to our brains, and to our lives?
What I want to draw attention to today are little loci that sit on the border of the hypothalamus called Hypocretin Neurons. Hypocretin neurons (also called Orexins–and note that the word “orexin” means “appetite increasing”) were discovered just 14 years ago in 1998, but they have radically altered the landscape of eating neurobiology since then. No, they are not the sole molecules responsible for sleep and waking. Mice that have had these neurons removed still sleep and wake in roughly normal patterns. But they never feel alert, and they never suffer insomnia. And when the neurons are activated, the mice leap into action. Hypocretin neurons wake animals up. This much is certain.
The lack of Hypocretin Neuron signalling is the cause of narcolepsy, while elevated Hypocretin levels induce arousal, elevate food intake, and elevate adiposity. Hypocretin Neurons upregulate the production of molecules down several other pathways, too: these include noradrenergic, histaminergic, cholinergic, dopamine, and serotonergic.
The anatomy of Hypocretin Neurons is also coming into greater light. When are the neurons active? What signals do they receive, and what signals do they produce? Research is beginning to show that Hypocretin Neurons are excited by excitatory synaptic currents and asymmetric synapses with minimum inhibitory input. The fact of asymmetry is important. It means that Hypocretin Neurons are instead always acted upon by mostly uniform – excitatory - signals they receive. Hypocretin Neurons only ever up-regulate and relax. They do not down-regulate. Excitatory signals outnumber inhibitory signals 10:1.
One notable source of excitation is corticotrophin releasing hormone, which suggests that stress activates the activity of Hypocretin Neurons. GABA neurons also create a bridge between Neuropeptite Y, which is the molecule that arguably has the strongest appetite-stimulating effect on the brain, and Hypocretin Neurons (more on Neuropeptide Y later this week). From there, Hypocretin Neurons project to all regions of the brain, including the hypothalamus, cerebral cortex, brain stem, and spinal cord. It seems as though Hypocretin Neurons may act as a nexus of signal input for the appropriate synchronization of various autonomic, endocrine, and metabolic processes.
Food restriction further augments recruitment of excitatory inputs onto Hypocretin cells. This explains the relationship between insomnia and adiposity: because of the easy excitability of Hypocretin Neurons, any signal that triggers their activity, regardless of homeostatic needs, will elevate the need to feed in brain circuits such as the locus coeruleus and the melanocortin system while also promoting wakefulness through activation of noradrenaline-stimulating neurons. Anything that promotes the release of corticotrophin releasing hormone (CRH) such as reduced sleep will further trigger Hyocretin Neuron firing and Appetite. This is a vicious cycle. Hypocretin Neurons play the role both of trigger and of accelerator, taking states of wakefulness, insomnia, stress, and obesity into continual positive feedback loops.
So how does leptin factor in? Hypocretin Neurons express leptin receptors. Moreover, some recent complicated neurobiological work done on mice has shown that injecting them with leptin decreases the activity of their Hypocretin Neurons. What this means is that Hypocretin Neuron activity is stimulated in part by decreasing levels of leptin in the blood, and that increased leptin levels reduce the level of excitation running through Hypocretin Neurons. This is coupled by ghrelin activity, which is also detected by Hypocretin Neurons. Ghrelin, which originates in the gut and is known to stimulate appetite, also excites Hypocretin Neurons. What does feeding do, then, for Hypocretin Neuron excitation? Experiments on mice show that re-feeding restores normal Hypocretin activity, to an extent. Repeated abuse takes longer to recover from, but the simple presence of leptin in the blood normalizes the brains of mice.
Hooray! This is good for fasting, right? So long as one re-feeds appropriately, everything should be fine? Well, yes. In a healthfully functioning individual. But not in a) someone who is both stressed and leptin resistant, since increased leptin levels from the re-feed might not be powerful enough to offset other excitatory pathways b) someone who is currently emerging from yo-yo dieting or caloric restriction c) someone who is dealing with an over-stimulated appetite, d) someone experiencing stress, e) someone who has had a history of insomnia, f) someone who is underweight, since they have low leptin levels, g) anyone who has ever had an eating disorder, particularly bulimia or binge eating disorder or h) anyone with HPA axis or endocrine dysregulation, particularly women, including overt stress, hypogonadism, hypothalamic amenorrhea, hypercortisolism, or hypocortisolism (adrenal fatigue.) I am sure the list is incomplete.
