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“How Do I Know When It’s Working?” A Quick Troubleshooting Guide to Paleo

April 15, 2013 in FAQ, FAQ, How To Get Started

yoga1It’s a question that many people new to paleolithic nutrition ask either while they are going through that initial adjustment period (especially when jumping into paleo with both feet but also with gradual transitions) or as the months wear on and the difference is not as magical as anticipated.  How do I know when it’s working?  When will I start to lose tons of weight and have lots of energy?  When will my health conditions miraculously disappear?

Well, the answer is “it depends”.

How different did you eat before committing to paleolithic nutrition?  Generally, the more different you are eating now to before you discovered paleo, the harder and longer your adjustment period.  This is especially true if you ate a lot of carbohydrates before.  It can take up to a month for your body to switch over to a metabolism that runs better on fat and in the meantime, you may feel tired, lethargic, have headaches, and generally feel pretty terrible.  But, this isn’t true for everyone.  And of course, the opposite can also be true:  some people are made so sick by the foods they were eating before that they notice an instant improvement to their health.

What health issues are you challenged with?  In my personal experience, most gut health issues will improve dramatically the first couple of weeks on paleo and then continue to improve slowly over the next six months as your gut continues to heal (for more posts on gut health, see here and here).  Issues relating to inflammation typically take longer to show significant improvement depending on how well you are sleeping and managing your stress (typically another month or two).  Remember that for many health issues, you need to address all of the tenants of a paleolithic lifestyle (get good sleep, manage stress, get outside).

Are you in autoimmune denial?  I was.  While out-of-the-box paleo tackled most of my health issues, I still had unresolved autoimmune issues even after four months of strict paleolithic nutrition.  I had to do the autoimmune protocol (I’ve written about the autoimmune protocol extensively and this is also the topic of my book), in which you also exclude all the gray area foods.  If you have been eating a strict paleolithic diet for two months and are still dealing with health issues, you might have to do this too.  The good news is that after a few months of no eggs, no nuts, no seeds, no nightshades, no alcohol, no NSAIDs, low caffeine and no cheating, with a concurrent focus on eating extremely nutrient-dense foods (lots of vegetables, grass-fed meat, organ meat, fish and bone broth), most people can add at least some of those things back in.

Is your gut in REALLY bad shape?  It is possible that your gut was very leaky before you started paleo, so healing is just plain ol’ going to take a while.  Especially, if you suspect that you have Small Intestinal Bacterial Overgrowth or extensive gut damage, you’ll need to focus on Repairing The Gut, which can take 6 months to 2 years (although you should see continuous gradual improvement).  For all of the posts I’ve written on gut health, click here.

stomach acidHow is your digestion?  You might need to add some digestive support supplements for a little while to help your body heal.  These include digestive enzymes, ox bile, and stomach acid supplements (which are contraindicated for those with ulcers, blood clotting disorders, or taking NSAIDs).  Digestive enzymes and ox bile, while they can be expensive, are generally very safe to take as directed on the bottle (just make sure you actually eat once you take digestive enzymes because taking them and then not eating can cause damage to your gut).  If you are interested in a stomach acid supplement, check out my post on stomach acid here and this post by Steve Wright.

Do you have unknown food sensitivities?  If you’ve had a leaky gut for some time, you may have food sensitivities that you are unaware of.  Many alternative health care practitioners will order an IgG and/or IgA antibody screen which tests for food sensitivities.  The good news is that if you leave those foods out of your diet for a while, you can usually add them back in after your gut has fully healed.  If you have symptoms of Irritable Bowel Syndrome (like diarrhea, constipation, gas, bloating, acid reflux), another possibility is a FODMAP sensitivity.  Other potential culprits include salicylate sensitivity and food allergies (such as latex allergies, citrus, fish and shellfish, tree nuts, eggs, and dairy).

Do you need liver detox support? If you had/have an overgrowth of bacteria or yeast in your gut that are now dying off in great numbers, your liver might be working in overdrive.  B-vitamins (rich in red meat and organ meat), sulfur (rich in cruciferous vegetables and vegetables from the allium family), selenium (rich in seafood and organ meat) molybdenum (rich in organ meat) are important to support the liver.  Milk thistle (extract or tea) may also be helpful.  Choosing foods rich in these substances (or supplements) to help support liver detox is also useful for anyone losing weight, especially if the weight is coming off quickly.  This is because the body uses the fat tissues to store some toxins and excess hormones like estrogen (which gets them safely out of the body’s circulation) and rapid weigh loss has the potential to release these putting an additional strain on the liver.

