Appetite and your period

Appetite and your period

American culture is nothing but confused about the effect that the menstrual cycle has on women.  We have rumors about mood swings, weight gain, appetite, athelticism, acne, depression, anxiety, insomnia, inflammation, and more. But we really don’t know much about any of them at all, let alone if they are true in the first place. Does the menstrual cycle really have that great a grip on a woman’s physical and mental health?

 

There are in fact grains of truth to many of the vague beliefs we have about the menstrual cycle. Some are bigger than others. Today, I investigate one of those grains:

Does appetite fluctuate according to the time of the month?

Actually, it does.

There may actually be something to wanting to eat ALL THE THINGS during your period. I love this chocolate since it’s gluten, dairy, and soy free.  And these chips when I’m craving something salty.

If you take a look at the graph below (click to enlarge), made by Hirschberg for her 2012 article reviewing appetite in women, you’ll notice that appetite is complicated. It’s influenced by many different sources, such as gut flora, hormones secreted from the gut, insulin secreted in response to a meal, and leptin from fat cells. Yet hormones are most certainly one of them. Hormones interact with leptin, as well as feed directly into the brain to stimulate or suppress appetite.

HIrschberg 2012.

HIrschberg 2012.

 

The two primary hormonal mechanisms of action are estrogen and progesterone.

Contrary to what you might guess – and what I originally guessed – estrogen is an appetite suppressant How is not totally understood, though it is widely thought that estrogen spontaneously decreases calorie intake by increasing the potency of the satiating actions of some gut peptides, especially cholecystokinin. The more cholescytokinin produced by the gut, the more full the brain feels. Furthermore, estradiol stimulates anorexigenic (stop eating) POMC/CART activity and inhibits orexigenic (keep eating) NPY/AgRP neurons.

There is evidence that estrogen does all of of these things in both rodents and humans. Rats that have had their ovaries removed, and thereby lost their estrogen-producing capabilities, for example, spontaneously eat more and gain weight. When injected with estradiol, their normal feeding and weight behaviors are restored.

In contrast to estrogen, progesterone appears to increase appetite. When administered high doses, ovariectomized rats eat more. This happens in humans as well, and most especially when in the presence of estrogen. Unless a woman has had her ovaries removed, she will always have at least some estrogen in her bloodstream.

 

So what about the menstrual cycle?

It seems clear from studies on both rodents and humans that estrogen decreases appetite and progesterone has the power to increase it. Do estrogen and progesterone fluctuations during the menstrual cycle make this happen? Hirschberg put together a graphic to approximate the feeding effects documented in women (again, click to enlarge):

Hirschberg 2012

Hirschberg 2012

You can see from this graph how feeding decreases when estrogen spikes and increases when progesterone does. This model is supported by data from several studies, including, a meta-analysis that revealed that mean food intake is lowest during the periovulatory phase of the menstrual cycle, when estradiol levels are high (see here), and other studies that have demonstrated that there is typically a peak in food intake occurs during the premenstrual period, when progesterone levels are high (hereherehere, and here).

 

Hormones and appetite in pregnancy and lactation

It’s not the explicit topic of this post, but I thought I’d throw in some notes on pregnancy and lactation. They are fascinating periods of hormone regulation. Learning about them demonstrates a bit more about the ties between hormones and appetite.

Both animals and women eat more during pregnancy to ensure health fetus growth. Rats will eat up to 200 percent their normal intake! In humans, the increase is more moderate, at about 10–15%. This effect is greatest from about week twelve until midgestation, when physical activity and food intake both decline.

No one knows quite for sure what biological factors cause this increase in food intake. Of course the fetus causes an increased caloric need, but the body doesn’t leave anything to chance. It doesn’t wait for the fetus to demand food in order to provide it — this could result in starvation for both the woman and the fetus. Instead, it uses hormones to get the woman to start eating more at the right time. Progesterone appears to be a primary component of this. It does so via specific receptors in the brain.

During lactation, progesterone becomes less important and prolactin possibly more so (though, again, simple energy demands from the fetus are likely the greatest factor.)  At this time, energy requirements are even higher than during pregnancy, with breastfeeding demanding approximately 500 extra kcal per day. This elevated need is generally met bya number of mechanisms: 1) being less physically active, 2) by eating 20–25% more (which makes sense, since most women consume approximately 2000 calories/day), and 3) by mobilizing fat tissue, which is an excellent natural way to burn off pregnancy weight.

so.. what?

