Hormonal Acne: Where It’s Coming From, and What to Do about It
One common trope in the paleosphere is that acne is caused by irritants to the gut lining and inflammation. The idea is that food toxins create a permeable gut, which in turn permits toxins to enter the bloodstream and wreak havoc on our skin. Several advocates have a good point when they say that “virtually everyone who has acne has a gut issue” — yet based on my own reading and experience I do not yet know if I can get 100 percent on board with that, having seen so many women’s acne cured by fixing their hormonal issues. What I do know is that women experience acne at greater rates than men, that hormones can be significant contributors to acne, and that in women with any hint of hormone issues, hormones should be the first culprits targeted in the war against acne. Guts should be attended to. But there is only so much a healed gut can do when a woman’s hormones have jumped ship.
Hormonal Acne Presentation
When: Hormonal acne in many cases presents at certain times of the month. Popular times include 1) at ovulation, which occurs ~week three of the cycle (which can be discerned by body temperature variations) (with the menstrual cycle starting on day one of blood flow), 2) the few days before a period, and 3) at the start of a woman’s period. Cyclicity is not the only way acne manifests, however. For women with hormonal problems such as PCOS and HA, hormonal acne can persist all of the time.
Appearance: Hormonal acne usually presents as cysts–which are those lovely, pus-filled, painful and inflamed sacks. Hormonal acne may also present in more mild forms as comedones–those whitehead “bumps” that never break the surface–or even in some cases as smaller lesions that are not quite as angry and painful as full out cysts, and may appear more rash-like or just smaller than typical acne.
Location: And in terms of location, hormonal acne occurs first and foremost around the mouth: on the chin, below the nose, around the sides of the mouth, and sometimes up the jawline. As hormonal acne worsens, however, it can spread to the cheeks and the forehead. Other body parts can be affected, too, but only in severe cases, and once it has advanced. If acne is presenting in locations on the body without being present around the mouth area, there’s a decent chance hormones are not the primary culprit.
The physiological mechanism of hormonal acne
Hormonal acne comes from up-regulation of oil production within the oil glands beneath the skin. The glands become over-burdened by the oil when this happens–there’s just too much of it–and it erupts to the surface, having to simply “go somewhere.”
Inflammation can exacerbate this process. The worse inflammation is, the more irritated the oil gland can become, and thus the more red, and the more painful. Yet eruptions do not occur first without an oil problem. This is the reason no amount of washing will ever clear up hormonal acne. It comes from underneath. The only way to fix it is with interventions in the bloodstream.
What causes increased oil secretion
In the case of hormonal acne, the primary drivers of oil secretion are androgens (male sex hormones), specifically when they are elevated relative to other hormones, particularly estrogen, in the blood. When skin cells detect higher levels of androgens in the blood, their DNA responds by up-regulating oil production.
The most prominent androgen is testosterone. Testosterone-driven acne is most obvious in women with PCOS, who often only find out they have PCOS once they experience acne and ask their primary care doctors or dermatologists about a cure. Acne is one of the clearest indicators of PCOS and of the underlying hormonal imbalance for this reason. This is also, interestingly, why men on steroids often experience acne around the mouth area. Excess testosterone causes hormonal acne, plain and simple.
Yet it is not the only androgenic culprit. Another androgen, called DHEA-S, causes acne production as well, though DHEA-S serves the female body less as a male sex hormone and more as a precursor hormone. DHEA-S is produced primarily in the adrenal glands. From there, DHEA-S acts as a building block for virtually all other hormones. For this reason, HPA axis dysregulation is usually the first place to look to as the origin of DHEA-S problems. Women with high stress levels, dysregulated HPA axes, or hypothalamic amenorrhea often experience increased DHEA-S levels. Some women with PCOS do as well, depending on their etiology. (See my post on the inter-related nature of HA and PCOS). The presentation of elevated DHEA-S is less well-defined and understood than testosterone, but it is still crucial in understanding the relative balance between androgens and female sex hormones in the body. Moreover, because it is produced by the adrenal glands, it speaks volumes to the amount of dysregulation and stress upon a woman’s HPA axis. DHEA-S increases oil production when present in disproportionately high amounts.
