Okay, okay… I know it’s not paleo per se…
To talk about making your bed…
But actually I think it is!
Nowadays, we have beds.
BUT WE DIDN’T USED TO.
Beds aren’t paleo!
I mean, obviously beds are fine. But since beds have only existed for a few thousand years and people have existed for millions of years, beds are pretty new things.
And so with beds, comes problems for our evolved bodies.
Here is one of the problems:
Allergies and bugs.
Specifically, allergies and dust mites.
Dust mites are incredibly common in beds. In fact, it is nearly impossible for a bed to exist without them. On average, it appears as though a single bed contains between 1 and 2 million dust mites.
Dust mites are microscopic, so even while they are gross to think about, they don’t normally impact your life. The exception is that when dust mites poop, humans often react to them as allergens.
For this reason, dust mite poop has been hypothesized by many researchers to be a factor in causing asthma (though of course there are many).
How do you minimize the amount of dust mites in your bed?
You might think that you should wash your sheets every day, but the answer is in fact far simpler:
Don’t make your bed.
If you don’t make your bed, and you leave your top blankets all crumpled up or off to the side or what-have-you, then you will air out your sheets. Dust mites thrive off of skin cells in warm, damp environments. They actually die if their environment becomes too dry. If you don’t make your bed, you dry out the dust mites and they die.
If, however, you make your bed after getting out of it, you trap warmth and moisture in the sheets, which creates a veritable breeding ground for these asthma- and allergy- causing dust mites.
So be paleo!
Don’t make your bed!
Your sinuses may thank you.
(Or I guess the real paleo thing to do would be to sleep in a tree or a cave… whatever.)
What do you think? What are your bedding preferences? Do you think about paleo and how it might impact your life in areas more than just food? I’d love to know!
Of all the things in the body that hormones affect, sleep is one of the most important.
Without quality sleep, it is difficult to regulate appetite, to burn fat, to feel good, and to be happy and calm. Poor sleep can cause inflammation, poor blood sugar control, depression, anxiety, and a whole host of other issues.
Women suffer from insomnia at nearly twice the rate of men. This may in part be due to social and psychological factors, but it is also no doubt also due to the physiology of female hormones.
Fortunately, even though it’s nearly impossible to find great information about female hormones and insomnia on the web, the basics of are actually quite simple. Here is what you need to know about female hormones and insomnia.
Female hormones and insomnia: low estrogen levels cause insomnia
Low estrogen levels cause insomnia. Why? Because estrogen helps move magnesium into tissues. Magnesium is crucial for catalyzing more than 300 reactions in the body, the synthesis of important sleep neurotransmitters and the sleep hormone melatonin included.
When this happens, it is both harder to fall asleep as well as harder to stay asleep throughout the night.
Female hormones and insomnia: when estrogen levels get low
Estrogen levels can fall for a number of reasons. Here are the most common:
Female hormones and insomnia: psychological stress
High amounts of psychological stress can cause the female body to shut down reproductive function. This happens because the body would prefer to wait until less stressful time before becoming pregnant. It is much easier to become ill or die while pregnant if you are in a stressful environment.
You can read more about psychology and how it can affect sex hormone function in this post: psychological stress and hypothalamic amenorrhea.
Female hormones and insomnia: metabolic stress
High amounts of physical stress like under-eating, over-exercising, low fat or low carb diets, intermittent fasting, dramatic weight loss or low body fat percentage can all cause estrogen levels to drop precipitously.
It is super important for the female body to feel relaxed and fed. If it does not feel fed, it will think that it is starving. And if it thinks that it is starving, it will stop producing reproductive hormones, so as to stop you from becoming pregnant at a time in which it may be dangerous.
All sorts of activities that involve undereating of some sort – whether from calorie counting or chornic dieting – thus become a threat to your ability to sleep, especially if they are a chronic problem.
You can read more about the threat of starvation to female sex hormones in this post: metabolic stress and hypothalamic amenorrhea.