I’m not sure. For one, this biochemistry might explain a little bit why there’s that mythic “go wild for chocolate” part of the menstrual cycle.

bugdocmom.com

bugdocmom.com

Second, it is totally cool that the reproductive system is so powerful! I am a firm believer that there’s no need to try and resist any enhanced cravings that you feel throughout your cycle. Typically the body will burn through the extra calories consumed on this level, especially if it is demanding it because of energetic and hormonal demands.

In fact, listening to these appetite fluctuations is one of the best things you can do for your body. Your body wants you to feed it when it asks to be fed. There are lots of ways to feed it in a healthier way, like some of the fantastic looking things in this book.  But if not fed, the body down-regulates thyroid activity, slows metabolism, and may even decrease the potency of reproductive organs.

The lesson here isn’t to start counting calories.  It isn’t to weight and measure while you’re PMSing. It is, instead, to understand how your hormones vary throughout the month, appreciate the wonder of your reproductive body, and do your best to be its partner and provide what it needs.

And for god’s sake, just eat the chocolate!

Are you really more hungry during your period? Find out what the deal is with your appetite during your period.

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Want to learn more about hormones, food, and fat? If you haven’t heard yet (and sorry if you have like a million times) there’s a super kick ass this week only collaboration between my favorite paleo thinkers (Kresser, Wolfe, Sanfilippo, me, etc) on female fat loss. Check out everything – which, btw, is competely free – @ the site where it’s all available:

http://forwomenonly2014.com

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.

How Probiotics Helped Reduce my Sugar Cravings

How Probiotics Helped Reduce my Sugar Cravings

I recently became a bit obsessed with gut flora research via a long story:

I began getting migraines again this winter after eating a lower-potassium diet to help with my electrolyte problem. Low potassium is associated with migraines. It didn’t help that I was visiting my father, who likes to cook with MSG. To help with the migraines, I took Aspirin, which is an NSAID. It worked, so I began taking Aspirin for my regular headaches, and that helped, too. However: NSAID’s are notoriously bad for your gut flora. My skin began breaking out a little bit. This could have been caused by anything (I thought: weight loss, fiber in my diet, increased progesterone, poor sleep, dirty towels… skin is complicated!), but I thought “maybe it’s the NSAIDs depleting my gut flora.”

I went to Whole Foods post haste and got kombucha on tap.

(My favorite brand available both in stores and online is THIS one)

I’m drinking a couple of jars a week.

My skin looks great – I’m not sure if its from the kombucha.

Something I did most definitely notice, however, is that my cravings for food, and particularly sweet food, have somewhat dramatically decreased. After just my first few gulps, I felt a difference. These days  I walk around during the day, not even thinking about food, and I stop eating meals without needing willpower, and I wonder: is this how ‘normal’ people feel?

So I asked myself if there was a connection. Could my increased freedom from cravings be a result of kombucha’s notorius bifidobacterium?

Turns out, it most certainly can.

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How it works: your gut flora

Gut flora–which are the bacteria that live in your gut and that number in the trillions–are responsible for a whole host of functions in the body. They play a role in digestive comfort, in being constipated or having diarrhea, in immune system health, in depression and anxiety, in insulin resistance, in obesity, and in inflammation. Because these critters are so significant for these issues, they are significant for just about every noncommunicable disease you can imagine.

Probiotics.org knows what's what.

Gut flora are incredibly important–perhaps the most important aspect of your body–for fighting off disease.

Why are gut bugs so important? Because your gut is the barrier between you and the outside world. Good gut flora help you process nutrients and protect yourself from toxins. When good gut flora populations decrease (as mine may have with my aspirin use), and/or when bad gut flora infiltrate the gut and outnumber the good guys, health problems ensue.

How it works: gut flora and cravings theory #1

One theory for how gut flora influence your gut – and there seems to be reasonable evidence for this – is that your gut flora condition you to continue to feed their own specific populations. Carrot-loving gut bugs beget carrot-loving gut bugs, for example (if a fair bit oversimplified.)

So gut flora from particular foods may make you continue to crave those particular foods. This is great if you eat a lot of natural, healthy foods. This is less good news if you eat a lot of processed foods. The more processed foods you eat, the more bad bacteria will reproduce. They will hijack your cravings, and you’ll crave even more of the same old bad food.

If you are a processed food / sugar junkie, it may be hard to switch your diet, but being sure to include good, natural, healthy foods like fruits, vegetables, animal products and fermented may help you crave those more and more.  Read my book, Sexy By Nature or Weight Loss Unlocked for my advice on the healthiest diet.

How it works: gut flora and cravings theory #2

The second theory, which is not exclusive but complementary to the first, is that good gut bacteria like bifidobacterium (these are the famous good guys) cause the body to produce satiation hormones.