Are you sleeping enough?  Yes, this has nothing to do with diet.  But sleep has a profound effect on every system in your body and if you are not getting enough of it, you can’t heal properly.  Aim for 8-10 hours per night in a pitch black room (see this post if you’re having trouble getting good sleep).  You can read more about the importance of sleep on the immune system in this teaser excerpt from The Paleo Approach.

Are you stressed? If you are not taking adequate measures to manage your stress (like getting activity but avoiding excessively strenuous exercise, spending time outside, having fun, getting enough sleep and developing strategies to manage psychological stressors), then your stress hormones might be out of whack.  If you have been under high stress for a long time and have trouble sleeping, you may have adrenal fatigue.  Both www.RobbWolf.com and www.BalancedBites.com have lots of great suggestions for healing from adrenal fatigue.

Did you go too low carb? What types of carbs (fruit versus starchy vegetables versus both versus neither) and how many carbs we should eat (varying from ketogenic diets and 20g per day to plenty of “safe starches” and upwards of 300g per day) is probably the most hotly debated topic within the paleo community.  One of the reasons for there being no clear answer as to what is best is that the carb intake of historically-studied and modern hunter-gatherer populations varies wildly.  On one end of the extreme are the Eskimos, who consume a diet composed approximately of 50% fat, 35% protein and 15% carbohydrate.  On the other end of the extreme are the Kitavans, who consume a diet composed approximately of 20% fat, 10% protein and 70% carbohydrate.  And of course, everything in between.  This probably reflects the fact that macronutrient ratios are not as important as food quality and nutrient density.  So, if your introduction to the concept of paleo was through a resource that expounded on the benefits of low carb, it is important to understand that this view is not representative of the entire paleo community and no consensus exists.  It’s also important to understand, that while blood sugar regulation is extremely important, going too low carb can be tough on your thyroid and can decrease leptin sensitivity (see this post and this post).  Also, eating adequate carbohydrates and especially insoluble fiber is important for proper regulation of ghrelin levels (see this post).  So, what is a good carbohydrate intake?  That’s actually highly individual (you can read this series of posts about optimizing your carb intake here, here and here), but if you are not feeling very good on a standard paleo diet, adding a little fruit or starchy vegetables is a good idea to try.

Are you inappropriately IFing? There are many enthusiastic supporters of Intermittent Fasting, but it’s important to understand that this is only appropriate for very healthy people.  If your sleep is not great, if your stress in not managed, if you are substantially overweight or if you have any kind of chronic disease, skipping breakfast (or breakfast and lunch) can cause dysregulated cortisol and undermine your other efforts.  This is not something to experiment with early on in your paleo journey.

What are your goals and how far away from them are you?  If you have a lot of weight to lose, you will probably notice a big drop in weight fairly quickly.  This will be mostly water weight, but don’t worry, fat is also being burned and you should eventually settle down into some nice steady weight loss (slow and steady wins the race, so there is no reason to be frustrated with weight loss if you are “only” losing a half pound per week-that’s actually very healthy!).  When your body seems resistant to weight loss, try addressing sleep quality and stress levels, but also be aware of the impact of female hormones and hunger hormones (levels and sensitivity).  For more tips and tricks for losing weight, see this post.

gray foodsAre you truly complying with paleolithic nutrition?  There are few things worse than being “almost paleo” (depending on your health challenges and what “almost” actually means for you).  While many people can successfully navigate the murky waters of cheats and occasional gluten consumption, if you are asking the question “when will I feel fabulous” while not actually following a paleo diet as strictly as you can, then you might be a person who just can’t cheat or tolerate occasional gluten exposure.  And from a metabolism, hormone and taste-bud adaptation standpoint, allowing yourself the occasional slice of pizza or pie a la mode can really derail your efforts to get healthy and perpetuate cravings, food addictions, and feelings of deprivation.  I advise eating very strict paleo for at least a month before you play with eating small amounts of dairy or legumes or allowing yourself cheat meals (and I recommend a lifelong avoidance of gluten for most people).  If strict paleo isn’t enough to make you feel great, look at the gray area foods in your diet (eggs, nuts, seeds, nightshades, alcohol, caffeine).  Maybe one of them is the culprit (nightshades are my number one suspect).  But if you are truly sticking to it, my guess is you are already feeling much, much better!