Female hormones and insomnia: fluctations with the menstrual cycle
Women of reproductive age often experience fluctations in their ability to sleep on a monthly basis. I know that I certainly do.
Most women report most difficulty sleeping in the day or two before menstruation, and during the first days of menstruation.
This is because these are the days in which estrogen levels are the lowest.
On day 1, the day of bleeding, all sex hormone levels are very low. Over the course of the next two weeks, before ovulation, estrogen levels rise. After ovulation, estrogen and progesterone levels fluctuate. Sometimes during this phase, progesterone levels may be elevated enough in order to off set any benefits from the estrogen, but usually the estrogen is strong enough to enable you to sleep.
At the end of the cycle leading up to the days of bleeding, however, most hormone levels are back down very low, including estrogen, making sleep difficult during these days and in the days that follow.
Female hormones and insomnia: menopause
Menopause is infamous for causing insomnia. Hot flashes often play a role in this, but even without hot flashes many women and toss and turn for years.
Menopause causes insomnia because the ovaries stop producing estrogen and progesterone at this time. Very often, after menopause the body readjusts to low estrogen levels and more easily picks up on a light estrogen signal. But it can take a significant amount of time for that to happen, which can be super problematic if you enjoy sleeping.
One solution to this problem is to try hormone replacement therapy. I am not an expert in pharmaceutical solutions to menopause, however – so I cannot in good conscience recommend particular brands or dosages. I will say that I think a low dose for a short period of time is probably okay and will not cause any problems, though HRT can cause symptoms such as breakthrough bleeding and is also under investigation for being linked to incidences of female cancers such as breast cancer.
One more natural solution is to experiment with phytoestrogens like legumes (chick peas, black beans), nuts (macademia nuts, cashews), small amounts of soy or flax in your diet, or even moderate alcohol consumption. These foods act like estrogen in the body and may be able to help give your sleep the estrogenic edge you need. Each woman’s body is different so you won’t know how these affect you until you give them a shot.
I recommend starting with one bowl of chickpeas a day if you are coming from a ‘clean’ paleo diet, and with something a bit more robust, like a tablespoon of flax, a day if you are coming from a Standard American Diet. The reason there is a difference in those recommendations is that women who have been ‘clean paleo’ will be more sensitive to phytoestrogens than ones who regularly consume them as a part of the SAD.
You will also want to make sure you are eating at least 40 grams of fat a day so your body has all the fat it needs to make estrogen, as well as at least 50 grams of carbohydrate (100 for women who are still of reproductive age), to keep your metabolism, thyroid, and reproductive hormones burning strong.
For more on some recommendations I make for menopause, check out this post on menopause and hot flashes.
Other hormones, systems, and insomnia
Of course, there are other hormone problems that can cause insomnia. Disorders of testosterone production, growth hormone production, and thyroid hormone – especially if hyperthyroid – can all have a negative effect on your ability to sleep.
Plus of course there are many other causes of insomnia beyond hormones. Neurotransmitter imbalances, electrolyte imbalances, stimulating substances like caffeine or MSG, blood sugar spikes, stress, anxiety, and dysregulated circadian rhythms can all be significant problems. I have suffered from each of these in my own journey with insomnia.
Nevertheless, the menstrual cycle, menopause, and the sensitivity of the female body to stress are all very common reasons that women lose sleep. And it all boils down to one thing: estrogen.
Estrogen, estrogen, estrogen.
Working on correcting or taking care of the estrogen-lowering issues discussed above can and will go a long way towards soothing your insomnia needs.
And, as ever, I am super curious as to what you think! Do you have experience with female hormones and insomnia? What things have worked for your insomnia?
I spend a disproportionate amount of my time telling women to eat carbohydrates.
In the paleosphere, it is incredibly common to eat a low carbohydrate diet. Plenty of people use low carbohydrate diets to lose weight, to sharpen insulin sensitivity, and to reduce appetite in the short term.
A low carbohydrate diet can also be 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 effects of this are significant: adrenal glands work overtime, livers get tired from performing so much gluconeogenesis, insulin sensitivity drops, body fat levels fluctuate, sleep quality decreases, and libido and fertility decrease.
