Archive for the ‘Women’s Health’Category

HPA axis dysfunction

Hi friends! What up.  Today is another doozy.


There are two primary ways in which the HPA axis can malfunction.  It’s activity can increase, or it’s activity can decrease.

The HPA axis jumps into action when stressed or stimulated.   This is a good thing when the body is faced with short-term stressors.   In this event, adrenal activity increases.   Along with several other key responsibilities, the adrenal glands’s primary purpose is to help us survive in the face of a threat: they rally all of the body’s resources into “fight or flight” mode using cortisol and adrenaline.   Healthy adrenals instantaneously increase heart rate and blood pressure, release energy stores for immediate use, shut down digestion and other secondary functions, and sharpen the senses. But since they are programmed to respond to every kind of stress — physical, emotional, perceived, psychological, environmental, infectious, or any combination of these — a person under chronic stress can get into a fair bit of trouble.  It can knock the whole HPA axis off kilter.  Conditions related to increased activity are: Chronic Stress, Depression, Anorexia, OCD, Anxiety disorders, Excessive exercise, Alcoholism, Withdrawal, Diabetes, Obesity, Metabolic Syndrome, Hypothyroidism.  

The converse is perhaps just as bad.  The HPA axis suffers decreased activity either when hormones tell it to down regulate (as is the case with low leptin signalling!), or it has simply become exhausted by being in a high-stress, hyper-active mode for too long a time period.  Conditions related to decreased activity include: Chronic fatigue, Fibromyalgia, Adrenal insufficiency, PTSD, rheumatoid arthritis, hypothyroidism, asthma, and eczema.

Since cortisol plays a big role in our health and feelings of well-being, and since it also plays a crucial feedback role in up or down regulating the activity of the hypothalamus, stress will be a big piece of the rest of this post.  I’ll talk about different kinds of stress here, and then later detail the effects of cortisol on our bodies.

Clinicians generally divide stress up into four primary categories: emotional stress, sleep disorders, metabolic dysregulation and chronic inflammation.  In my book, they are virtually inseparable.  If you’re signed up for one, you’re almost always signing your life away to all of them.  BUT: they are each handled somewhat differently by the HPA axis.

Mental-emotional stress originates in the brain, and it eeks into the rest of the body via the hypothalamus, which is the hub of connectivity between your brain and the endocrine system.  This drives up the production of ACTH, which stimulates cortisol production later down the line.  Fortunately, this kind of stress is mediated by personality, perception of novelty, uncertainty, control in the situation, and how threatening the stimulus seems.  Low self esteem also makes it easier for the hypothalamus to jump into high gear.

Slow-wave sleep suppresses cortisol release, which is I believe the primary reason sleep is so important for health.   Exposure to chronic stressors results in a disruption of normal hormone fluctuations that occur throughout the day.   This means that cortisol will often jump up at night, creating a vicious cycle of decreased sleep, and therefore increased cortisol, and further decreased sleep, and even great cortisol levels.  No wonder I’ve been such a wreck for the last twenty years.

The most accepted model of how HPA axes dysfunction  asserts generally that stimulation drives the axis into an overactive state for some time, but that after a while the system becomes unresponsive.   Cells become cortisol-resistant.  This is where the popular term adrenal fatigue comes from, though much of the literature verges on pseudo-science.  While “adrenal fatigue” is certainly problematic, many scientists believe that this is an adaptive, and maybe even productive, response.  Hypercortisolism is bad.   Decreased HPA axis gives the body a bit of a break.  Or at least is intended to.

Why hypercortisolism bites

1)  Cortisol is immunosupressive.  It impairs cytokine production and function, induces the loss of tissues important to immune cell production, and may in fact play a causative role in the development of autoimmune disease.  Being immunosupressive means that cortisol inhibits inflammation.  Generally this is a good thing, but when it goes on for too long, important inflammatory reactions, including the immune reactions I just mentioned, fail to function when they are needed.