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Teaser Excerpt from The Paleo Approach–The Importance of Sleep

April 4, 2013 in Practical Tips, Stress and Sleep, The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneThere are many topics that I am researching and writing about for the book that I’ve been meaning to write about for the blog for ages (the book just gives me a firm deadline). I have decided take some of these topics (especially the more blog-sized ones) and publish them as teaser excerpts for the book (also because I think this information should be here too).

The book also contains a detailed (yet easy-to-follow) description of the components of the immune system, including a great quick reference guide to help you as you read through the book.  So, when you read this section in the book, you’ll already know why modulating Th1, Th2 and Th17 cells is important and you’ll already understand the essential role that regulatory T-cells play in the immune system.  

For a quick primer: Th1, Th2 and Th17 cells are subtypes of lymphocytes (white blood cells) that can be over-activated in autoimmune disease and cause damage. Regulatory T-cells are another subtype of lymphocyte that are supposed to keep all the other immune cells in check and suppress both over-activation of the  immune system and autoimmunity (they tend to be deficient in autoimmune disease). Cytokines are chemical messengers of inflammation. Monocytes and neutrophils are types of white blood cell responsible for generalized inflammation (part of the innate immune system whereas B-cells and T-cells are part of the adaptive immune system).  B-cells are the type of lymphocyte that produce antibodies.

So, forgive the references to Chapter 7 and page numbers with no number. While you’ll have to wait until the book is out in September to read those sections, in the meantime, please enjoy this part of Chapter 4:  Lifestyle Factors That Contribute to Autoimmune Disease.

Excited to read The Paleo Approach?

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Want to help spread the word about my book?  Please share this post and other teaser excerpts.  Thank you!

“A good laugh and a long sleep are the best cures in the doctor’s book.”

–Irish Proverb

In the last 50 years, the average amount of time that Americans sleep each night has decreased by 1.5–2 hours.  That’s a staggering amount of sleep—equivalent to a full month of continuous sleep every year—that we need but are not getting.  Epidemiological studies show a strong correlation between short or disturbed sleep and obesity, diabetes and cardiovascular disease.  In fact, lack of adequate sleep has been associated of increased morbidity and mortality from all causes.  This means that if you consistently don’t get enough sleep, you have a much higher risk of getting sick and/or dying.  Period.  Studies have also evaluated the role that sleep plays in healing from specific diseases, like breast cancer, and show that the less you sleep, the less likely you are to survive.

Frankly, scientists still don’t really understand why we need sleep, why we need as much as we do, and what our bodies are actually doing while we sleep.  But, it is obvious that sleep is important for human health.  Studies that evaluate the physiological changes caused by not sleeping or not getting enough sleep can be very instructive in understanding just how critically important sleep is.  For those with autoimmune disease, it is especially important to understand the role that sleep has in inflammation, stimulating the immune system, and regulating hormones (which themselves modulate the immune system).

Just plain old not getting enough sleep causes inflammation even in young, healthy people.  A variety of studies evaluating the effects of acute sleep deprivation (typically by restricting sleep to 4 hours per night) for several consecutive days (typically 3 to 5) have shown increases in markers of inflammation and the numbers of white blood cells in the blood.  Specifically, even just three consecutive nights of not enough sleep can cause increased monocytes, neutrophils and B-cells in the blood, increased proinflammatory cytokines (including cytokines known to stimulate maturation of naïve T-cells into Th1, Th2, and Th17 cells), increased C-reactive protein (a marker of inflammation), increased total cholesterol and increased low density lipoprotein cholesterol (LDL).

Even just one night of lost sleep (40 hours without sleep) causes inflammation in young, healthy people.  Just pulling a single all-nighter dramatically increases markers of inflammation in the blood, including C-reactive protein and proinflammatory cytokines.  Studies that evaluated not just sleep deprivation but also recovery after sleep restriction (with the idea of simulating a typical workweek where someone might get less sleep for 4 or 5 nights straight and then try to make up for it on the weekend) have also shown that the proinflammatory cytokine known to stimulate Th17 cell development persists for at least two days after increasing sleep to 8 hours per night, even though other markers of inflammation have recovered.  This means that even if you try and “catch up” on your sleep during the weekend, the stimulation to the immune system keeps going.  If you follow this stereotypical pattern of not getting enough sleep during the week and sleeping in on the weekend, you still run the risk of cumulatively causing detrimental changes in the immune system.  Certainly, you can recover from lack of sleep, but it takes persistence, consistency and commitment—even during the week.

Sleep deprivation is also associated with increased susceptibility to infection.  In fact, the less sleep you get, the more likely you are to catch the common cold.  Getting adequate sleep can also protect you from infection.  One study even showed that the longer the sleep duration, the lower the incidence of parasitic infections in mammals.