The problems that come from a low-carbohydrate diet of course don’t affect every woman. Each of us is different. But women who experience stalled weight loss, 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.
If you are trying to lose weight, take a look at my program, Weight Loss Unlocked, which will help you lose weight in a healthy, safe, and balanced way. Check it out here.
Also, this is my favorite paleo cookbook with plentiful carbs in it. It’s by Russ Crandall, and he’s an amazing chef, as well as one of my favorite people of all time.
Carbohydrates are beneficial for fertility and health because…
-Glucose is necessary for the conversion of T4 to T3 in the liver.
Without adequate glucose, the liver struggles to make enough T3, which is the form of thyroid hormone critical for healthy thyroid function.
Without sufficient T3, hypothyroidism results. Hypothyroidism is implicated in mood disorders, reproductive irregularities such as PCOS and amenorrhea, in skin conditions, and in weight gain, among other things. (For more on how to figure out your particular type of PCOS and how hypothyroidism may be at play, see my program PCOS Unlocked or read my post on the causes of PCOS)
Many women, contrary to popular paleo belief, in fact lose weight once they add carbohydrates back into their diets. This is because the carbs help the body produce more T3.
(Now, low carb dieters might be quick to point out that the liver can manufacture its own glucose. Certainly, the liver is capable of producing its own glucose with gluconeogenesis, but that process can become taxed over time, particularly if the liver is already taxed from poor eating habits in the past, mineral deficiencies, stress, or calorie restriction.)
-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. Leptin is absolutely crucial for reproductive function. Without leptin, the hypothalamus does not tell the pituitary to produce sex hormones, so it doesn’t.
–Insulin is also an important signaler of the “fed” state.
In addition to leptin, the hypothalamus also responds to insulin. These two hormones are largely responsible for the female body determining whether it is in a “fed” state.
Being in a fed state is critical for convincing the body it is in a healthy enough environment to reproduce, have a libido, and also lose weight.
–Moderate carbohydrate intake is associated with better mood, stress-reduction, and sleep quality.
I see this in my work and in anecdotes, as well as in many controlled studies.
Carbohydrate intake boosts tryptophan levels in the brain, and tryptophan is the protein precursor to serotonin. Getting at least some carbohydrate in the diet helps with the vast array of issues associated with serotonin deficiency which include moodiness, stress, and insomnia. People have been shown to sleep better if their dinner includes carbohydrates in it.
This is especially true for women.
For a look at the details and complexities of the issue, see Emily Deans writing 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.
Carbohydrates for fertility and health
The main point here is 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 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.
This concept is central to my program Weight Loss Unlocked. If you are interested, it will help you figure out which path to weight loss is best for your unique body and metabolism.
Carbohydrates to eat:
-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.
These starches are composed primarily of glucose.
–Fruits. All fruits! Berries and cherries tend to have more glucose than fructose, other fruits tend to have more fructose than glucose. This is not a huge point of difference but I have noticed that some women tend to do better on glucose-heavy or fructose-heavy carbs. I personally have an easier time with weight maintenance with fruits than with starches. I talk about this idea more in depth in that Weight Loss program for women I use with my clients.
-Rice 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. Wild rice is another option that I like. Pink rice is something that my friend Noelle from Coconuts and Kettlebells really loves and is a unique way to incorporate rice into the diet! (By the way, if you haven’t listened to The Paleo Women Podcast featuring myself and Noelle, you need to! We are the BEST and we will explain to you ALL THE THINGS. Find us here!)
-Vegetables of course are great, but they do not count for carbohydrate consumption. I know that most of the carbs in vegetables are glucose, but much of it them are 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 fruits work the best.
How much carbohydrate to eat for women:
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.
I typically recommend that women start with 100 grams of dense carbohydrate like starches and fruits and experiment from there. You can definitely eat more than that – I know that I do. But you could also eat a bit less, especially if you prefer a lower carbohydrate appraoch to health.