2)  Cortisol decreases hormonal output.  It signals to the hypothalamus to down-regulate, such that growth hormone, thyroid releasing hormone, and gonadotropin releasing hormone are released at much lower rates by the hypothalamus.  Yikes!  Without GH you don’t grow; without TSH your thyroid doesn’t work properly; and without GnRH your pituitary fails to signal reproductive activity.   GnRH is a factor in just about every single endocrine disorder.   YEAH.  To top it off, these hormones act as cortisol antagonists.   They typically mitigate the effect of cortisol in the blood.  This makes their absence is even more insidious.  Without them, cortisol can increase without ever being checked.

3) Cortisol increases insulin levels.  This fact, coupled with the decrease in androgens from decreasing hormonal output in general, leads to fat deposition. Visceral fat has buckets full of glucocorticoid receptors, which makes it very easy for cortisol and insulin to shuttle more and more triglycerides into fat cells.  I can’t emphasize how important this is.   The cardiovascular and all adipose-related issues from cortisol hyperactivity increase the aull-cuase mortality risk of patients two to three times and decrease life expectancy by several years.

4) Increases in cortisol-induced abdominal fat are associated with an increase in both total oxidative stress and in the number of inflammatory cytokines.

5)  Cortisol can destroy healthy muscle and bone tissue.

Why hypocortisolism bites

1)  Immune system up-regulation.   This can really improve health in some cases.  But up-regulating cellular immunity can induce tissue damage and excessive inflammation via the over-production of pro-inflammatory cytokines.    Low cortisol also makes catecholamine (epinephrine and norepinephrine) levels go unchecked.  These further increase inflammatory cytokines.  They also disrupt T-cell signalling.   The result is susceptibility to inflammatory diseases, including autoimmne diseases, mood disorders, malignancy, obesity  and chronic pain syndromes.  This can also increase susceptiblity to assaults by infectious and environmental pathogens.

2)  Bowel disturbances, PTSD, fibromyalgia, low back pain, burn out, and atypical depression.

3)  High-stress sensitivity, chronic fatigue and chronic pain.    These three occur so frequently and in such concert with low cortisol states that they are referred to as the “low cortisol triad” by some authors.  I know.  Catchy.


DHEA-S is produced in the adrenal cortex.  It is an androgen, and it is considered one of the dominant precursor hormones.  This makes it critical for endocrine and reproductive function.   DHEA-S is produced in other organs, but it’s primary source is the adrenal glands.

High levels of DHEA-S are often associated with hyper-activity of the adrenal glands- so in this case both cortisol and DHEA-S are elevated in the blood.   The HPA axis has started pumping, and it doesn’t know how to stop. Women with PCOS often have high levels of DHEA-S precisely for this reason.   This is bad for them because it makes it much easier to create androgens such as testosterone.  And without parallel increases in estrogen from the ovaries, the excess testosterone will wreak havoc.

Calorie restriction and exercise both also increase DHEA-S levels.   DHEA-S is the primary hormone, and DHEA is the active form.   When calories are consumed, more DHEA is recruited form DHEA-S.   This depletes DHEA-S stories.  So calorie consumption reduces DHEA-S, but calorie restriction will keep levels higher longer.

This is important to note for those of us who restrict calories and exercise frequently.  If we have hormone problems, particularly issue with excess, we might want to think about how to optimize our DHEA-S production.  Too much DHEA-S?  Eat more.    Too little?  Try eating a bit less, or intermittent fasting.

Low levels of DHEA-S are associated with adrenal fatigue and hypocortisolism.  In this case, the HPA axis just can’t do much of anything anymore.   This is bad.  DHEA-S is considered the best “feel good” hormone by many endocrinologists.    And it is a precursor to many hormones.  Moreover, there is a growing body of evidence that healthy levels of DHEA and DHEA-S may help stave off Alzheimer’s disease, cancer, osteoporosis, depression, heart disease and obesity.   You can supplement with DHEA-S if you feel as though you desperately need it.  However, perhaps the best course is to supplement in the meantime while you address the underlying issue of decreased HPA axis activity and adrenal exhaustion.


The pituitary

Because stress is a big deal and everyone wants to know about it, most of the HPA research has focused on cortisol and the adrenals.   But the rest of the axis is important, too.

Decreasing hypothalamic activity down-regulates pituitary activity, which means that the production of sex hormones decreases.   And what causes decreased HPA activity?