Inadequate sleep also has profound effects on hunger hormones and metabolism (recall that hunger hormones such as insulin, leptin, ghrelin, and cortisol are important modulators of the immune system, see page ##, ## and ##).  For example, when food intake is measured following sleep deprivation (5 consecutive days of 4 hours sleep), people tend to eat substantially (20%!) more than normal.  However, it doesn’t take five full days of inadequate sleep to see dramatic effects on insulin, cortisol, and leptin.  One study showed that even a single night of partial sleep (4 hours) causes insulin resistance in healthy people.  Another study showed that a single night of partial sleep (3 hours, in this case) caused reduced morning cortisol levels (when cortisol should be its highest) and elevated afternoon/evening cortisol (when cortisol should be gradually decreasing) and elevated morning leptin levels.  This means that one night of three or four hours sleep causes insulin resistance, dysregulated cortisol and increased leptin.  One late bedtime because you went to a late night movie or a party at the boss’ house.  One.

Inadequate sleep has also been investigated as a possible cause of autoimmune disease. In an animal model of psoriasis, sleep deprivation caused significant increases in proinflammatory cytokines, cortisol levels, and increases in specific proteins in the skin associated with symptoms of psoriasis (like the flaking, dry, scaly skin).  In an animal model of multiple sclerosis, mice subjected to sleep deprivation developed the disease earlier than mice that slept normally.  Once the mice developed multiple sclerosis, sleep deprivation caused increased disease activity and pain sensitivity.  Furthermore, sleep disturbances are commonly reported by people with chronic inflammatory conditions (such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease and asthma).  Whether the sleep disturbances cause the disease or the disease causes the sleep disturbances is not well understood.  However, such sleep disturbances are known to worsen the course of the disease, aggravate disease symptoms such as pain and fatigue, increase disease activity and lower quality of life.  Yes, sleep is important.

So, how much sleep do you need?  There is no clear answer to this.  Consensus is that healthy adults need 7-10 hours of sleep per night.  If you are trying to heal from an autoimmune disease, don’t be surprised if what your body needs is on the longer end of that range (say 9 to 10 hours) or even exceeding that range (some people with autoimmune disease report needing 12 hours of sleep every night to heal).

Getting enough sleep isn’t just about preventing inflammation; it’s also about repairing the body and modulating the immune system.  Certainly, the process of tissue repair in the body is predominantly performed during sleep.  However, an important study showed that regulatory T-cell activities follow a circadian rhythm, meaning that, just like many functions within the human body, they increase and decrease throughout the day.  In healthy people, regulatory T-cells are highest in the blood at night with lowest numbers in the morning (similar to melatonin production and the opposite of cortisol). The activity of the regulatory T-cells also follows a circadian rhythm, having the highest suppressive activity during sleep and lowest in the morning.  When volunteers were subjected to sleep deprivation, the suppressive activity of their regulatory T-cells was decreased (even though the actual numbers of T-cells remained the same).  This implies that sleep is required for the suppressive activity of regulatory T-cells, meaning that if you want to modulate your immune system and reverse your autoimmune disease, sleep is critical.

If you have an autoimmune disease (I generally assume you do if you are reading this book) and aren’t getting 8 hours of good sleep every night, I cannot emphasize enough the importance of putting sleep on the top of your priority list.  You need sleep.  Now.  Tonight.  Every night.  Seriously, stop reading and go to bed.  Strategies for prioritizing sleep and what to do if you are trying to get more sleep but just can’t are discussed in Chapter 7.

Bollinger, T., et al., Sleep-dependent activity of T cells and regulatory T cells, Clin Exp Immunol. 2009 Feb;155(2):231-8

Bosy-Westphal, A., et al., Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women, Obes Facts. 2008;1(5):266-73

Boudjeltia KZ, et al., Sleep restriction increases white blood cells, mainly neutrophil count, in young healthy men: a pilot study, Vasc Health Risk Manag. 2008;4(6):1467-70.

Donga, E., et al., A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects, J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8.

Frey, D.J., et al., The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults, Brain Behav Immun. 2007 Nov;21(8):1050-7

Heslop, P., et al., Sleep duration and mortality: The effect of short or long sleep duration on cardiovascular and all-cause mortality in working men and women, Sleep Med. 2002 Jul;3(4):305-14.