Because hormonal balance is in large part what cells detect when determining how much androgen is floating in a woman’s bloodstream, low estrogen (relative to androgen levels) is also a significant driver of hormonal acne. Estrogen has the power to off-set high testosterone levels in the blood. This occurs via increased testosterone binding activity, which estrogen enables by increasing the activity of sex hormone binding globulin (SHBG). For this reason, if low estrogen levels are restored–either in women with PCOS or HA or some mixture of the two–then testosterone levels are mediated and hormonal acne decreases. Because hypothalamic amenorrhea often sends estrogen levels into the basement–particularly if a woman has low body fat levels–this is the primary mechanism by which women with hypothalamic amenorrhea cure their acne. Because menopause significantly decreases estrogen levels, this is also the primary reason women in menopause can see a re-emergence of hormonal acne after decades of clear skin.
As a final cause, progesterone can also play a role in hormonal acne. Progesterone, in high doses, acts as an inflammatory agent, and in this way causes acne to flare up. Progesterone levels being highest during the days leading up to menstruation explains why many women experience outbreaks at this time.
Moreover, testosterone levels peak at ovulation, while estrogen levels simultaneously hit their low, which is why the other common time for women to experience cyclic breakouts is at the start of week three of their cycles.
Aggravators of hormonal acne
Stress: Stress plays an important role. It acts as an inflammatory agent, especially if cortisol levels remain high for a long time, and then also if a woman then enters into adrenal fatigue, which triggers a chronically inflamed state. Stress may also dysregulate DHEA-S production. For this reason, stress is not necessarily the cause of hormonal acne, but does exacerbate it, and prevent proper healing.
Heat. Heat is inflammatory, and also causes us to sweat, such that pores become clogged.
Inflammatory foods: grains, dairy, omega 6 vegetable oils.
Dairy: While being inflammatory, dairy is also the most androgenic of foods. Pregnant cows produce a protein that inhibits normal testosterone processing in the human body, such that testosterone can rise beyond normal levels with high dairy intake. This is true of women with pre-existing hormonal imbalances, yet it is also true of the general population. Many people at least anecdotally least respond to dairy with acne more strongly than any other food.
Phytoestrogens: soy, flax, legumes and nuts in high quantities. While phytoestrogens have the power to act as estrogens in the body, this role is ambivalent and should be treated with caution, especially with the skin. Different estrogen receptors read different kinds of phytoestrogens differently, such taht phytoestrogens usually perform estrogen-lowering effects in skin tissue.
Low carbohydrate diets: Having sufficient glucose stores is important for skin healing, and can speed the recovery of acne lesions. Glucose is also helpful for preventing hypothyroidism.
Poor sleep: Sleep both enables healing and promotes hormonal production (and as such helps restore hormonal rhythm and balance).
Hypothyroidism: Without sufficient levels of T3, the active form of thyroid hormone, in the blood, a woman’s skin cells lack the ability to heal properly. Many women who suffer hypothyroidism suffer chronic acne.
Dealing with hormonal acne
The way forward with hormonal acne is to get blood work done and work through the primary imbalances. In general, hormone dysregulation that leads to acne can be broken down into a few categories: 1) high testosterone from PCOS (specifically overweight and insulin resistant PCOS), 2) low estrogen from low body fat levels, chronic restriction, or living in an energy deficit, 3) low estrogen from menopause, 4) high progesterone from general hormone imbalance, possibly as a result of an overactive pituitary and estrogen dominance, 5) any of these conditions worsened by stress or hypothyroidism, and 6) any combination therein.
The solution to all of these problems is to correct the hormone imbalance. I have discussed methods of doing so above and elsewhere. (See my posts on PCOS causes and treatment options, and some of my work on hypothalamic amenorrhea.) For most sufferers of hormonal acne, testosterone is elevated due to insulin resistance and PCOS. The solution, then, is to eat an insulin sensitizing diet, to exercise, and to decrease stress. For other sufferers, DHEA-S may be too high, so stress should be a big factor to examine. And for many others, low estrogen relative to testosterone is the primary problem, and modes of increasing estrogen levels should be examined. These include weight gain, stress reduction, and improved sleep quality. For women with menopause, it may just “take time” or perhaps medical interventions are appropriate, depending on the severity of the problem.