One factor is a decrease in leptin levels.  If leptin signalling is weak–ie, if our body fat levels are too low, or if we exercise too often–then the lack of leptin crossing the blood-brain barrier into the hypothalamus signals to the hypothalamus that the body is starving, and certain extraneous bodily functions such as reproduction cease.

A second factor in decreased HPA axis activity is high cortisol levels.  I know that I told you earlier that high cortisol levels are associated with hyper-activity of the HPA axis, so this might be confusing, and you might think they lead to increased sex hormone production, but this isn’t necessarily the case.  Cortisol still always exhibits a dampening effect on the hypothalamus.   The amount of cortisol produced by the body relative to the general activity of the HPA axis is complicated, and has to do with the amount of stress the body is under, how long it has been under that stress, and whether or not the body has lost any of its sensitivity to cortisol.

And finally, HPA axis activity can decrease if it has become exhausted.  This is adrenal fatigue, plain and simple.

In all of these cases, the hypothalamus stops telling the pituitary gland to produce sex hormones.  The pituitary, in turn, stops telling the gonadal tissue to produce hormones themselves.  The end result is overall decreased sex hormone levels.  Sex hormones are necessary for reproductive function, as well as for a variety of other important roles such as waking the body up, putting it to sleep, being in a good mood, and having a good memory.   When sex hormones decrease,  many things can go wrong.  PCOS is one them.  Acne is another.  Loss of libido, too, and also, fertility.   Depression.  Weight gain.  Miscarriage.  Yikes.

The final big system affected by HPA axis dysfunction is the thyroid.  When the hypothalamus is suppressed, thyroid releasing hormone doesn’t get released.  And when the pituitary is suppressed, thyroid stimulating hormone doesn’t get released.  The result is wholesale decrease in thyroid activity, all the way from TSH through T4 and to T3.


So the solution?  Sleep as much as possible.  Eat the appropriate amount of food.   Rest often.  Refuse to be stressed.  I am a firm, firm believer in the power of positivity to make us healthy human beings, and the HPA axis probably plays a big role in that.  Don’t let your co-workers, your boss, whatever, all that nasty crap in your life get you down.  I mean– it’s a million times more complicated than that.  I understand.  But I really do think mitigating those stressors (especially the ones you impose on yourself!) transforms physical health.  No self-hating, no anxiety about your looks, no worries about being perfect.  Your cells will thank you.


*Thank you WomenToWomen for the awesome graphics!



04 2012

The HPA axis: an introduction

I have been serving up diatribes for several weeks now.  It’s time to bring it back to physiology for a while.  I feel this way especially because I am so interested in how we might best mitigate hormone dysfunction.  One way is by investigating the means by which cells communicate to each other.   The HPA axis, for this reason, is a very big deal.  From my perspective, for those of us who suffer hormonal imbalances, it is the most important part of our bodies to pay attention to. Here’s why:

If our cells are a kingdom, and our hormones the governors, and leptin the bitchy king, then the HPA axis is the divine law that enables and justifies the whole damn thing. Or we could call it the flashy green code of The Matrix. Or the binding of a book. The point being that when the HPA axis is good it’s good, and when it’s bad all the king’s subjects die. No one wants to die. How do we stop everyone from dying?

The abbreviation HPA axis stands for Hypothalamic-Pituitary-Adrenal axis. It is sometimes called the Limbic Hypothalamic Pituitary Adrenal axis, and also the Hypothalamic Pituitary Adrenal Gonadotropic axis. (Gonadotropic, ladies!) This axis describes the complex interaction between the vast diversity of your hormone hubs, via direct influences and feedback mechanisms.

The Hypothalamus

The hypothalamus, at the core of our brains, is the primary point of connection between the central nervous system and the endocrine system. The hypothalamus releases hormones into the bloodstream. Some of them act on distant tissues, but others go directly to the pituitary gland and in turn tell it what to do. This is why it is often said that the hypothalamus controls the pituitary gland. The secretion of hypothalamic hormones GnRH, gonadotropin releasing hormone, GHRH, growth-hormone releasing hormone, TRH, tryptophin releasing hormone, dopamine, somatostatin, TRH, thyrotropin-releasing hormone and CRH, corticotropin releasing hormone all influence the action of the pituitary and adrenal gland. Hence why they are called “releasing” hormones. The job of the hypothalamus is to conduct the orchestra. It asks for certain things to be played, and if all things are running smoothly, the whole orchestra plays in beautiful concert.