Hirotsu, C., et al., Sleep loss and cytokines levels in an experimental model of psoriasis, PLoS One. 2012;7(11)

Lehrer S, et al., Insufficient sleep associated with increased breast cancer mortality, Sleep Med. 2013 Mar 4 pii: S1389-9457(12)00384-X. doi: 10.1016/j.sleep.2012.10.012. [Epub ahead of print]

Lucassen EA, et al., Interacting epidemics? Sleep curtailment, insulin resistance, and obesity, Ann N Y Acad Sci. 2012 Aug;1264(1):110-34

Meier-Ewert HK, et al., Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk, J Am Coll Cardiol. 2004 Feb 18;43(4):678-83.

Palma, B.D., et al., Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus, Am J Physiol Regul Integr Comp Physiol. 2006 Nov;291(5):R1527-32.

Palma, B.D. & Tufik, S., Increased disease activity is associated with altered sleep architecture in an experimental model of systemic lupus erythematosus, Sleep. 2010 Sep;33(9):1244-8.

Ranjbaran, Z., et al., The relevance of sleep abnormalities to chronic inflammatory conditions, Inflamm Res. 2007 Feb;56(2):51-7.

Reynolds AC, et al., Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men, PLoS One. 2012;7(7)

van Leeuwen WM, et al., Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP, PLoS One. 2009;4(2)

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The Hormones of Hunger

January 29, 2013 in Hormone Regulation

I want to delve into the effects of diet and lifestyle on hunger and satiety signals in a series of upcoming posts.  I am mostly interested in the hormone dysregulation that occurs during metabolic syndrome, but also in how to optimize diet, exercise, sleep and stress management to achieve an ideal weight.

The feeling of hunger is regulated by a complex system of hormones that interact with neurotransmitters and neurotransmitter receptors within the hypothalamus region of the brain.  These hormones essentially activate or deactivate specific neurons in the hypothalamus that control hunger.  These neurons have receptors to Neuropeptide Y (NPY), the essential neurotransmitter in regulating hunger.  The hormones can increase or decrease hunger either through binding the receptors for NPY or increasing or decreasing NPY itself.  Essentially a hormone will increase hunger if its expression activates these NPY neurons whereas you will feel satiated if a hormone’s expression deactivates the NPY neurons.  The interplay between these hormones and your brain is complex and only partially understood.  However, what scientists do know about these hormones can help inform our decisions and compulsions regarding diet and other lifestyle factors. 

New hormones continue to be discovered and their roles in regulating appetite, satiety, metabolism and digestion continue to be studied.  As the full list of hunger hormones grows, understanding the complex interplay between these hormones, the types of food you eat, and the amount of muscle and fat on your body quickly becomes overwhelming.  I have tried to summarize the key players (at least as scientists currently understand them):

Hormones that tell your body you’re satiated:

Cholecystokinin (CCK) is secreted by the cells that line the duodenum (the first segment of the small intestine) when they detect the presence of fat.  This causes the release of digestive enzymes from the pancreas and bile from the gallbladder.  Increased levels of CCK signals to the stomach to slow down the speed of digestion so the small intestine can effectively digest the fats.  CKK is also a neuropeptide similar to NPY and has a direct action on neurons in the brain to signal satiety.  This is the most immediate hunger suppressing signal and is the reason why eating fat with your meals is so important.

Oxyntomodulin is released in response to protein and carbohydrates in the stomach and signals a change in energy status to the brain.  Oxyntomodulin enhances digestion by delaying gastric emptying and decreasing gastric acid secretion.

Peptide YY (PYY) is released by cells that line the jejunum, ileum (the next two segments of the small intestine) and colon in response to feeding and is especially sensitive to protein.  PYY signals to the gallbladder and pancreas to stop producing digestive enzymes.  PYY is important in increasing the efficiency of digestion and nutrient absorption after meal by slowing down gastric emptying, slowing down the speed of digestion, and increasing water and electrolyte absorption in the colon.  PYY interacts directly with NPY receptors in the hypothalamus in an inhibitory fashion, thereby turning off hunger signals.

Glucagon-Like Peptide-1 (GLP-1) is secreted in the ileum in response to carbohydrate, protein and fat.  It rapidly enters the circulation and is one of the fastest and shortest-lived satiety signals.  It inhibits acid secretion and gastric emptying in the stomach.  GLP-1 also increases insulin secretion and decreases glucagon secretion.  GLP-1 decreases hunger signals by reducing the amount of NPY.