Remember, you do not necessarily need to eat high carbohydrate. You can, but you don’t have to. It is only that a diet with at least some carbohydrates can really help with fertility, hormone balance, thyroid, and weight loss problems.
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: What the bleep do we know about carbs
While you’re at it, go read Melissa’s post on Why Women Need Fat.
Don’t forget this is my favorite paleo cookbook full of good carbs.
And especially don’t forget to check out Weight Loss Unlocked if weight loss is one of your main goals right now, The Paleo Women Podcast, which is just so much fun, and my best-selling book Sexy By Nature, all great resources for all things women’s health, happiness, and fertility!
Neurotransmitters: Exciting and Inhibiting
Gamma-Amino-Butyric-Acid, or GABA, is the chief inhibitory neurotransmitter in the human brain. Along with serotonin, dopamine, glutamate, glycine, histamine, and norepinephrine, among dozens of other neurotransmitters, GABA regulates brain function.
Different neurotransmitters are in relationship with different types of receptors, and these receptors signal excitation or inhibition. For this reason, neurotransmitters are commonly classified by their excitatory or inhibitory activity. Some neurotransmitters signal to both kinds of receptors and play both excitatory and inhibitory roles. Others are just one or the other. GABA is one of these. It is powerfully inhibitory.
GABA: Calm, Resilience, and Sleep
The GABA neurotransmitter tells the brain to be quiet. The vast majority of inhibitory synapses in the brain employ GABA. For people who are depressed and fatigued, therefore, GABA might seem like a problematic molecule. But that ends up not being the case. GABA malfunctioning has been shown to play a role in almost all mood disorders, including depression.
GABA is strongly associated with well-being, calmness, proper memory function, proper circadian rhythms, and good sleep. GABA inhibits amygdala activity, too, so it has also been shown to inhibit pain and fear. For this reason, people have talked about GABA as being a molecule that promotes resilience and personal strength.
GABA is well known to be a prominent factor in mental well-being and feelings of calm. Officially it results in “sedative, hypnotic (sleep-inducing), anxiolytic (anxiety reducing!), anticonvulsant, muscle relaxant and amnesic” effects. For this reason, a whole host of drugs that mimic GABA, called benzodiazepines, have been designed and proscribed prolifically. Valium is one of them.
The long-term effects of these drugs are unpleasant, as they almost always result in withdrawal. The symptoms of benzodiazepine withdrawal parallel GABA deficiency. These iclude anxiety, tension, high blood pressure, insomnia, agitation, seizures, muscle spasms, and panic disorders. For example, GABA-inhibited mice tested for anxiety demonstrate “a model of anxiety characterized by harm avoidance behavior and an explicit memory bias for threat cues, resulting in heightened sensitivity to negative associations.”
GABA is also one of the prominent molecules involved in sleep. During sleep, many parts of the brain need to be quieted, and they need to do it all at once. This is, in part, GABA’s job. Without GABA, excitatory neurotransmitters continually keep different parts of the brain and the body firing, such that it can never shut down fully enough for deep sleep.
Valerian root, a natural herb and supplement, “encourages” the production of GABA. It’s one of the most successful sleep aids one can use. Melatonin is also powerful and is bio-identical, but it’s effects wane more markedly over time as the body becomes more and more used to higher levels of melatonin. Over-the-counter and prescription drugs, while knocking people out, also inhibit the deep restfulness of REM sleep. Valerian does not replace, but instead stimulates GABA production. This is why it is so naturally (and without causing addiction) effective in promoting deep sleep.
GABA and The Pituitary
GABA, even while it inhibits frenetic activity in the brain, also stimulates activity in the anterior pituitary. The anterior pituitary is where most of an individual’s hormone production takes place. GABA, therefore, is crucial for people who would like to boost hormone production. ACTH, TSH, FSH, LH, prolactin, and Human Growth Hormone are all secreted from the anterior pituitary.