The hormones released by the hypothalamus have specific effects. There are a few that are more relevant for our purposes here. GnRH stimulates LH and FSH activity in the pituitary, which are directly responsible for ovarian activity, ovulation, and menstruation. TRH stimulates the release of TSH–thyroid stimulating hormone–so without this the thyroid gland does not produce what you need. Dopamine inhibits prolactin release, which also acts on the ovaries. And CRH stimulates the release of adrenocorticopin, a precursor to stress hormones. We might say that CRH is the first line of activity in the stress response.

The Pituitary Gland

The pituitary gland is generally divided into two parts, the anterior pituitary and the posterior pituitary. The posterior pituitary releases those distant-action hormones (ADH and oxytocin) which are less relevant for the axis. The anterior pituitary is the one that produces the relevant hormones. Follicle stimulating hormone stimulates the development of follicles on the ovaries and the production of estrogen. Luteinizing hormone triggers ovulation. TSH stimulates production of T4 and T3. In all cases, it’s clear that the receipt of stimulating hormones from the hypothalamus to the pituitary is crucial for reproductive function.

So direct central nervous system stimulation affects pituitary function. One example of this is circadian rhythms and the release of adrenocorticoid to stimulate waking. Yet there is another mechanism that tells the pituitary what to do, and this is feedback from its own system. The hormones directly secreted by the pituitary indicate to the pituitary how much of the product is in the bloodstream. This acts on the pituitary, but also on the hypothalamus, such that high estrogen, progesterone, and testosterone levels can all inform the hypothalamus to reduce production of GnRH. This is helpful often. But in other cases it is absolutely NOT, since high testosterone levels can inhibit GnRH in general, which reduces the production of all pituitary hormones.

The Adrenal Glands

The adrenal glands consist of two distinct parts: the adrenal medulla, which secretes catecholamines directly into the blood, which I’ll touch on a bit later, and also the adrenal cortex, which secretes steroid hormones. The primary steroid hormones are cortisol, corticosterone and DHEA, the precursor to adrenal sex hormones.

Approximately 90 percent of the cortisol in our systems is “bound.” The remaining 10 percent is free, and it’s what is biologically active. Cortisol is metabolized in the liver, and it has a half life of 60-90 minutes! Isn’t that amazing? If we are not constantly stressed, then the hyper-stressed states we enter into from an immediate event are only supposed to last for 60-90 minutes. Amazing.

Cortisol is important for a number of reasons. Without it, we die. Here are some of its functions:

1. Metabolism.  Cortisol and other glucocorticoids exert anabolic effects– that is, gluconeogenesis and glycogenesis– on the liver, and catabolic effects– or proteolysis, and lipolysis– in the tissue. What this means is cortisol stimulates activity that utilizes energy sources. Proteolysis eats muscle tissue, which is generally bad, but lipolysis eats fat tissue, which is usually good. Gluconeogenesis and glycogenesis make glucose and glycogen in the liver.

2.  From the stimulation of cortisol, glucose output by the liver increases and glucose uptake by other tissues decreases. Another way to say this: cortisol increases blood sugar. Insulin is secreted in response to blood sugar, in order to mitigate the effects.

3.  Cortisol influences the immune system and inflammatory responses. Cortisol and all other glucocorticoids suppress the synthesis of arachnidonic acid, the precursors to a number of compounds involved in the inflammatory response.  They also decrease the key compounds interleukins and gamma interferon, which are crucial for the immune response.

4.  Cortisol also decreases REM sleep significantly: high concentrations in the blood can cause insomnia and, duh, decrease mood. Cortisol secretion increases in response to stressful stimuli. It is in fact crucial for survival in extreme circumstances. The reasons for this are not well understood, especially in light of the fact that cortisol inhibits immune function. The best guess is that cortisol is required for initial metabolic responses to stress–but that, right, we overdo it. Surprise.