Medication
There are drugs designed to help with hormonal acne. Spironolactone and flutamide are the two primary ones that come to mind, as well as birth control.
The reason birth control pills are helpful for acne is because they enforce hormone regularity on a woman’s system. The precise pill that is helpful for each woman varies by her particular condition– but in general, BCPs are comprised of estrogen and of progesterone. BCPs can for that reason 1) raise estrogen levels–which either corrects an estrogen deficiency or helps balance the activity of runaway testosterone–and they can also 2) restore proper balance between estrogen and progesterone, which is important for keeping progesterone levels within their proper parameters. Some BCPs also contain anti-androgenic substances, such as spironolactone, which is an added benefit for women who are living with androgen excess. In all cases, I do not generally recommend that women get on BCP, as it can cause worse hormonal dysregulation in the long run (sort of like handicapping a delicate hormonal system), and does not solve the underlying problem.
Flutamide acts in a similar way to spironolactone, but less effectively, and with more side effects. So spironolactone is typically the drug of choice.
Spiro has been hailed by many women as God’s gift to womankind. For many women it begets truly miraculous effects. Yet one should step cautiously with spironolactone. If a woman’s primary problem is not testosterone excess, spironolactone will very likely do more harm for her skin than good. (Check out the panicked discussion forums at acne.org to see what I’m talking about.) Moreover, even for those who have testosterone excess as their primary problem, spironolactone merits caution for a variety of reasons. First, spiro usually induces an infamous “initial breakout” which can last anywhere from weeks to months. This isn’t always the case– sometimes women improve immediately. Sometimes they never really do. But the typical case is for women to see an initial worsening of their acne, followed by relief in the upcoming months, especially if they increase their dosages. Secondly, spiro cannot be taken by pregnant women because it induces birth defects, so women cannot stay on spironolactone indefinitely. This is problematic because spironolactone acts as a bandaid on the hormone problem, and does nothing to fix it whatsoever. What spiro does simply is block testosterone receptors. In a few cases, it cures women. Yet in very many cases, if the underlying problem is not addressed while a woman is taking spironolactone, her acne will return once she comes off of the drug. This is why I recommend that women only consider taking spironolactone if they want a “quick fix” while they work on their diet and exercise in order to improve their PCOS. As a final note, spironolactone has a couple of other health concerns. First, it lowers blood pressure, since spiro is actually a blood pressure lowering drug proscribed “off label” for acne. Secondly, it acts as a diuretic, so women on it need to drink water constantly, and may not be able to consume alcohol anymore. And finally, spiro acts as a potassium-sparing diuretic, such that women cannot eat potassium rich foods, lest they risk the chance of becoming hyperkalemic, which can–I swear to God–lead to sudden death. It’ll probably lead to muscle weakness first, but an imbalance of electrolytes in the blood is no laughing matter, so women on spiro should limit their potassium rich foods as well as get their potassium levels checked periodically. Potassium rich foods include bananas, potatoes, avocadoes, tomatoes, and leafy greens.
For these reasons, spiro can help, but it cannot be relied on long term. It does not get at the root of the issue–drugs rarely do–and the true path to hormonal help is diet and lifestyle modifcation.
As a final note, bio-identical hormone supplementation can be helpful for women going through menopause. Estrogen patches can release small amounts of hormone into the bloodstream, and can lessen acne considerably. I do not think this is detrimental to a woman’s health, if it is in fact the case that her estrogen levels have simply dropped off during menopause. However, it does, in my opinion, make it difficult for estrogen levels to rise and hormone balance to re-establish itself on its own. This is a decision best left to the individual and to her doctor.