Low TSH is profoundly implicated in hypothyroidism; having low FSH, LH, and prolactin levels is the root biological cause of hypothalamic amenorrhea; and growth hormone is one of the primary molecules responsible for healthy metabolism. It’s activities include up-regulating fat utilization, protein sparing, and glucose-insulin sensitivity. One study at the University of Milan found that 90 minutes after 5 grams of GABA supplementation, HGH levels increased 5-fold.
Increasing GABA with diet
-GABA itself is not present in foods, but one of its key constituents — glutamic acid/glutamate — is available in a wide array of readily available foods. Glutamate-containing foods are plants and vegetables. Examples include: broccoli, spinach, lentils, walnuts, citrus, tomatoes, cheese, corn, and mushrooms. There are other foods in this category, such as wheat, wheat bran, soy, and cottonseed flour, and peanuts, but I do not recommend eating them (find out why in my book). High glutamic acid containg foods are generally animal products. They include eggs, particularly the whites, many varieties of cheese, cod, gelatin, whitefish, and chicken, beef, and scallops.
–L-theanine also increases GABA activity. This amino acid is found in high doses in green tea.
-Foods rich in B-complex vitamins, particularly inositol, also prompt GABA production. In fact, B-vitamins are necessary for the functioning of nearly all brain processes and chemicals. Foods containing B-vitamins comprise a rich and varied list. They include: fruits such as bananas, figs, cantaloupe oranges and figs, and vegetables, particularly cruciferous vegetables, such as beets, broccoli, kale, and spinach, and nuts, and seafood, and beef and beef liver, chicken liver, all organ meats, and all game/ruminant meats.
-A lower protein diet in general is associated with increased GABA activity.
-Finally, exercise and meditation can enhance GABA activity. GABA is a lot like other body systems and muscles in that it has positive feedback effects. The calmer someone is, the more likely it is that he will be able to produce proper amounts of GABA. Some physical activities allow the mind and body to enter into calmed and relaxed state. For this reason, many natural health practitioners recommend yoga as a means of increasing GABA. Meditation and light forms of exercise such as walking also fit into that recommendation.
Night Eating Syndrome isn’t something that gets talked about very often. But disordered eating researchers are hyper aware of it. It’s also an enlightening topic for a variety of reasons, least of which being the relationship between the endocrine system, circadian rhythms, and feeding schedules.
The diagnosis and experience of night eaters is now well-parameterized, though the causal factors are not. Night eaters usually eat very little in the mornings, eat more snacks during the day time than others, and wake up often several times each evening in order to eat. They usually sleep at normal times, but their sleep is disturbed by their need to eat. Night eaters experience lower levels of leptin both at night and during the day, lower levels of growth hormone, and higher levels of TSH. In general, insulin and glucose are elevated, and rates of depression are also higher. But still the crux of the night eating problem is timing: Leptin and insulin are delayed between 1 and 3 hours. Melatonin is delayed by a couple of hours. Ghrelin, the primary hormone that stimulates food intake, is phased forward by as much as five hours. Glucose rhythms are almost entirely reversed. Night eaters also experience several “amplitude” attenuations. What this means is that both the spikes and the troughs of different cycles are minimized, such that hormone levels flatten out and disrupt the endocrine system’s ability to hit the triggers for normal functioning.
Researchers are not sure what causes night eating syndrome. Metabolic dysregulation for sure, but “obesity” still doesn’t provide the answers. What is clear is that the central timing of circadian rhythms (via the suprachiasmatic nucleus in the brain) undergoes some kind of disconnect with other clocks located throughout the body, particularly those found in the stomach and the liver. Many researchers recommend using lighting and other environmental triggers to get NES sufferer’s clocks back on schedule, but that only addresses one portion of what controls timing. The SCN is the ruler of the circadian system, but it cannot force peripheral organs into line. I believe liver and stomach signalling need to be addressed independently. For an excellent discussion of what mechanisms may be at play in peripheral clock signalling, check out this review.