Glucuagon-like-peptide-1 is one such satiation hormone. It increases in the “colonal mucus” (sexy, right?) of rats fed oligofructose, a laboratory carbohydrate that resembles the carbohydrates found in many fruits and vegetables.  PYY and ghrelin, two other satiation hormones, may also increase in response to oligofructose. Rats that consume oligofructose spontaneously eat less, cease creating fat cells, increase insulin sensitivity, and improved glucose tolerance.

As for humans…we already know that probiotics help with obesity. This happens via biochemical modulation of fat metabolism. Yet it also appears to probably happen via increased satiation and spontaneously reduced food intake.

The more bifidobacteria and other good gut flora you have, the more satiation hormones they will create in response to a meal.

A good probiotic supplement can help with this if you aren’t always able to include raw fermented foods.  This is my favorite supplement.  And here is my favorite book on fermented foods, if you’re interested in giving it a try!

Moral of the story

There are a lot of different physical and psychological components of food cravings.

For one – you need to eat food. I talk way too much to women who want to reduce food cravings but are eating 1200 calories a day. So be sure you eat when you are hungry all of the time, probably at least 1800 calories a day (though this varies widely), before you address any other issues.

Second, emotional issues should be dealt with. Is food your mother? Your addiction? Your stress-relief? Your boredom? Your celebration? Or  do you eat because you spend so much willpower trying not to eat that you end up overeating in the end? Psychological issues with food are also supremely important.

Third, you may consider physiological approaches. Sometimes the issue cannot be resolved psychologically because there’s an underlying problem. Amino acid therapy — boosting serotonin and dopamine levels by consuming precursors 5HTP and tyrosine — can help regulate appetite if your serotonin and dopamine levels are low.

Gut bugs can also help, as we’ve seen. (They can also boost your serotonin levels! Two birds with one stone!)

Consume fermented foods like kombucha, sauerkraut, kimchi, natto, or grass-fed yogurt or kefir. If those are not available to you, consider a probiotic supplement that contains at least bifidobacterium, as well as other varieties.

You can also try a probiotic supplement. I prefer whole foods since they provide they provide a high degree of variability of bacterial species. Nonetheless probiotics have been shown to improve weight loss and support mental health in studies, so if you go this route (like this option or this one) you can also benefit.

You can also support your gut flora population not only by eating the bugs themselves – which is what you do with the fermented foods – but by consuming their preferred foods. Gut flora love to eat fibrous fruits and veggies, particularly those which contain inulin. These are greens, summer squash, onions, garlic, leeks… and jerusalem artichokes are also a particularly good source. This article demonstrates just how effective this strategy is.

Kombucha (linked to my favorite brand on Amazon)  is really helping me. I can’t say if it will help you. Really, I cannot. We all have different bodies and we all have our own unique cures. But I love how much more stable my blood sugar feels and my meals are. I no longer feel so much like I must eat a sweet with every meal. I love my gut bugs very, very much. For this reason, as well as for so many others.

soft.net

soft.net

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.

The Physiology of Women’s Weight Loss Part II: Appetite and Weight Regulation

The Physiology of Women’s Weight Loss Part II: Appetite and Weight Regulation

In the first post I wrote on the physiology of women’s weight loss, I focused on the role estrogen plays in fat stores.  I noted at the end of the post that estrogen is involved with sending appetite-regulating signals to the brain.  This is an important factor in female weight loss.  Men have hormonal feedback that dictates their satiation, too, but their body is less attached to how much fat it has.  For a woman, having fat is crucial for pregnancy and childbirth.  For this reason, a woman’s body errs on the side of caution with respect to fat stores.  When in doubt, it screams “eat!”

I’ve done a lot of research on women’s weight loss and hormonal health.  My book Weight Loss: Unlocked can help you to lose weight, if you so choose, in a healthy and hormonally sound way.  My bestseller Sexy By Nature is also filled with incredibly beneficial information on women’s health.

What this means is that it is much easier for women to be barraged with physiological demands to eat.  These drives are not malicious things, and a woman can never be upset with her body for having them.  It’s natural, and it’s necessary for health.  Only by accepting our strong biological need for food as physiological fact can we women truly move forward with love, holistic healing, and positive, even pleasurable weight loss.

What follows below is an overview of the mechanisms by which women’s bodies “hang on” to fat stores.   This is not to say that the body wants to be overweight.  The body actually wants to be a proper, fit, attractive weight.  What happens is that normal weight-regulating factors get dysregulated by an inflammatory diet, and prolonged abuse drives a system further and further off-track.  The good news is that because a woman’s body wants to be an appropriate weight, once the woman starts treating her body with proper love and nourishment, the pounds naturally slide off.