ACTH and cortisol are released in irregular pulse throughout the day. The biggest pulse occurs in the early morning, and starts a few hours before waking. The lowest levels of ACTH in the blood occur right around the time of falling asleep (in someone with regular circadian rhythms.) Spikes in cortisol about half as large as though during waking occur each time you eat, roughly correlated to how much you eat. DON’T freak out about your meals because of this. Your body handles cortisol quite well. No irrational panics allowed. Just– take note. This is one reason why both grazing and bingeing are not optimal behaviors.

This whole system is moderated by negative feedback, as in most of the body’s systems. When the hypothalamus detects enough cortisol, CRH (in the hypothalamus), and therefore ACTH (in the pituitary), and therefore cortisol (in the adrenals) production, are all decreased. You understand, then. The HPA axis is a delicate flower.

Finally, there is a whole class of adrenomedullary hormones, such as catecholamines (epinephrine and norepinephrine), we haven’t talk about. But they’re important, too. The first step in their biosynthesis is catalyzed by tyrosine. Don’t be in tyrosine (an amino acid). It’s important.  Epinephrine and norepinephrine both increase blood glucose concentrations and metabolic rate.  Epinephrine increases cardiac output, vasodiliation in skeletal muscle and liver but vasoconstriction in other vascular tissues– so essentially it shunts blood to skeletal muscle and the liver. Norepinephrine causes primairly vasoconstriction, which results in increases in blood pressure–ie, a reduction in cardiac output.

Epinephrine and Norepinephrine are activated by “fight or flight” situations, ie, our regular lives. Their production is, here’s another surprise, initiated by the hypothalamus. BUT these babies aren’t regulated by negative feedback. This is important. Cortisol will decrease in response to high cortisol levels. Epinephrine and norepinephrine instead can just keep on rising.  Ack, ack, ack.

So that’s a review of the HPA axis.  It’s complicated as all hell.  But even more than complicated, it is important.  The HPA axis runs the whole hormonal game, and therefore the vast majority of your reproduction and metabolism.    It responds to stress, and it helps you mitigate stress.  It responds to hormonal input, and helps you mitigate hormonal problems.   It is sensitive to signalling from all over your body.  These are all awesome things, but it also means that disruptions, can really throw you off.

The HPA axis significantly effects your thyroid gland, how you metabolize food, how much estrogen and testosterone you produce in your ovaries, and how much stress hormones and sex hormones you produce in your adrenals.  I’ll talk about those issues in my next post.


04 2012

Emerging from starvation: Why I can no longer fast

Some of the craziest shit has been happening to me recently.   Literally, the craziest.  I have no idea what’s going on.  That’s a lie.  I have a lot of ideas.  One of them has even been emerging over the last few days as the strongest contender, but that’s only after duking it out in the sea of idea-mediocrity for some time.  It’s like the island of misfit toys, but for insane hypotheses.

Never let it be said I have anything other than insane hypotheses.

Okay.  I have to wind it back a bit for you.  You can scroll down to the last section of the post for the punch line if you’re an overly eager beaver.  What follows is a recap of my eating and PCOS history, with recent developments highlighted near the end.


In 2009 I stopped menstruating.  This month, March 2012, marks the 29th month in a row that I haven’t had a period.  This is because I have the hormone disorder Polycystic Ovarian Syndrome, which means basically that my ovaries are constantly on the fritz.  Back in 2009, this condition was sent into hyperdrive. I lost ~25 pounds in 3 months on a low fat low calorie diet.  That’ quite an achievement for a 5’2 frame.  My already sluggish ovaries boarded up their windows and got the hell out of Dodge, leaving me alone to deal with the wreckage.

My body fat got down to probably around 18 percent, as a guess; it probably dipped to 17 at times, and at others rising to 19.  I’m not sure.  In any case, from that unhealthy low point in 2009 I adopted a paleo diet, though that didn’t trigger menstruation, and I built muscle, and I travelled and my hair stopped falling out and every man in the world started tripping over himself to put his tongue in my mouth.  (This actually happened.  It happened so frequently in fact that it developed it’s own name: the drive-by make out.   This is not a joke.  I was in Italy. Italian men are handsy, presumptuous little grabby primates.)