In conclusion
Hormonal acne is terrible, and for many women can seem incessant, and never ending. Girls are assured growing up that they will eventually out-grow their acne, yet many women see it persist throughout their twenties and thirties, and some actually do not even see the acne manifest until their twenties and thirties. Some women do not even see acne appear until after the birth of their first children, as their progesterone and estrogen levels are flying all over the map.
For this reason, drug interventions can serve as decent placeholders in moving forward. It can help the pain and awkwardness of acne while diet and lifestyle fall better into place. Yet there are downsides to medication, and large ones. Medication is only ever a band-aid, and it can be a band-aid that in the long run leads to more harm than good. One point I did not even touch on above is that playing with hormones is like playing with fire. Sometimes things can go horribly wrong– on spironolactone and BCPs alike some women suffer weight loss or significant weight gain, increased acne, and significant–even frightening and life-threatening–mental health disturbances. For this reason, meds may be best left alone, depending on the circumstance and the level of risk a woman is willing to bear. On the other hand, there is in all cases a natural, food-based solution. What it takes is time, experimentation, good blood work, and patience. As in all things.
Read MorePCOS 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.
I disagree.
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.
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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.
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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).
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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.
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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.
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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.
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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.
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Carbohydrates for Fertility and Health
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.
Here’s why:
-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.
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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.
Still afraid of carbohydrates and insulin? Read Weightology’s take on insulin, or, better yet, Stephan Guyunet’s thoughts on fructose being the sole driver of insulin resistance, rather than glucose.
Read MorePaleo and Amenorrhea: How Extremity Can Make even the Best Diet Fail
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 MoreThe HPA axis: Psychological Stress and Hypothalamic Amenorrhea
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 MoreThe HPA axis: Metabolic Distress and Hypothalamic Amenorrhea
If it hasn’t been clear yet, the hypothalamic-pituitary-adrenal (HPA) axis is one of the leading contributors to poor reproductive health. The pituitary gland tells the reproductive organs what to do, and the hypothalamus tells the pituitary gland what to do, and the adrenals produce cortisol which influences the activity of both the hypothalamus and the pituitary glands. Yikes.
Hypothalamic amenorrhea– or the loss of menstruation via disturbance to the HPA axis–affects 5 percent of women of reproductive age. Subclinical women I suspect double that number, at least. Many problems emerge as a result of HPA axis dysregulation that do not go as far as HA. If it does advance to that stage, recovery from HA requires the restoration of normal cortisol function, the normalization of glandular tissue, and also rectification of the hypothyroidism that usually follows from hypothalamic dysregulation.
The HPA axis is dysregulated by all types of stress. Acute stress is handled fairly easily, as the HPA axis is typically stable and in fact built to optimize an individual’s response to stress. But chronic stress is– as we are all well aware– half of one of Satan’s eyelashes away from downright insidious.
Yet chronic stressors are divided by themselves into even more particular categories: psychosocial stress on one hand, and metabolic distress on the other. Psychosocial stress is caused by mental, emotional, and social factors. Metabolic distress is caused by living in an energy deficit, which is in turn caused both by calorie restriction and excess exercise. These two forms of stress affect the HPA axis via different mechanisms. Yet it should be another obvious fact for you that psychosocial stress and metabolic distress almost always go hand in hand.
This post is going to focus on metabolic distress. I’ll treat the psychosocial and how these two are interrelated in the following post.
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I talked a bit in my previous posts about the HPA axis and how different pathologies can emerge from hyper-activity of the axis and hypo-activity. Metabolic distress pushes the axis in hyper activity, at least for as long as the system can handle it before burning out.