Fat as a vital organ

Not too long ago, scientists thought that fat cells were simple units of energy storage.  Metabolism would grab the energy stored in the fat cells when it needed it, and then the fat cells would continue lying there inert.  Metabolism might deposit more energy into them at another time, and then later it would come grab the energy back.   Fat cells were considered storage units, and not anything more.

Since 1994 with the discovery of leptin, science has gradually unearthed the surprising notion that fat tissue is not just a storage space but is also an endocrine organ in and of itself.  Fat receives signals from hormones; it is actively involved in how much fat gets stored within its own reserves, and how; and it sends out potent signals of its own.  These signals are crucial.  They tell the brain how much energy is currently being stored in the form of fat.  Higher levels of leptin signal to the hypothalamus that an organism does not need to eat anymore.   Potent appetite stimulators such as neuropeptide Y and anandamide are inhibited by leptin in the hypothalamus, and the production of alpha-MSH, an appetite suppressant, is encouraged.  Though there are dozens of hormones and neurotransmitters involved in signalling appetite to and from the brain, what this demonstrates is that leptin more or less runs the show.   More leptin = less eating.

That is, unless the organism is leptin resistant.

Leptin resistance

Leptin resistance occurs when leptin has flooded a system.  In addition to originating in fat stores, leptin levels in the blood rise with food consumption.  Leptin 1) spikes after consumption of a large meal, particularly a carbohydrate-heavy meal, since leptin works in tandem with insulin, and 2) it sort of dribbles into the bloodstream if food is eaten in smaller quantities throughout the day.   So leptin levels rise whenever the body really thinks it has been well-fed.

Over-secretion of leptin is the primary means by which people dysregulate their leptin signalling, for example, if they eat too many meals without waiting for hunger to return in between them, or if they graze on food all day, or if they have a couple of snacks each day.   Basically, leptin resistance develops when normal weight-regulating drives are ignored.  This is easy to do in the presence of highly palatable food and drink.  Other factors that can throw someone’s leptin signals under a bus are stress, loss of sleep, problems with neurotransmitters, or nutrient deficiencies.   Under the influence of these factors, or perhaps several of them in conjunction, it becomes difficult for a woman to hear the leptin signalling in her hypothalamus.

Once people begin ignoring their leptin signals, they get easier and easier to ignore.   This is because constantly elevated leptin levels cause leptin receptors to become insensitive to the leptin floating around in the bloodstream.  Then, as the body realizes that it’s normal leptin signalling isn’t getting the job done, it incites more eating, more weight gain, and higher leptin levels in hopes that an increased leptin signal will get through.   For this reason, obesity is correlated with high leptin levels, even though many obese people complain of constant hunger.

Leptin resistance is a problem for everybody.  Both men and women.  Without fixing leptin sensitivity problems, it’s very difficult to lose weight, and it’s even more difficult to enact any kind of dietary restriction.   But women, who have higher levels of leptin than men (having higher body fat percentages) and who have HPA axes more attuned to energy conservation, are particularly sensitive to fluctuations in leptin levels.

Leptin and menstruation

Achieving a certain leptin level is the primary trigger for menarche (the first incidence of menstruation)   Stress, genetics, being exposed to smoking, and not being breast fed are other important factors.  So far as researchers can tell, throughout evolutionary history a woman’s period likely started around 15 or 16 years of age.  A few studies were conducted in the nineteenth century documenting menarche.    In 1850, girls began menstruating at an average age of 17;  by 1960 that age decreased to 13 years old.  Today in America,  approximately ten per cent of girls start to menstruate before 11 years of age, and ninety per cent of all US girls are menstruating by 13.75 years, with a median age of 12.43 years.   Both black and latino girls begin menstruating before white girls.

Many suspect that the higher body weights and higher leptin levels are responsible for the change in menarche.  A 2011 study found that each 1 kg/m2 increase in childhood BMI can be expected to result in a 6.5 per cent higher risk of menarche before  reaching 12 years of age.

Leptin and the reproductive set point

Knowing about puberty and menarche is so important for adult women because a woman’s reproductive functioning for the rest of her life is influenced by the conditions of her early reproductive years.  Having started menstruation with a certain leptin concentration in the blood, a woman’s body treats this as a “set point ” of sorts later on.   Having had a certain level of leptin, too, influences the young girl’s estrogen and progesterone levels,  such that these also become reproductive set points.  Therefore, if a woman drops too far below her set leptin or estrogen levels later in life by losing too much weight, her body will do its damndest to get those levels back up.  A similar phenomenon happens if she becomes overweight and leptin resistant.