My sex drive was also in the shitter; I got moderate-severe cystic acne; I was (am) infertile.

But I was paleo.  I was healthy.  I started doing reading on PCOS and found loads of information– but it all was hard to dig up, and it was totally scattered, and even the people with the best ideas really didn’t have any kind of certainty.  The problem was that there’s lots of information out there, and also that PCOS is a bit complicated, such that the reason I was suffering my symptoms “could have been anything!”    I tried loads of things to fix the PCOS naturally: I ate super low carbohydrate for a while; I eliminated dairy and soy completely; I ate coconut; I ate fish; I cut out non-organic animal products; I ate “fertility” foods; I built muscle; I exercised; I fasted. 

Yeah.  So one of the things I did was fast.  I was told that PCOS is usually a disease of insulin dysregulation (true), so I figured I should fast in order to fix my sensitivity.  Okay!  Awesome.    Now I had scientific justification for my life of disordered eating, restriction, obsession, and hunger.   Hell to the y. e. s.!

Fast forward to the end of 2011.

Nothing has worked.  I’m fed-up.  I’m broken and pock-marked and frustrated like I’ve never been.  Tired of fighting and looking for answers.  I decide to try drugs.  They fuck me royally.  

One of the things that happens is I develop anxiety issues and the worst insomnia I’ve ever suffered.  I know this doesn’t sound like a big deal, but of all the health issues I’ve ever dealt with, this one of the worst.  I couldn’t possibly wish this kind of panicked existence on anyone.  Trying desperately to make it stop, I drop the thyroid medication.  It helps.  The anxiety dissipates, more or less.  All that is left is insomnia.  But it’s BATSHIT CRAZY INSOMNIA.  Like: Don’t-sleep-for-days insomnia.  It’s absurd, completely absurd– I really don’t know how to articulate just how fucked everything in your life becomes when you stop sleeping.  Don’t let this happen to you.  It’s fucked.

Did I mention being fucked?


I think it’s a good thing.

Now who’s fucked?

I’ve stayed on the testosterone blocking drug Spironolactone.  This has some potential to increase my estrogen levels, which is really important.  Yet far more important than being on this drug, I think, are some other “desperate” measures I have undertaken, finally, in submission to  last resorts.  I have added significant carbohydrate to my diet: 40-50 percent of calories, and my BMI has risen to 21.7.  I have also endeavored to eat more frequently, specifically whenever I am hungry, and to stop exercising, and do my best to convince my body that I am not starving.

And guess WHAT.  I think it’s working.

I think, too, sometimes, that I am detecting hints of a menstrual cycle.  (!)  By gauging the activity of my skin, my vaginal secretions (no longer dry as Oscar Wilde !), sensation in my clitoris (imagine… Jesus Christ… no, don’t imagine Jesus, I mean: imagine OMG not having any sensation down there for three years), and emotional changes…. well, it looks like my hormones are up to something.

Which brings us to the topic of today’s post: emerging from starvation.

These days, I absolutely can not sleep unless I am fed.   This fact scares me for a number of reasons, and it seems crazy, but really, the evidence is clear.  At night, I lay awake literally until the sun comes up unless I’ve had a full, satiating meal beforehand.  On nights I do sleep, I wake up energized and ravenous, usually quite early.  During the day, I might feel exhausted, but I can’t sleep unless I eat.  Often I will lay down to nap or to sleep, and I just know that my body is too energized, and I feel sort of caffeine-type jittery, but then I’ll eat an avocado and I’ll be instantaneously exhausted and fall asleep on the spot.


What’s happening to me is on the surface clear, even if the reasoning is less so: it’s adrenaline.  Nothing in the world I think has the ability to keep the body running like this for so long except for adrenaline.  I have gone now several days at a time where I hardly sleep at all but am never tired…. it’s adrenaline, it’s got to be, and I have a theory.  Surprise.