The mechanism by which these clocks become de-coupled is not quite known. First, it is generally assumed that a switch in feeding times tells the body to expect different signals, such that moving meals around really can phase shift organs. Yet it goes deeper; most everyone with night eating syndrome still eats at regular mealtimes. Something must account for what’s making them so hungry at nighttime. In investigating the link, some researchers injected the glucose-receptor agonist dexamethasone into mice at different times during the day. Dexamethasone is a synthetic glucocorticoid, stronger than cortisol. With the dexamethasone in their systems, the mice’s livers became phase-shifted within a day or so. With less, it took longer. What this demonstrates is that the presence of cortisol in a system accelerates whatever phase changes might be occurring. The SCN is capable of arousing CRH (a precursor to cortisol) production. Many researchers speculate that this is a mechanism by which the SCN generally attempts to modulate peripheral organ activity. Yet if cortisol runs amok, the effects can occur absent the usually cause.
The same goes for people. One study tested CRH levels in night eaters. They found that in night eaters compared with controls, the CRH-induced cortisol response was significantly decreased. In conclusion, disturbances in the hypothalamic-pituitary-adrenal axis with an attenuated ACTH and cortisol response to CRH were found in subjects with night-eating syndrome.
Lesions on the SCN abolish glucocorticoid and feeding rhythms. In “clock mutant” mice, the feeding schedule is distorted in a way that almost doubles calorie intake. Mice typically eat 75 percent of their calories in the nighttime, yet when they become Mutant Clocks they end up consuming the same volume of food also in the day time. These mice also experience diurnal variation in glucose and triglyceride levels. Their gluconeogenesis is almost entirely suppressed. Why this happens is not known, though it is clear that the signalling from the SCN clock must be received and interpreted in the liver in order for gluconeogenesis to function properly. This is especially interesting because we see that feeding-stimulating (orexic) and feeding-inhibiting (anorexigenic) genes in these mice are both decreased as a result of the clock mutation. We would think, then, that these two decreases would balance each other out. And maybe they do. What seems to be the real problem with night eating syndrome is the dysregulation in the communication between the SCN and the digestive organs.
Throwing off glucose metabolism in this way begets leptin problems as well. And how does leptin dysregulation contribute to the development of night eating syndrome? It’s a slow but insidious process. Sleep curtailment inhibits the leptin response. Decreased leptin levels leads to an increased need to eat–particularly of carbohydrates. This is likely due to a whole host of types of neurons that respond to starvation signalling (ie, low leptin levels or poor leptin sensitivity) with drives toward carbohydrate refueling, particularly Neuropeptide Y and hypocretin neurons. When sleep-curtailed individuals wake up in the morning, they have impaired glucose tolerance and crave carbohydrates right away. Throughout the day, blood sugar swings and inhibited leptin signalling and responsiveness lead to incessant snacking. Additionally, an altered cortisol profile from the disturbed sleep disrupts the liver and stomach clocks. These several phenomena result in an increased need for food and for calories late in the day. Leptin levels have dipped, glucose and insulin functioning has been impaired, cortisol has been on the rise, and the brain has been told it’s starving. Then, so late in the day, the individual eats because he is hungry. His leptin levels will rise, particularly in response to a high carbohydrate, high insulin meal. This can help him sleep, via calming hypocretin neurons, as well as sooth his cravings. But it’s not over. With other timers off in the stomach and the liver, the brain will get appetite and waking signals (again, partly facilitated by hypocretins) strong enough to rouse the individual from sleep. If hypocretin neurons are significantly stimulated, the organism will always rise. Continually then throughout the night hypocretin neurons respond to all of the hormones coming out of the liver and the stomach and get the organism up to feed.
This all results in a vicious cycle. What needs to be done about it is not exactly known. Patients can supplement with 5 HTP and tyrosine in order to raise brain neurotransmitter levels, which can curb appetite. Patients can do light therapy in order to strengthen the power of the suprachiasmatic signalling. And patients can perhaps take melatonin or valerian, or any other sleep aid, in order to try and get a full night’s rest and a full night’s recovery of leptin signalling capabilities. Mealtimes can be gradually shifted and snacking reduced such that the individual can still fall asleep and sleep well at the appropriate times. Finally, reducing stress is also–as always–one of the most helpful factors.
