One of the most common problems I encounter in my audience is binge eating. This is also one of the most common concerns Noelle and I field for our podcast. Everybody wants to know: How do I stop?
I have written about overcoming binge eating at great length before. In the article Binge/Restrict: The Most Common Pattern of Overeating and How to Stop, for example, I argue that while most people think the solution to binge eating is simply to be disciplined enough to get over it, the answer is actually the opposite. The answer, I argue, is to allow yourself abundance. The answer, I argue, is lots of food. Once you stop restricting your diet, you no longer feel the deprivation and obsession that inevitably cause you to overeat later on.
I do still believe that this is one of the most important things you can do to overcome binge eating. But I would like to discuss here the great, biochemical heft behind these processes.
Because here’s the thing: as much as society (and you!) may call you undisciplined, stupid, lazy, gluttonous, fat, insert demoralizing adjective here, for bingeing on whatever kind of food has hooked you, it’s wrong. It’s just plain wrong. You’re up against a huge set of biological, habituated compulsions. Bingeing behavior has now been proven to have potent biological motivators. And you must know it. I believe — I hope — that as you know it, so you may forgive yourself. Then you may more easily walk the path of healing.
To that end, I am going to describe two separate studies. These were both done on rats, so of course we cannot assume they to apply to humans. But there are human analogues and other human studies (such as on the science of sugar addiction – a topic for another time), that indicate the models may well apply.
Binge-Like Consumption of a Palatable Food Accelerates Habitual Control of Behavior and Is Dependent on Activation of the Dorsolateral Striatum
This study investigates the difference between constant, non-restricted access to palatable foods versus restricted access to palatable foods. It ends up revealing that just a few weeks of occasionally being exposed to bursts of sweetened milk cause rats to binge on it, as well as to maintain these eating habits even after the time restrictions have been taken away. It happens because of neural changes that have taken place during the “burst” period. These changes cause long-term habits to form.
Teri Furlong and colleagues at the University of Sydney gave rats a diet of either normal chow or chow plus sweetened condensed milk. The “normal chow” rats were the control group. The rats that received the sweetened milk were divided into two groups: half got milk all day every day, as much as they wanted. The other half got access to the sweet stuff for only two hours every day.
After five weeks, the scientists trained all of the rats to press levers. There were two levers: one for sweet sugar pellets and one for simple grain pellets. In the test, the animals feasted on one of the types of food (either the sugar or the grain) and then exposed to a lever. In the first scenario, rats saw the lever for food they hadn’t yet had. If they had eaten sugar, they got grain. If they had eaten grain, they got sugar. In this scenario, all the rats ate a lot of the new food. Tastebuds like variety.
In the second scenario, the rats were given access to levers for the food they had already eaten. So if they had eaten sugar, they got a lever for sugar, and if they had eaten grain, they got a lever for grain. And this is where things really get interesting: rats who had had constant access to the sweetened milk in the training phase ate to satiety. They stopped pressing the lever. They had no interest in either the grain or the sugar. But, rats who were only allowed access to the sweet milk for two hours a day (and for the rest of the day, as much unsweetened food as they wanted), responded differently. They kept pressing for grain, even though they were already full of grain, and they kept pressing for sugar, even though they were already full of sugar. They weren’t pushing these levers because they were hungry. They were pushing these levers because having restricted bouts of access to sweet foods rewired their brains.
Interestingly enough, the researchers found that the obsessive lever-pressing was associated with an area of the brain called the dorsolateral striatum–an area of the brain associated with habitual behaviors. The researchers therefore hypothesize that rats develop long-lasting bingeing behaviors because of the repetitive training they had from the easier phase of the study. In that phase, they simply learned that the sweet stuff was rarely available, so they stuffed their faces when they could. This imprinted in them a long term habit.
Importantly, chemicals injected into their brains that interfered with glutamate and dopamine activity in the dorsolateral striatum caused the bingeing behavior to stop.