I have sworn very recently to never let my body go hungry.  Today, I eat whenever I get the urge to, come hell or high water… or– holy hellfire, Batman!– a size 27 jean.   I have to make this happen.   Literally.  It feels so unnatural.   And it is brand new for me.  Even though I’ve been fasting under the guise of healthy eating for a significant chunk of time now, I have actually been denying myself food, dieting, counting calories, and cycling in and out of severe restriction since I was ~15 years old.

I have been hungry since I was 15 years old.  I think my body had rather gotten used to it.  Up until…hell, yesterday, I thought it was the normal state of existence.

But now… now… with the added weight, with the dedication to reduced stress… certain hormone systems I think are kicking back into life.   My body is having none of starvation.  It’s just completely done; it won’t let me do it anymore; the jig is up– I’m packing up my skinny pants forever.   In some ways this is really sad, and still it’s really difficult, but in other ways it’s the best thing that has ever happened to me.

The most amazing thing happened to me last night:

I went out to dinner with some friends, and I did not finish my pho because I did not WANT to. 

Holy shit.  Holy shit.  I’m shaking my computer, guys.  If you’re a disordered eater, you know how big of a deal this is.  I did not want to keep eating!!11!1!!!1!!sin(90)1!!1!!!  Now that  I am treating my body with respect, it’s respecting me right back.  Is my obsession with food waning?  After almost ten years?  Was the answer really as simple as making a commitment to reduced stress and consistent satiation?


I’m not getting my hopes up.  It’s early.  My hormones are in giant flux.  I really have no idea what is happening.   Honestly, I don’t understand any of it.  Why the adrenaline, why now?  Why wasn’t it working this way before?  Is it because other hormones are fluctuating?  Because my cells are emerging from a several-year period of semi-starvation and, in their new energy state, are steadfastly refusing to go back?  Maybe.  I know that I’m grasping at straws.  But I don’t know what else to grasp at.  Only time will tell.

For now, I’m going to continue to eat when I’m hungry.  This sounds like a completely normal idea, but for me and for all the other people out there with disordered relationships with food, it seems almost impossible.   I’ll try to keep at it, and I’ll let you know how it goes.  Who knows.  Maybe now that I’ve got that side of the equation, I’ll be able to continue to stop eating when I’m full.  And this will, in the very least, enable me to keep getting rest at night.  That’s the most important part.   I really can’t say that enough.  Sleep is important.  I’ll do anything to get it back.

I’ll write more on starvation in a while.  I’ll keep you posted.  It’s interesting; it’s abnormal; I’m freaked out and nervous as shit; but also I’m tentatively psyched.   The future is scary, but if I can manage to trust my body just a little while longer, I may in fact be saved.





03 2012

PCOS and diet part 600, a summary of sorts

PCOS and your diet are huge.  Your doctor might tell you that the food you eat doesn’t matter, and that it’s all a matter of “hormonal regulation” or “ovarian dysfunction,” — but we all know that those these are a function of poor diet and lifestyle, too.  Food’s a big deal.

In general, if you are overweight and have PCOS, chances are good you suffer insulin dysregulation of some sort, and you’re going to want to consider diabetes-type diets and treatments.  Lower carbohydrate (usually, specifically HFCS), higher fat, some intermittent fasting if you’re up for it, and exercise.

In general, if you are thin and have PCOS, chances are good your testosterone is sky high and your estrogen is locked in a cellar in the basement.  Erm– that’s not exactly true.  PCOS is hugely complicated, and no one really understand why so many thin women suffer hormonal dysregulation.  I would chalk it up, I think, to -poor diets and to stress throughout life, to -in-womb and infancy nutrition, to -nutrient and hormonal profiles at the time of menarch, and to -weight fluctuations and food in the adult years.  Generally– generally!–the important things to hit here are limiting phytoestrogens (overweight PCOS patients need to watch out for this as well), limiting stress, increasing thyroid activity via whichever mechanism is appropriate to you, probably one being eating carbohydrates, and making sure you aren’t exercising too much or are underweight.  If you were ever heavier at a point in your life, and you menstruated then, do a little Aristotle:

Syllogism EG:

1)  Heavy Stef menstruates.

2) Thin Stef does not menstruate.