The pathology of Hypothalamic Amenorrhea in general
The point of the HPA axis is to metabolically mobilize individuals in stressful circumstances. So in them, stress levels rise. In one study, the degree of ovarian compromise women suffered was in a precise inverse relationship with observed cortisol levels. That’s pretty amazing. What the cortisol does is perform negative feedback on the hypothalamus, such that the hypothalamus releases GnRH (gonadotropin releasing hormone) in decreased quantities. Without GnRH, the pituitary doesn’t get the signal to more of its own hormones. These include LH and FSH, hormones that in turn signal to the ovaries how much estrogen they should be producing according what time of the cycle it is. The Pituitary is also responsible for secreting thyroid stimulating hormone (TSH). Ordinarily, TSH levels rise or fall in response to changes in T3 and T4 levels in the blood. In HA, the pituitary never receives these signals, so TSH levels do not increase when they should. This leads to the HPA axis setting an altered hypothalamic set point: it decreases as much as what is seen in hospitalized patients who develop what is called “sick euthyroid syndrome.” Additionally, due to HA, the secretory patterns of growth hormone, prolactin, and melatonin vary. This is problematic for a wide variety of reasons, not the least of which are sleep, tissue repair, and hormone development.
Exercise, weight loss, and metabolic distress
When compared with normally menstruating but sedentary women, amenorrheic athletes demonstrate less progesterone secretion, fewer LH pulses from the pituitary in a day, and higher cortisol levels. Amenorrheic athletes that are anovulatory have the fewest LH pulses in a day of all groups of women and the highest cortisol levlesl despite comparable leves of exertion and fitness among these athletes and others. This is all to say that athletes experience greater risk of amenorrhea.
Though both sorts of stress are important for the ovaries, there is no doubt that exercise and weight loss serve as stressors all their own. In monkeys trained to run, it has been shown that caloric supplementation reversed the anovulation induced by training. Interestingly, the monkeys did not spontaneously develop a compensatory increase in appetite and had to be bribed with colorful candy to consume more calories. The HPA axis was downregulating their drives to eat. Studies in women also indicate that exercise and weight loss cause anovulation, probably through decreased GnRH release. One team of researchers, Louks and Thurma, quantified the amount of energy restricted (absent of psychosocial stress*) needed to impact GnRH release in normally menstruating women. They fed the women an energy stasis of 45kcal/kg of mean body mass per day. This amounts to approximately 2200 calories for a woman weighing 110 pounds. They administered graded daily energy deficits of 10, 25, or 35 kcal/kg. This yields absolute values for the 110 pound woman of 1750 calories per day, 1000 calories per day, and then, Yikes!, 500 calories/day. An energy deficit of 33 percent showed no impact in LH pulse frequency after 5 days, and an energy deficit of 75 percent showed a 40 percent decrease in LH in 5 days. I imagine that both of these numbers would be more signficiant with longer time periods. Much more significant. For all energy deficits cortisol levels rose. At the 75 percent reduction, cortisol levels rose by 30 percent. For the women who had the lowest progesterone levels at the start of the study, the cortisol levels and reductions in LH were impaced the most. Most women, I’d imagine, who enter into such deficits do not have them imposed, but rather choose them. This indicates to me that they are under a great deal of stress as well, such that the “stressed” women tested in this study probably closer approximate the majority of real American women.
*(On the other hand, modest dietary restriction accompanied by small amunts of exercise greatly increased the proportion of monkeys who become anovulatory when presented with social stress. Social stress is also a significant factor in amenorrhea.)
The question remains: Is it the stress of exercise or the energy deficit that alters LH pulsatility in exercising women? This key question has been answered maybe by controlled studies in which women undergo dietary caloric restriction imposed in the face of increasing exercise demands. It would appear that LH pulsatility is not disrupted by the stress of exercise but rather by reduced energy availability. With increased calories, the women don’t experience as much LH disturbance as when they don’t meet their caloric needs. Presumably, then, sufficient calorie ingestion would really help mitigate the problem for women suffering exercise-induced HA. According to this one spate of studies. Honestly, I’m not sold. Muscle tear down and growth, and any repair that occurs on joints and other tissues, involves the activation of inflammatory responses. Cortisol rides along with those. If the exercise and the resulting cortisol is significant enough, supplementation with calories cannot cure everything. Additionally, the psychosocial stress that accompanies excess exercise plays a role. Additionally, thyroid function may be negative impacted by trying to make up for fluctuating caloric intake. And finally, I find it implausible that women outside of controlled studies will know precisely how much they need to add to their diets in order to achieve the proper balance.