In this study, MM Hagan and DE Moss subjected rats to four different patterns of 12-week restriction-refeeding cycles. The animals were either food restricted–constantly on a diet–or restricted plus some free-access binge days. After 12 weeks all rats underwent a re-feed period.
There were four different groups of rats: 1) “normal diet” eating with normal chow in the refeed period, 2) cyclical restricted eating (bingeing) with normal chow in the refeed period, 3) “normal diet” eating with palatable food in the refeed period, and 4) cyclical restricted eating (bingeing) with palatable food in the refeed period.
The rats that ate the “diet eating” consistently received 75% of their normal calorie intake. The rats with cyclical restricted eating went through 4 days of restriction of 75% of their normal intake, then two days of a refeed where they could eat ad libitum.
After 12 weeks of this kind of entrainment, the rats were given 3 tests: 1) 24 hour deprivation and chow feeding; 2) 24 hour deprivation then chow and cookie feeding; 3) spontaneous chow and cookie feeding.
In the first test, with 24 hour deprivation and chow feeding, the rats which had gone through restricted cycles of feeding (on both normal and sweet food) ate 10% more food than the control rats. Interestingly enough, the rats that had been conditioned on sweet food were not all that interested in the chow feeding, and actually ate 20% less chow than the control group.
In the second test, with 24 hour deprivation and cookie feeding, rats that had been in sweet restricted cycles ate almost 20% more food than the control group.
In the third test, in simple spontaneous feeding without a 24 hour deprivation window, rats conditioned by sweet foods ate more than rats on normal chow, regardless of whether they had been restricted or not. The rats who ate non palatable chow and were on normal “diets” were perfectly fine; the rats who had eaten sweets but were on a normal diet ate about 20% more; the rats who had been in restricted cycling patterns and refed on sweets ate 80% more than control mice on normal diets. 80% more.
Researchers in this study conclude, therefore, that “of all the conditions, the restricted/palatable group showed the most bulimic-like eating behavior. That is, a history of restricted eating (dieting) and refeeding on palatable food (bingeing) predicted a persistence of bingeing-eating behavior even after a 30-day period of normalization.”
Other Studies and implications
Of course, these are just two studies, and have been conducted on rats. There are plenty of indicators that similar phenomena are at play in human beings. Recall perhaps most strikingly of all the Minnesota semi-starvation experiment in which “normal men” were food restricted and showed binge eating and insatiable appetites for sweet foods even after many days of unrestricted eating during the rehabilitation phase (Franklin et al 1948). In the 90s, Polivy et al “found that uncontrollable bouts of binge eating were significantly more common among prisoners of WWII who had, over 50 years earlier, experienced severe food restriction compared with nonrestricted combat veterans” (1994).
Via experiments on rats, we can see more clearly mechanisms by which this takes place. Apparently, pleasure neurotransmitters (such as dopamine) are definitely involved, as are, to a significant extent, the parts of the brain that are associated with habit formation.
The bottom line is this: your history of dieting, of binge eating, of restricting and refeeding, has had a concrete affect on the functioning of your brain. I can’t tell you how many thousands of women have expressed terrible guilt and shame with respect to their bingeing behaviors. They are all incorrect. If you feel this way, you are also incorrect. Your biology compels you, and powerfully so.
As I indicated in the start of this post, literally the best thing you can do for yourself is to forgive yourself. Give yourself access to food, and unlimited. Accept your body and delight in how hard it tries for you. Provide it with the nourishment it needs to develop new habits. It may feel rough at first, but over time the body can actually learn to eat well. You may also find that staying away from sweets or certain palatable foods is important. So long as this does not cause you to develop obsessions with these foods, that could be good. It would remove the biological trigger of habit that you have imprinted in your brain. Even switching to a different set of palatable foods could help (so long as your access is unrestricted). They key here is developing a positive, loving, forgiving attitude and helping your body create new habits.