There is a hell of a dichotomy occurring in the Paleo blogosphere this month. 99 percent of the time I am pleased as Pooh stuck up a honey tree, nestled in my esoteric corner of paleo-feminist rage, but every once in a while I wish more people could hear what I have to say. Today is one of those days.
The split I am talking about is not all that nefarious. In most cases, it’s benign and can be ignored. But in general I would like to draw attention to it, because I think there’s a lot going on beneath the surface (and here, the depths are not just Nemo and Dory but are instead people’s lives), and that depth requires speaking to. Immediately.
Mark’s Daily Apple has recently done a beautiful series on the benefits of fasting. I loved it. I learned plenty, as I always do on MDA. The series was well-written and -organized, and in fact I ended up directing people who are unfamiliar with fasting to the site in hopes of swaying their opinions. (So let it be clear: I am not against fasting per se.) Yet Chris Kresser has also done an April “Best your Stress” challenge. Serendipitously enough, it concludes today. And it is exactly what it sounds like: an endeavor to spend 30 days taking practical steps to counteract stress. Chris’s idea was that people often spend 30 days trying to get their diets in line. But what about their stress, and their lives? I couldn’t agree more. This man is a gale of fresh, important ideas.
The reason I say these two Big Themes are at odds is because they are. Fasting is a stressor. Period. Mark Sisson would agree. All people who advocate fasting would agree. But all they ever do is put an asterisk at the end of their posts: *people who are stressed should probably not fast, they say. But why? Who is affected, and how? What can fasting and other forms of restriction do to our brains, and to our lives?
What I want to draw attention to today are little loci that sit on the border of the hypothalamus called Hypocretin Neurons. Hypocretin neurons (also called Orexins–and note that the word “orexin” means “appetite increasing”) were discovered just 14 years ago in 1998, but they have radically altered the landscape of eating neurobiology since then. No, they are not the sole molecules responsible for sleep and waking. Mice that have had these neurons removed still sleep and wake in roughly normal patterns. But they never feel alert, and they never suffer insomnia. And when the neurons are activated, the mice leap into action. Hypocretin neurons wake animals up. This much is certain.
The lack of Hypocretin Neuron signalling is the cause of narcolepsy, while elevated Hypocretin levels induce arousal, elevate food intake, and elevate adiposity. Hypocretin Neurons upregulate the production of molecules down several other pathways, too: these include noradrenergic, histaminergic, cholinergic, dopamine, and serotonergic.
The anatomy of Hypocretin Neurons is also coming into greater light. When are the neurons active? What signals do they receive, and what signals do they produce? Research is beginning to show that Hypocretin Neurons are excited by excitatory synaptic currents and asymmetric synapses with minimum inhibitory input. The fact of asymmetry is important. It means that Hypocretin Neurons are instead always acted upon by mostly uniform – excitatory – signals they receive. Hypocretin Neurons only ever up-regulate and relax. They do not down-regulate. Excitatory signals outnumber inhibitory signals 10:1.
One notable source of excitation is corticotrophin releasing hormone, which suggests that stress activates the activity of Hypocretin Neurons. GABA neurons also create a bridge between Neuropeptite Y, which is the molecule that arguably has the strongest appetite-stimulating effect on the brain, and Hypocretin Neurons (more on Neuropeptide Y later this week). From there, Hypocretin Neurons project to all regions of the brain, including the hypothalamus, cerebral cortex, brain stem, and spinal cord. It seems as though Hypocretin Neurons may act as a nexus of signal input for the appropriate synchronization of various autonomic, endocrine, and metabolic processes.