Stimulating appetite in response to low leptin levels

The way a body tries to increase leptin and estrogen concentrations is to increase fat mass.  The way to increase fat mass is to increase appetite.  This is why leptin is such a potent signal in a woman’s brain.    With decreased leptin levels (or leptin insensitivity), appetite-stimulating neurons up-regulate powerfully.

Importantly, more women profess sugar addiction than men.  One of the neurons that detects decreasing leptin concentrations in the blood is called Neuropeptide Y.  Neuropeptide Y stimulates carbohydrate craving.   Women who are experiencing starvation– or at least women who’s hypothalama are detecting lower leptin levels than their bodies think are optimal — experience insidious carbohydrate cravings.

Are women stuck in leptin set points?

No.  Not necessarily.

The thing is, it’s complicated.  A woman’s body will never “want” to be overweight.   Women start menstruating at a certain leptin level and at a certain age, but even if this occurs at a very young age, the leptin is still around the same absolute level that another woman might experience, just many years earlier.   So her leptin levels, if higher earlier than optimal,  still are not shooting through the roof at menarche.

Moreover, if a young girl is overweight when she starts her period, at that time her body is probably fighting for and signalling a desire to lose weight.  It’s just not working because some of the signals have been disturbed by poor diet and lifestyle.   This woman’s body’s need for and desire to lose weight will persist for the rest of her life.   The hormone and appetite pathways are all still in place.  They are just begging to be restored to their normal function.   All the woman needs to do is listen, and to nourish her body properly.  In this way, it will be her partner in weight loss, rather than her adversary.

Other appetite stimulators

Appetite is stimulated via a few other important pathways.  They are not limited to women.  For example, an individual’s cravings for certain foods increases as a result of nutrient deficiencies.   Fluctuating insulin and blood sugar are important.  Stress is important.  Social conditioning, negative thought patterns, psychological responses to hardship, and body image issues also powerfully stimulate cravings.

Neurotransmitters as appetite stimulators

Perhaps most significant, however, is the relationship between neurotransmitters and food, specifically for women. When serotonin levels drop, cravings, again, particularly for carbohydrates, increase.  Serotonin levels can be disrupted by a vast number of problems.  These span from nutrient deficiencies to an omega 6 – omega 3 imbalance to poor sleep to obesity to exercise and to stress.    Serotonin levels also fluctuate with the menstrual cycle.  A drop in serotonin during the luteal phase (the last two weeks) of the menstrual cycle is thought to be by many the dominant cause of PMS.  This would explain why many women experience increased cravings for sweets throughout PMS.   These are natural, up to a point.  But PMS is an extreme fluctuation, and solving the underlying diet and lifestyle factors causing PMS should also decrease the wild swings in cravings that many women suffer throughout their menstrual cycles.

The role of neurotransmitters in appetite deserves several posts of its own.  They are forthcoming.  For now, it suffices to note that neural mood regulators are strong links between a woman’s reproductive system and her weight regulation mechanisms.  Sub-optimal serotonin levels in particular increase carbohydrate cravings.

All that said…

Women come equipped with a system designed to maintain adequate fat mass.  If a woman is overweight, it’s because the normal weight regulators she has in place are not receiving the proper nourishment required for effective signalling.    Leptin insensitivity, in the case of an overweight woman, or low leptin levels, in the case of an underweight woman, compel her to eat and to eat and to eat.  Estrogen, as I noted in a previous post, is also a significant weight-regulator unique to women.  It, too, is disrupted with diet and lifestyle.  Therefore, with the restoration of the proper functioning of all of the underlying mechanisms at work in a woman’s body, specifically with leptin and with estrogen levels, a woman’s weight can slide off.  More on that in my upcoming post on the easiest, most natural way (paleo diet! decreased stress! self-love!) for women to lose weight.

Take a look at my latest book Weight Loss Unlocked for my plan to help women lose weight and my book Sexy By Nature for more on all things women’s health, confidence, and self love!

 

 

 

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.

Neuropeptide Y: Appetite, Macronutrients, and Yo-Yo Dieting, or, Why Restriction Breeds Carb-Addicts and Disordered Eaters

Neuropeptide Y: Appetite, Macronutrients, and Yo-Yo Dieting, or, Why Restriction Breeds Carb-Addicts and Disordered Eaters

Neuropeptide Y is one of several neuromodulators involved in regulating feeding.   These include classic neurotransmitters such as serotonin, GABA, or dopamine, molecules derived from fatty acids like endocannabinoids, and neuropeptides.   (All of which I will discuss at length eventually.)   Every neuromodulator can be classified as orexic or anorexic.  Orexic cells drive feeding.  Anorexic cells do the opposite.  Neuropeptide Y is one of the orexic cells, and it is in fact one of the strongest.