In animals, Hypocretin Neurons serve an important evolutionary function. Arousal is a vital behavior in all species. And normally, Hypocretin Neurons respond quickly to changes in input. But in situations of chronic metabolic or endocrine stress, or of recovering from a stressor, they can lead to hyper-activity and hyper-feeding.
Researchers have long known about the link between leptin, sleep, and obesity. The less someone sleeps, the lower her leptin levels, so the more she eats, and the heavier she gets. Hypocretin Neurons may serve as one of the answers to the question of exactly how that phenomenon comes about. Or at least it plays a role. Because 1) Hypocretins simultaneously stimulate appetite and wakefulness, particularly through orexigenic output of the melanocortin system, and subsequent release of CRH, which activates the stress response, and 2) while Hypocretin Neurons wake us up, they also need to be quiet enough for people to go to sleep.
Finally, I raise the questions: how many disordered eaters have trouble sleeping? How many anorexics, binge eaters, calorie restrictors, exercise-addicts, stressed-out individuals, and very low-carb dieters have trouble sleeping? How many people try intermittent fasting and find that it disrupts their sleep or circadian rhythms? How many people wake up in the middle of the night or early in the morning, even though they still need sleep, but for the life of them feel so awake? Part of that answer lies in blood sugar metabolism, for sure. And in other places. Sleep is a hell of a complex phenomenon. But here– Hypocretin Neurons can become overburdened by excitatory signals. They get hyped up in the face of both decreasing leptin levels and leptin insensitivity. They are upset by restriction, and they are upset by fasting. Hypocretin Neurons demonstrate why so many people have difficulty with their appetite and their sleep. If you find that fasting disturbs your sleep, or that you are suffering disordered circadian rhythms along with stress or appetite problems, do you best to relax your system. Don’t fast. Relax. Exercise less. Reduce stress. Eat more. Put on weight. Eat more carbohydrates. Don’t graze. Increase your leptin sensitivity. And listen to your body.
Coming up next: nighttime eating syndrome, and how it’s all related.
The literature on sleep and obesity is becoming dense. Lots of things happen to people when they sleep. One of them has to do with appetite regulation, so many researchers are coming to believe that sleep plays a dominant role in today’s vast American Overfeed.
This hunch is supported by striking correlations.
In 1960, a survey of over 1 million people found a modal sleep duration of 8-9 hours. In 2002, polls conducted by the National Sleep Foundation indicated that the average duration of sleep for Americans had fallen to 6.9-7 hours. Recent data indicate that a higher percentage of adult Americans report sleeping 6 hours or less. In 2005, in the US, more than 30% of adult men and women between the ages of 30 and 64 years reported sleeping on average less than 6 hours each night. This decrease in sleep duration has occurred over the same time as the increase in the prevalence of obesity and diabetes.
Leptin has a distinct diurnal and circadian rhythm. It has minimum values during daytime and a nocturnal rise with maximum values during early to mid sleep. The amplitude of the circadian variation averages approximately thirty per cent. Leptin levels rise during the night to suppress appetite while sleeping. Moreover, the reduction of leptin at night spells bad news for the rest of the day: it sets the individual up not just with lower leptin levels in general but also decreased glucose tolerance and an increased craving for carbohydrates.
In order to test the effects of sleep deprivation on leptin production, a number of studies have been conducted. They’re all fascinating, so I have provided a quick review of some of the more revealing studies.
1) Many studies are conducted on people with sleep apnea. Epidemiological studies show that they are heavier than the rest of the population. They have greater rates of diabetes and metabolic syndrome. Yet when their sleep apnea is corrected, these people lose weight naturally, and their metabolisms normalize. This probably has to do both with decreased appetite as well as improved metabolic functioning.
2) In one study at the University of Chicago, doctors measured levels of leptin and ghrelin in 12 healthy men. They also noted their hunger and appetite levels. Soon after, the men were subjected to two days of sleep deprivation followed by two days of extended sleep. During this time doctors continued to monitor hormone levels, appetite, and activity. The end result: When sleep was restricted, leptin levels went down and ghrelin levels went up. Not surprisingly, the men’s appetite also increased proportionally. Their desire for high carbohydrate, calorie-dense foods increased by a whopping 45%.
3) In another study at the University of Chicago, a similar protocol was conducted but men were asked to return a year later for a comparison. For six days they got four hours of sleep — their week of sleep deprivation. The men’s food and activity levels were strictly regulated and hormone levels were taken during the day and while they slept. One year later, the men returned for a six-day study with an 8-hour sleep period, so they served as their own comparison group. The results: After their six-day sleep deprivation period, volunteers had a leptin decrease ranging from 19-26 percent.