Food restriction further augments recruitment of excitatory inputs onto Hypocretin cells. This explains the relationship between insomnia and adiposity: because of the easy excitability of Hypocretin Neurons, any signal that triggers their activity, regardless of homeostatic needs, will elevate the need to feed in brain circuits such as the locus coeruleus and the melanocortin system while also promoting wakefulness through activation of noradrenaline-stimulating neurons. Anything that promotes the release of corticotrophin releasing hormone (CRH) such as reduced sleep will further trigger Hyocretin Neuron firing and Appetite. This is a vicious cycle. Hypocretin Neurons play the role both of trigger and of accelerator, taking states of wakefulness, insomnia, stress, and obesity into continual positive feedback loops.
So how does leptin factor in? Hypocretin Neurons express leptin receptors. Moreover, some recent complicated neurobiological work done on mice has shown that injecting them with leptin decreases the activity of their Hypocretin Neurons. What this means is that Hypocretin Neuron activity is stimulated in part by decreasing levels of leptin in the blood, and that increased leptin levels reduce the level of excitation running through Hypocretin Neurons. This is coupled by ghrelin activity, which is also detected by Hypocretin Neurons. Ghrelin, which originates in the gut and is known to stimulate appetite, also excites Hypocretin Neurons. What does feeding do, then, for Hypocretin Neuron excitation? Experiments on mice show that re-feeding restores normal Hypocretin activity, to an extent. Repeated abuse takes longer to recover from, but the simple presence of leptin in the blood normalizes the brains of mice.
Hooray! This is good for fasting, right? So long as one re-feeds appropriately, everything should be fine? Well, yes. In a healthfully functioning individual. But not in a) someone who is both stressed and leptin resistant, since increased leptin levels from the re-feed might not be powerful enough to offset other excitatory pathways b) someone who is currently emerging from yo-yo dieting or caloric restriction c) someone who is dealing with an over-stimulated appetite, d) someone experiencing stress, e) someone who has had a history of insomnia, f) someone who is underweight, since they have low leptin levels, g) anyone who has ever had an eating disorder, particularly bulimia or binge eating disorder or h) anyone with HPA axis or endocrine dysregulation, particularly women, including overt stress, hypogonadism, hypothalamic amenorrhea, hypercortisolism, or hypocortisolism (adrenal fatigue.) I am sure the list is incomplete.
In animals, Hypocretin Neurons serve an important evolutionary function. Arousal is a vital behavior in all species. And normally, Hypocretin Neurons respond quickly to changes in input. But in situations of chronic metabolic or endocrine stress, or of recovering from a stressor, they can lead to hyper-activity and hyper-feeding.
Researchers have long known about the link between leptin, sleep, and obesity. The less someone sleeps, the lower her leptin levels, so the more she eats, and the heavier she gets. Hypocretin Neurons may serve as one of the answers to the question of exactly how that phenomenon comes about. Or at least it plays a role. Because 1) Hypocretins simultaneously stimulate appetite and wakefulness, particularly through orexigenic output of the melanocortin system, and subsequent release of CRH, which activates the stress response, and 2) while Hypocretin Neurons wake us up, they also need to be quiet enough for people to go to sleep.
Finally, I raise the questions: how many disordered eaters have trouble sleeping? How many anorexics, binge eaters, calorie restrictors, exercise-addicts, stressed-out individuals, and very low-carb dieters have trouble sleeping? How many people try intermittent fasting and find that it disrupts their sleep or circadian rhythms? How many people wake up in the middle of the night or early in the morning, even though they still need sleep, but for the life of them feel so awake? Part of that answer lies in blood sugar metabolism, for sure. And in other places. Sleep is a hell of a complex phenomenon. But here– Hypocretin Neurons can become overburdened by excitatory signals. They get hyped up in the face of both decreasing leptin levels and leptin insensitivity. They are upset by restriction, and they are upset by fasting. Hypocretin Neurons demonstrate why so many people have difficulty with their appetite and their sleep. If you find that fasting disturbs your sleep, or that you are suffering disordered circadian rhythms along with stress or appetite problems, do you best to relax your system. Don’t fast. Relax. Exercise less. Reduce stress. Eat more. Put on weight. Eat more carbohydrates. Don’t graze. Increase your leptin sensitivity. And listen to your body.
Coming up next: nighttime eating syndrome, and how it’s all related.