In the photo below (a snapshot I took of a page in an excellent textbook–Appetite and Body Weight by Tim C Kirkham) orexic and anorexic drivers are compared.  On the left are the orexics, on the right, anorexics.  Note how Neuropeptide Y and Leptin are situated at the top of the respective sides, demonstrating their antagonistic behaviors against each other.

 

So NPY is strongly orexic.  When injected into the brains of several species of animals, NPY induces several-fold increases in food intake at any time in the dark-light cycle.  Additionally, it is highly involved in the motivation and search for food.  NPY-injected animals are ravenous and incessant: they will eat even when they have to work really hard for it, even if they have to tolerate electric shocks, and even when the food is altered from the natural product and may in fact contain substances they have aversions to, such as quinine.   In animals lacking NPY, eating is delayed and the animal’s efforts at attaining food are sluggish.

NPY delays satiety throughout a meal.  Thus it augments meal size, time spent eating, and meal duration, irrespective of what food is provided.   Animals certainly have preferences for what to eat, but they will take anything and eat it at length if they cannot get their paws on sweet foods.  This action of NPY, along with other orexins, explains why many disordered eaters need to eat and eat and eat, regardless of how much they like the food.

The most fascinating aspect of NPY, however, in my opinion, is the way in which it interplays with macronutrient cravings.    NPY increases carbohydrate cravings first and foremost: NPY-injected animals show an enormous preference for sweet foods.   But NPY also has a fed-fasted-state feedback mechanism: after weeks of being fed either a high-carbohydrate or a high fat diet–so long as it is high calorie–NPY levels fall (though the animals certainly prefer the high-carbohydrate diet), and the animals stop craving carbohydrates that much.

This all occurs in light of the fact that when one is starving at all, NPY levels rise.  They rise in response to fasting, in response to chronic food restriction, and in response to any sort of starvation signal whatsoever, for example, a drop in leptin levels.   NPY levels also continue to increase as the time spent in the fasting state gets longer and longer.   This means that the NPY-driven craving for sweets increases as the fasted state endures.

Once regular feeding is restored, however, NPY levels fall back to baseline.  In this way,  NPY is meant to moderate energy consumption, with a clear preference for carbohydrates.  Why?  Because glucose is the fastest way to get a “fed” signal firing in the brain, at least on an immediate time-scale.   Glucose spikes insulin levels and therefore leptin, which in turn  signals to the NPY right away that the organism is fed.  However, the “fed” state must endure through longer time scales than one simple meal in which leptin levels spike.   Therefore, a long-term undertaking of feeding with any type of macronutrient ratios should be sufficient to mitigate NPY-related problems, so long as energy intake is sufficient to account for energy expenditure.    In the short-term, however, as mentioned, sometimes glucose is the only way to get the NPY neurons (as well as the hypocretin neurons responsible for wakefulness while hungry) to shut up.

This phenomenon explains in part the failure of so many diets.  Neuropeptide Y is one of the strongest stimulators of appetite, and is it triggered first and foremost by low leptin levels and caloric restriction.  Any detection of a fasted state will lead  to the organism craving carbohydrates moreso than usual, and the cravings won’t really subside unless the organism can convince the NPY neurons that it’s not starving.   Herein lies the rub: people restrict, and drives toward feeding rise.  In particular because of NPY-type drives, that drive is focused on carbohydrates.  The more successful a person is at restriction and at willpower, the harder and harder it gets to maintain that level of restriction.   Eventually the stamina fails, and the organism caves, often to a sweet food.  Recall that NPY delays satiation and prolongs feeding quantity and duration.  What this means is that this one bite of sweet food the person allows himself is all-of-the-sudden one thousand bites of sweet foods.  This willpowering individual feels awful about what he’s done, so he gets back into his routine of chronic restriction.   This is a hell of a cycle to be caught in.  My Pepper readers know this all too well.

Re: what NPY-type activity means for fasting and for ketogenic diets:

Glucose availability in the brain is important for NPY regulation.    Glucoprivation- that is, deliberately blocking glucose activity–has been shown to induce feeding and activate hypothalamic NPY neurons in rats.  What this means is that a brain that runs on limited glucose stores may have increased NPY activity.   Ketogenic organisms run on limited glucose stores.

Since many people who fast and/or undertake ketosis experience decreased appetite, there are clearly other, stronger mechanisms at play in the modulation of their appetite than NPY drives; for example, perhaps the simple strength of leptin sensitivity in signalling to the NPY is powerful enough in these individuals to squelch the drive to carbohydrates.   Or perhaps in some individuals moreso than others gluconeogenesis from the liver is functioning well-enough to get adequate glucose supplies to the brain.  I suspect that both of those ideas are in part true.  Nonetheless, NPY explains in part why some people binge so hard on sugar once they take a step off of the fasting or very-low-carb ladders, even if they are not in explicit restriction like the yo-yo dieters I mentioned above.