4) In another study — a joint project between Stanford and the University of Wisconsin — about 1,000 volunteers reported the number of hours they slept each night. Doctors then measured their levels of ghrelin and leptin, as well as adiponectin, insulin, glucose, a lipid profile, and they also charted their weight. The result: Those who slept less than eight hours a night not only had lower levels of leptin and higher levels of ghrelin, but they also had a higher level of body fat. What’s more, that level of body fat seemed to correlate with their sleep patterns. Specifically, those who slept the fewest hours per night weighed the most.
5) In the final study, young, healthy subjects who were studied after 6 days of sleep restriction where they were allowed four hours in bed. After full sleep recovery, their levels of blood glucose after breakfast were higher in the state of sleep debt despite normal or even slightly elevated insulin responses. The difference in peak glucose levels in response to breakfast averaged was large enough to suggest a clinically significant impairment of glucose tolerance. These findings were confirmed by the results of intravenous glucose tolerance testing. Indeed, the rate of disappearance of glucose post injection was nearly 40 per cent slower in the sleep-debt condition than after recovery, and the acute insulin response to glucose was reduced by 30 per cent.
How fast do leptin levels recover from sleep deprivation?
Leptin levels recover almost as soon as regular sleep is resumed, at least in controlled studies. In the first night. However, these studies occur over a week or two at most. If the sleep deprivation is chronic, it seems to have the same effect as fasting does on leptin. Levels remain low–at least for some time–despite resumption of “normal” sleep or eating. It takes time for the system to re-equilibrate after chronic stressors.
How does stress act on this system?
Stress activates cortisol secretion, but it also stimulates sympathetic nervous system activity. This gets adrenaline running in the system, increases heart rate, and increases blood pressure. These two things increase during both partial and acute sleep deprivation. It is well kown that andrenergic (adrenal-related) receptor activation is suppressive of leptin production, and that leptin is reduced in response to adrenaline infusions. For this reason, whatever dampening that stress puts on sleep negatively affects appetite activity.
There are other downstream effects of sleep deprivation. I’ll cover some of them briefly here, then hopefully return to them each on their own.
1) More cortisol dysregulation. One effect of sleep deprivation is a decrease early evening cortisol levels. Normally at that time of day, cortisol concentrations are rapidly decreasing in order to attain minimal levels shortly before habitual bedtime. Yet in one study the rate of decrease of cortisol concentrations in the early evening was approximately 6-fold slower in subjects who had undergone 6 days of sleep restriction than in subjects who were fully rested. This means, basically, that it takes longer for people who have lost sleep to ramp down from that stress and be able to go to sleep again.
2) Thyroid reduction. In one study, after 6 days of 4-hour sleep time, people experienced a striking decrease in the normal nocturnal TSH rise, and the overall mean TSH levels were reduced by more than 30%. A normal pattern of TSH release reappeared when the subjects had fully recovered. T4 was higher in the sleep-restricted condition than the normal condition, indicating that decreased sleep decreases the body’s rate of conversion from T4 to T3.
3) Growth hormone reduction. The temporal organization of Growth Hormone secretion is also altered by chronic partial sleep loss. The normal single GH pulse occurring shortly after people fall asleep splits into 2 smaller pulses, 1 before sleep and 1 after sleep. With decreased sleep, peripheral tissues are exposed to high GH levels for an extended period of time. GH has anti-insulin-like effects, so an increased overnight exposure to GH negatively impacts insulin sensitivity and glucose tolerance.
I’m going to pick up here where I left off on my last post. There, I covered the role that exercise and energy deficits play in HPA-axis-induced amenorrhea. Here, I cover the effects of psychosocial stress, and also how the two kinds of stress play off of each other.
Hypothalamic amenorrhea (HA) typically results from pschyogenic stress coupled with a mild energy imbalance– so generally both social stress and metabolic distress are present. These two stressors are too intertwined to separate out in studies. Hypothalamic Amenorrhea affects 5 percent of women of reproductive age, and subclinical women I suspect double that number, at least.
It is generally believed that psychosocial dilemmas activate neural pathways (ie, worrying about a job will stem from the prefrontal cortex) and hit the HPA axis that way, whereas exercise and weight loss disturb the HPA axis via metabolic disturbance. Although it seems logical that specific cascades exist for different types of stress, there is currently no method for clearly delineating psychogenic from metabolic stress. Psychogenic stress almost always has metabolic costs as well. These stem from perfectionism and body image issues, and they include stressors such as food restriction and excessive exercise. For this reason, it’s impossible, almost actually impossible, to study the two sources of HPA axis stress independently.