3) If thin Stef wants to menstruate*, she should become Heavy Stef.


No, it’s not that easy; it’s not that simple; putting weight back on doesn’t account for other factors like stress and wear and tear from earlier parts of your life and from basic ovarian sluggishness that might not ever go away.
I’ve talked a lot on here about particularities of different foods and how they affect our hormones.  And they do.  It’s amazing, but I really do break out if I eat a couple bowls of oats, since oats contain phytoestrogens.  I really do wake up in the morning with angry, painful cysts if I consume cream or milk.  When your hormone systems have become so sensitive, tiny disruptions to it from food really are noticeable.

BUT: They would not be noticeable if other things were in line.

The estrogens produced in our bodies is approximately a billion times stronger than those we eat in foods.  This is why most people don’t have PCOS.  Why we do have PCOS is that there’s something funny going on in our metabolisms.  The goal is to FIX these metabolic problems.    Diet is one of the most important mechanisms by which we can do that.  But the point is not to micromanage with foods but instead to holistically fix the metabolic problems.  Generally get your food in line.  Eat real shit.  Be an appropriate weight.  Don’t over exercise.  Don’t stop yourself from eating if you’re hungry.  

Foods important.  But it’s only important in the role it plays fixing everything else.  Don’t use food perfectionism as a scapegoat because you don’t want to look at bigger issues.



*I just typed masturbate…considering PCOS killed my sex drive, I guess that would be an appropriate word here, too.


03 2012

Female fitness clarification

A la my recent post on the masculinization of the ideal female body, people seem to think I’m advocating that whole paleo muscled, shredded woman as beautiful.

I’m not.

do think it’s sexy.  It’s why I worked so hard to achieve it.


But I think it’s overdone.  Strong does not = healthy.  Strong = strong.  Sated and energized and fertile = healthy.  This often means fat.  Fat in your chest, fat on your thighs, fat on your hips, maybe some fat on your abdomen.

Deal with it.

I refuse to hate my thighs.  You know– that’s why I had to get so skinny.  I couldn’t get that damn fat off of my thighs.   Fuck it.  I’m tired of hating my body for something that I did to it, and I’m tired of counseling women as thin as I am on how to stop obsessing over food when the most obvious answer is to eat more.   Yes, I think of course that disordered eating is still a problem.  I think emotional relationships with food occur at all weight levels.  I will always help and love you within the paradigm of your mindset and your goals.  Unconditionally.  But when your health is at stake, please please please please please consider all of the options.  Including this one: embrace fat.  Double zeroes are not ideal.  Threes are even not ideal.  What’s ideal is your body and comfort.  That I am certain is sexiest thing of all.



02 2012

Carbohydrates for fertility

Lots of talk going on in the web recently about carbs and fertility!  Women’s health ftw!

Paul Jaminet: Higher Carb Dieting Pros and Cons

Chris Kresser and Chris Masterjohn: Cholesterol, mostly, also: Telltale signs you need more carbs

Cheeseslave: Why I ditched low carb

Paleo Diet News: Sort of rehashing Paul’s argument

Julianne: 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.


Hey.  I haven’t emphasized this enough on this blog.   Hypothyroidism can be induced via a number of mechanisms.  One is a low carbohydrate diet.  If hypothyroid, or even subclinical thyroid, is at all a part of your PCOS pathology, consider eating a high carb (at least 100 g/day, IMHO).   Really.   Do it.  Reading the links above will give you helpful insight into the mechanisms.


My quick anecdote:

Since adding carbohydrates to my diet– call me crazy– I’ve been less sickly.  The acne scars on my face heal much more quickly than they used to.   My acne itself is way better, though my meds, in part, can account for that.   I sleep much much much much more peacefully.  Most importantly, my breasts and hips have gotten larger, and my thighs a bit I guess, but my stomach has stayed flat flat flat.  How nice is that?   (But I would still be healthy if I had some tummy fat!)   Clearly my estrogen profile has changed.

(Note: I am also on a diuretic, so this makes it easier to have muscle definition, especially in the abdominals, but– well, I’ll take what I can get.  I’m not giving up carbs again.)


02 2012