Many people talk about the addictive power of carbohydrates.  I agree–it’s horrible.  I’ve talked about it many times, and at great length.  Yet what might be worse in some cases is the physiological basis NPY demonstrates for carbohydrate longing.  And the role that restriction plays in the demonic need for sweet foods.   Being in a energy-restricted state might play one of the more powerful roles in why carbohydrate is so insidious in the contemporary American food psyche.

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.

Night Eating Syndrome: An Effect of HPA axis and Appetite Dysregulation (among other things)

Night Eating Syndrome: An Effect of HPA axis and Appetite Dysregulation (among other things)

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.  Thenso 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.

 

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.

Hypocretin Neurons: The Link Between Fasting, Stress, and Arousal, or, Why Fasting Breeds Insomniacs

Hypocretin Neurons: The Link Between Fasting, Stress, and Arousal, or, Why Fasting Breeds Insomniacs

There is a hell of a dichotomy occurring in the Paleo blogosphere this month.   99 percent of the time I am pleased as Pooh stuck up a honey tree, nestled in my esoteric corner of paleo-feminist rage, but every once in a while I wish more people could hear what I have to say.  Today is one of those days.

The split I am talking about is not all that nefarious.  In most cases, it’s benign and can be ignored.   But in general I would like to draw attention to it, because I think there’s a lot going on beneath the surface (and here, the depths are not just Nemo and Dory but are instead people’s lives), and that depth requires speaking to.  Immediately.

Mark’s Daily Apple has recently done a beautiful series on the benefits of fasting.   I loved it.  I learned plenty, as I always do on MDA.  The series was well-written and -organized, and in fact I ended up directing people who are unfamiliar with fasting to the site in hopes of swaying their opinions.   (So let it be clear: I am not against fasting per se.) Yet Chris Kresser has also done an April “Best your Stress” challenge.   Serendipitously enough, it concludes today.  And it is exactly what it sounds like: an endeavor to spend 30 days taking practical steps to counteract stress.  Chris’s idea was that people often spend 30 days trying to get their diets in line.  But what about their stress, and their lives?  I couldn’t agree more.   This man is a gale of fresh, important ideas.

The reason I say these two Big Themes are at odds is because they are.  Fasting is a stressor.  Period.  Mark Sisson would agree.  All people who advocate fasting would agree.  But all they ever do is put an asterisk at the end of their posts: *people who are stressed should probably not fast, they say.   But why?  Who is affected, and how?   What can fasting and other forms of restriction do to our brains, and to our lives?

What I want to draw attention to today are little loci that sit on the border of the hypothalamus called Hypocretin Neurons.    Hypocretin neurons (also called Orexins–and note that the word “orexin” means “appetite increasing”) were discovered just 14 years ago in 1998, but they have radically altered the landscape of eating neurobiology since then.   No, they are not the sole molecules responsible for sleep and waking.  Mice that have had these neurons removed still sleep and wake in roughly normal patterns.  But they never feel alert, and they never suffer insomnia.  And when the neurons are activated, the mice leap into action.  Hypocretin neurons wake animals up.  This much is certain.

The lack of Hypocretin Neuron signalling is the cause of narcolepsy, while elevated Hypocretin levels induce arousal, elevate food intake, and elevate adiposity.  Hypocretin Neurons  upregulate the production of molecules down several other pathways, too: these include noradrenergic, histaminergic, cholinergic, dopamine, and serotonergic.

The anatomy of Hypocretin Neurons is also coming into greater light.   When are the neurons active?  What signals do they receive, and what signals do they produce?     Research is beginning to show that Hypocretin Neurons are excited by excitatory synaptic currents and asymmetric synapses with minimum inhibitory input.   The fact of asymmetry is important.  It means that Hypocretin Neurons are instead always acted upon by mostly uniform – excitatory – signals they receive.    Hypocretin Neurons only ever up-regulate and relax.  They do not down-regulate.   Excitatory signals outnumber inhibitory signals 10:1.

One notable source of excitation is corticotrophin releasing hormone, which suggests that stress activates the activity of Hypocretin Neurons.    GABA neurons also create a bridge between Neuropeptite Y, which is the molecule that arguably has the strongest appetite-stimulating effect on the brain, and Hypocretin Neurons (more on Neuropeptide Y later this week).  From there, Hypocretin Neurons project to all regions of the brain, including the hypothalamus, cerebral cortex, brain stem, and spinal cord.   It seems as though Hypocretin Neurons may act as a nexus of signal input for the appropriate synchronization of various autonomic, endocrine, and metabolic processes.