One way to test the potence of pyschosocial stress on female fertility is with primate studies. They parallel humans closely. This is nice. It enables researchers to control for all of the variables that affect human lives.
This is how big of a deal it is:
In one study, across more than 1200 menstrual cycles in cynomolgus monkeys, the stressed out, socially subordinate monkeys consistently exhibited ovarian impairment, whereas others did not. The thing is, in primate societies, much as in our own, it is inherently stressful to be at the bottom of the social ladder. All that researchers have to do in order to study primate fertility is to monitor the behaviors and physiology of lower rung versus higher run monkeys. For the lower rung monkeys in this study, their cycles increased in length and variability, and both their levels of progesterone and estradiol dropped. Additionally, they experienced elevated cortisol levels (almost in a perfect inverse relationship with the estradiol), as well as osteopenia, which is the precursor to osteoporosis. The researchers also tested soy on the monkeys to see if it would help. It did not. These monkeys were not energetically stressed. They ate the appropriate amount of food. The only thing that had the power to change their reproductive capacity was psychosocial stress, and it made a significant impact.
The stressors associated with stress-induced amenorrhea are many. They include affective disorders, eating disorders, various personality characteristics, drug use, and external and intrapsychic stresses. “External and intrapsychic stresses” sounds clinical and like a small category of disease, but it is in fact huge. If you think you are fat, if you think you are stupid, if you think you are ugly, if you think you aren’t good enough, if you think other people think you’re fat, stupid, ugly, or not good enough… the list goes on and on. “Intrapsychic” stress is the nebulous stuff that women impose on themselves–encouraged by society or otherwise–and it kills their HPA axes. Almost literally. Cortisol blocks signalling to and activity of both the pituitary and thyroid glands, in addition to on hormones themselves while in isolation in the bloodstream. Moreover, we all know that cortisol acts on other systems and tissues in detrimental ways. The stress of living in today’s world is one of the greatest health threats a woman can face.
In one study, women with stress-induced hypogonadism were compared with a) “normal” women and b) women with hypothalamic hypogonadism from other pathologies. Those with stress issues were the only ones who measured unrealistic expectations and dysfunctional attitudes. They were both highly perfectionistic and sociotrophic, which is defined as (its amazing we even have a word for this)– a high need for social approval. Perfectionism and sociotrophy play off of each other. Perfectionism interferes with social approval, and social approval feeds back on notions of what being perfect is, such that women with stress-induced hypogonadism face an intrapsychic conflict that might be too difficult to resolve. Additionally, being perfect is, well, an unrealistic expectation. Unrealistic expectations are not, generally, good for the soul.
Women with stress-induced hypogonadism also test as having trouble realxing and having fun. They do not typically meet the criteria for eating disorders, but they do as a whole exhibit disordered eating. That’s almost as insidious, in my book. And they do exercise a lot. These two facts of disordered eating and excess exercise do not help the stressed out hypothalama.
Because other sources of hypothalamic stress, as we’ve covered, include caloric restriction, excess exercise, and low body fat, all of which signal to the hypothalamus that the body is starving. These very often act in concert with psychosocial stress, a la the perfectionism discussed above, and feed off of each other in nasty ways.
For example, women become amenorrheic when suffering from anorexia. Clearly this is a metabolic effect, but the self-tortured stress and the isolation that often accompany anorexia take huge tolls from the cognitive angle as well. And tellingly: once anorexic women both regain weight and supplement with exogenous hormones, such that their systems should be working normally, they still often do not experience bone accretion. Bone accretion is enabled by estrogen. The fact that these women still lack estrogen demonstrates that the normalizations these women experience from regaining weight are not whole sale. They are ineffective, and clearly not all parts of the HPA axis are working properly. This is likely because psychological stress is still high and the adrenal glands have not yet recovered. It may also be due to ongoing metabolic derangements such as altered growth hormone action, or hypothalamic hypothyroidism. These women’s systems need time to recover. But they also need psychological healing, or else the HPA axis will not run happily.
In one study, 88 percent of women with hypothalamic amenorrhea recovered menstruation with just 20 weeks of cognitive behavioral therapy. Amazing! Soon I will write a post on recovering from HA, and cognitive behavioral therapy will play a big part in it. Additionally, I am currently studying cognitive therapy for women with eating disorders–which is unsurprisingly close to what I’ve been doing with women for years–so once I am learned-enough I will share and use all of that information that I can, too.Read More