You may also wish to supplement with low doses of l-tyrosine and/or l-tryptophan. These are precursors to dopamine and serotonin, respectively. They have been demonstrated to sometimes be quite potent for curbing people’s compulsions to overeat (an argument famously made by Julia Ross in The Diet Cure). I have personally noticed that when I take L-tryptophan (I take it for sleep) my constant feeling of “I could eat” disappears, and I feel more like a “normal person.”
Do you have experience that lines up with what I’ve discussed here? Contradicts it? I’d love to hear about what you’ve gone through, and anything you share could be a great help to someone else in the community.
Today I want to talk to you about a very sensitive and challenging issue.
It’s an issue I see constantly. I get emails daily from women who struggle with this stuff.
And it SUCKS.
I see too many women in my life constantly battling with food and their weight.
Is that you?
If it is, I want to talk to you!
I want to talk to those of you who are constantly searching for the perfect diet, and constantly falling off the perfect diet.
Are you constantly swinging between “this time I’ve got it,” and “what the hell is wrong with me that I can’t stop eating peanut butter out of the jar?”
Are you always judging yourself based on what you ate that day or whether or not your skinny jeans fit?
Do you generally let food and weight concerns rule your world — the ups and downs of the diet-binge cycle dictating your “good” or “bad” days.
I’ve lived this stuff.
I’ve lived a life that revolved around the food I put in my mouth, the exact quantity and macronutrient profile.
I’ve lived a life of food obsession and poor self-esteem.
Isabel Foxen Duke, my friend and founder of Stop Fighting Food, calls this “feeling crazy around food.”
Isabel is one of the most well-respected pros in the emotional eating world, contributing some very new ideas about how we can change our thought-patterns around food and weight, and finally break out of the exhausting diet-binge cycling behaviors that too many women find themselves trapped in — behaviors like, sneak-eating ice cream in the middle of the night; yo-yo dieting; emotional eating, and emotional eating’s painful cousin:binge-eating.
Many of my readers have worked with Isabel and her programs and have found her to be uniquely supportive and able to help them understand what is going on in their minds, and get back on the right track.
She’s got a wonderful, witty perspective that will keep you laughing and she drops truth bombs like nobodies business.
Isabel’s offering a free video training series this month, (Find it here) covering some of her most important concepts in changing women’s relationship with food on an emotional and psychological level.
If this is a topic that speaks to you, I highly recommend you sign up to get her free vids.
You don’t have to live your life clinging desperately to diets, only to end up with your fingers in a jar of Nutella at the end of the day.
You don’t have to live the rest of your life feeling bat-shit crazy around food.
Here’s the link again to sign up for this free training.
Let us know how you try to fight feeling crazy around food!
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.
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):
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 (here, here, here, 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.
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.
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!
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:
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.
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.
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.
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!” So how is weight loss related to leptin resistance?
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 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, that once a woman starts treating her body with proper love and nourishment, the pounds naturally slide off.
The organ you never knew you had
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 the discovery of leptin in 1994, 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 signaling appetite to and from the brain, what this demonstrates is that leptin runs the show.
More leptin = less eating.
That is, unless the organism is experiencing leptin resistance
Could you be leptin resistant?
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.
1) Leptin spikes after consumption of a large meal, particularly a carbohydrate-heavy meal, since leptin works in tandem with insulin
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 signaling. For example, if they eat too many meals without waiting for hunger to return in between them, or if they graze all day, or if they have a couple of snacks each day. Basically, leptin resistance develops when normal weight-regulating drives are ignored.
Contributing factors of leptin resistance:
Under the influence of these factors it becomes difficult for a woman to hear the leptin signaling 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. As the body realizes that it’s normal leptin signaling 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. 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 resistance 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 10% of girls start to menstruate before 11 years of age, and 90% 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. This certain level of leptin influences the young girl’s estrogen and progesterone levels, that these also become reproductive set points. 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 experiences leptin resistance.
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 is 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. 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 signaling 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.
Unexpected 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 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 signaling. Leptin insensitivity and leptin resistance, in the case of an overweight woman, or low leptin levels, in the case of an underweight woman, compel her to eat more. 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 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!
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.