Food restriction further augments recruitment of excitatory inputs onto Hypocretin cells.   This explains the relationship between insomnia and adiposity: because of the easy excitability of Hypocretin Neurons, any signal that triggers their activity, regardless of homeostatic needs, will elevate the need to feed in brain circuits such as the locus coeruleus and the melanocortin system while also promoting wakefulness through activation of noradrenaline-stimulating neurons.  Anything that promotes the release of corticotrophin releasing hormone (CRH) such as reduced sleep will further trigger Hyocretin Neuron firing and Appetite.   This is a vicious cycle.  Hypocretin Neurons play the role both of trigger and of accelerator, taking states of wakefulness, insomnia, stress, and obesity into continual positive feedback loops.

So how does leptin factor in?  Hypocretin Neurons express leptin receptors.   Moreover, some recent complicated neurobiological work done on mice has shown that injecting them with leptin decreases the activity of their Hypocretin Neurons.   What this means is that Hypocretin Neuron activity is stimulated in part by decreasing levels of leptin in the blood, and that increased leptin levels reduce the level of excitation running through Hypocretin Neurons.   This is coupled by ghrelin activity, which is also detected by Hypocretin Neurons.   Ghrelin, which originates in the gut and is known to stimulate appetite, also excites Hypocretin Neurons.   What does feeding do, then, for Hypocretin Neuron excitation?   Experiments on mice show that re-feeding restores normal Hypocretin activity, to an extent.  Repeated abuse takes longer to recover from, but the simple presence of leptin in the blood normalizes the brains of mice.

Hooray!  This is good for fasting, right?  So long as one re-feeds appropriately, everything should be fine?  Well, yes.  In a healthfully functioning individual.  But not in a) someone who is both stressed and leptin resistant, since increased leptin levels from the re-feed might not be powerful enough to offset other excitatory pathways b) someone who is currently emerging from yo-yo dieting or caloric restriction c) someone who is dealing with an over-stimulated appetite, d) someone experiencing stress, e) someone who has had a history of insomnia, f) someone who is underweight, since they have low leptin levels, g) anyone who has ever had an eating disorder, particularly bulimia or binge eating disorder or h) anyone with HPA axis or endocrine dysregulation, particularly women, including overt stress, hypogonadism, hypothalamic amenorrhea, hypercortisolism, or hypocortisolism (adrenal fatigue.)  I am sure the list is incomplete.

In animals, Hypocretin Neurons serve an important evolutionary function.  Arousal is a vital behavior in all species.    And normally, Hypocretin Neurons respond quickly to changes in input.  But in situations of chronic metabolic or endocrine stress, or of recovering from a stressor, they can lead to hyper-activity and hyper-feeding.

Researchers have long known about the link between leptin, sleep, and obesity.  The less someone sleeps, the lower her leptin levels, so the more she eats, and the heavier she gets.  Hypocretin Neurons may serve as one of the answers to the question of exactly how that phenomenon comes about.  Or at least it plays a role.  Because 1) Hypocretins simultaneously stimulate appetite and wakefulness, particularly through orexigenic output of the melanocortin system, and subsequent release of CRH, which activates the stress response, and 2) while Hypocretin Neurons wake us up, they also need to be quiet enough for people to go to sleep.

Finally, I raise the questions: how many disordered eaters have trouble sleeping?  How many anorexics, binge eaters, calorie restrictors, exercise-addicts, stressed-out individuals, and very low-carb dieters have trouble sleeping?   How many people try intermittent fasting and find that it disrupts their sleep or circadian rhythms?  How many people wake up in the middle of the night or early in the morning, even though they still need sleep, but for the life of them feel so awake?  Part of that answer lies in blood sugar metabolism, for sure.  And in other places.  Sleep is a hell of a complex phenomenon.  But here– Hypocretin Neurons can become overburdened by excitatory signals.  They get hyped up in the face of both decreasing leptin levels and leptin insensitivity.   They are upset by restriction, and they are upset by fasting.  Hypocretin Neurons demonstrate why so many people have difficulty with their appetite and their sleep.  If you find that fasting disturbs your sleep, or that you are suffering disordered circadian rhythms along with stress or appetite problems, do you best to relax your system.  Don’t fast.  Relax.  Exercise less.  Reduce stress.  Eat more.  Put on weight.  Eat more carbohydrates.  Don’t graze.  Increase your leptin sensitivity.  And listen to your body.

Coming up next: nighttime eating syndrome, and how it’s all related.

 

 

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So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.