Nutriton and metabolism play critical roles in all of this. (Note: the few studies done on men in this realm suggest that undernutritional is as deleterious to reproductive competency in men as it is in women.) Metabolic imbalance occurs when energy expenditure exceeds energy intake, right? This is important for our bodies, so there are many different (and redundant) signals to the brain from metabolic systems. This makes it hard to suss out what system does precisely what, and which is the most important in studying these issues. Signals reflecting energy stores, recent nutritional information, and specific classes of nutrients are integrated in the central nervous sytem, particularly the hypothalamus, to coordinate energy intake and expenditure. Chronic energy deficiency alters thyroidal function to slow metabolism and correct negative energy balance.
Putative appetite suppressing and satiety signals include cortisol, CRH, insulin, glucose, resistin, leptin, proopiomelanocortin POMC, cocain- and amphetamine-regulated transcript CART peptide, peptide YY, and glucagon=like peptide 1. (Yikes!) The hormones from fat cells implicated in energy regulation include leptin, adiponectin, and resistin. Leptin, which we all know and love, is the dominant long-term energy signal informing the brain of fat reserves– it is also a satiety signal. It’s a big deal, and for women’s with HPA axis dysregulation, having lots of it, or at least good sensitivity to it, is helpful. Adiponectin acts as an insulin-sensitizing agent by reducing hepatic (liver) glucose production. This one, contra leptin, is reduced in obesity. Resistin is linked to insulin tolerance and decreases glucose uptake by fat cells. Ghrelin is produced by the gastrointestinal tract. Plasma ghrelin levels rise during fasting and immediately before anticipated mealtimes and then fall within an hour of food intake, suggesting that ghrelin is important for meal initiation.
Resistin levels correlate with free cortisol levels, indicating that in states of stress the body is trying to sensitize the body to insulin. Adoponectin correlates with insulin sensitivity, too, particulalry in studies of depressed humans. In women, ghrelin levels increase in both anorexia nervosa and exericise amenorrhea. No surprise there. The greater the energy deficit, the more the body wants to eat.
Leptin is crucial. Importantly, women who primarily suffer from psychosocial stress and not metabolic distress recover from hypothalamic amenorrhea without changing weight or leptin levels. What this tells us is that leptin is mostly a problem for women who suffer energy deficits. Studies of rodents as well as of women indicate that increasing leptin and leptin sensitivity induces regularity. When mice are injected with leptin during a fast, for example, their cycles remain the proper length. Without leptin, however, their cycles become longer and irregular.
Leptin is produced by fat cells. Some other tissue produces it as well, but not as significantly. Low body fat is a very significant problem for hypothalamic amenorrhea. This is indicated by the fact that while many athletic women experience HA, women who participate in sports that require thinner physiques have much greater rates of HA.
Depending on the type of sport and competition level, the incidence of amenorrhea varies from 5 to 25%. The rates of HA in sports that require low body weight are as high as 6-43 percent in ballet and 24-26 percent in long distance running. In less stringent sports, such ad bicycling and swimming, the rates of HA are both 12 percent. All that is to say that low body fat is a clear signal that the body is running in an energy deficit. When this is the case–that is, when the body is running at a deficit– it thinks its starving. No, I’m sorry, it doesn’t think it’s starving. It is starving. So all of the satiation hormones– in this case ghrelin, resistin, and leptin– they muster their collective powers and try to get the body to eat more. If that does not happen, and if leptin levels are too low, the hypothalamus will not receive the signal to start the reproductive hormone cascade.
All that said, the factors that cause, respond to and mitigate metabolically induced hypothalamic amenorrhea are many and complex. In the end, they can almost be reduced to a leptin problem. But leptin is an issue solely because of low body fat and energy deficits (*as well as any leptin insensitivity, which I will treat in another post). There are also the issues of inflammation and stress that arises from exercise, as well as psychosocial stress–all of which build upon each other in the complex interactions between the HPA axis and the body at large.
In the following post, I’ll deal with psychosocial stress, and how these two are related. Afterwards I will deal with recovering from hypothalamic amenorrhea.
Read More