Leptin plays a key role in regulating energy intake and energy expenditure, including appetite and metabolism.  Leptin is released both by adipocytes (fat cells) and by the cells that line the stomach, so it signals both that the body is fed and that there is sufficient energy storage.  This appetite inhibition is long-term, in contrast to the rapid inhibition of eating by CCK and the slower suppression of hunger between meals mediated by PYY.  Leptin both rapidly inhibits NPY production and deactivates NPY neurons in the brain to signal that the body has had enough to eat, producing a feeling of satiety. It is one of the most important adipose derived hormones (read more in this post).

Adiponectin is secreted from adipose tissue into the bloodstream where it signals decreased gluconeogenesis (when the body converts fats and proteins into  glucose for energy), increased glucose uptake, lipid catabolism (breaking down of fats), triglyceride clearance (storage of fats), increased insulin sensitivity, and control of energy metabolism.  Adiponectin acts directly on NPY neurons similarly to leptin but with additive effects.

Hormones that tell your body you’re hungry:

Ghrelin is considered the main hunger hormone.  It is secreted by the cells that line the stomach when the stomach is empty and also by the pancreas when it detects low blood sugar.  Also, the liver secretes ghrelin when its glycogen storage runs low (and glucagon is high).  When ghrelin is released into the circulation, it directly activates NPY neurons to stimulate appetite.  Increased levels of ghrelin are directly associated with the sensation of hunger. It is considered the counterpart of the hormone leptin.  Importantly, ghrelin is a potent stimulator of growth hormone (GH) secretion and regulates nutrient storage, thereby linking nutrient partitioning with growth and repair processes. Ghrelin activates several anti-inflammatory pathways in the body and promotes cell regeneration thereby promoting healing, especially within the gastrointestinal tract. Ghrelin regulates glucose homeostasis through a direct action on the pancreatic islet cells (the cells that secrete insulin).  It is also important for memory function and gastrointestinal motility.

Cortisol is well-known as a stress hormone, but it has key roles in regulating metabolism and hunger.  Cortisol levels determine whether the body uses glycogen stores or triglyceride stores for energy (stored carbohydrate or stored fat).  Cortisol can also stimulate gluconeogenesis, the process of converting amino acids (proteins) and lipids (fats) into glucose in the liver.  It is believed that cortisol directly influences food consumption by acting on NPY neurons in the brain as well as affecting the levels of NPY and leptin.  Cortisol seems to have a particular effect on the desire to eat foods high in fat and sugar.  This is why stress management (which really means controlling any factor that might mess with your natural cortisol levels) is so important.

Glucagon is a hormone secreted by the pancreas when it detects low blood glucose levels (typically between meals, but this can also happen as part of that “sugar crash” after eating something very high carbohydrate).  Glucagon signals the liver to convert stored glycogen into glucose, which is released into the bloodstream, a process known as glycogenolysis.  When glycogen stores are low, high glucagon levels drive gluconeogenesis, the process of creating glucose from amino acids and fatty acids.  Increased glucagon amplifies the hunger sensation.

Insulin is secreted by the pancreas in reaction to high blood glucose levels (for more on insulin, see this post).  Insulin causes cells in the liver, muscle, and fat tissue to take up glucose (and fatty acids in the case of adipocytes) from the blood, storing it as glycogen.  While insulin is released as a result of eating carbohydrates, it paradoxically increases hunger as opposed to decreasing it.  This is caused by direct action on the NPY neurons and is the reason why eating a carbohydrate-rich meal is not as satiating as eating a meal that includes fats and proteins.  It also explains how quickly we feel hungry again after a high-sugar snack.

These hormones have important roles both in regulating aspects of digestion and signaling to the brain whether or not you need to eat.  Many of these hormones are also critical in regulating your blood sugar both after a meal and between meals (fed and fasted states).  Some of these hormones also affect other systems in the body, for example, interacting with the immune system and controlling inflammation.  Understanding how your diet and lifestyle affect these hormones will help you make choices that regulate these hormones properly, allowing yourself to listen to your hunger cues and trust that your body knows what it’s doing.  And regulating hunger hormones is a key part of healing and being healthy.

hunger hormones

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The Hormones of Fat: Leptin and Insulin

October 23, 2012 in Hormone Regulation, Weight Loss/Gain

Hormones tell your body whether to burn fat and lose weight or to store fat and gain weight or to find balance and weight maintenance in between.  When it comes to your body “deciding” what state to be in, there are two key hormones that regulate food intake and energy balance:  the adipocyte hormone leptin and the pancreatic hormone insulin.  While there are many other hormone players with complex interactions between them, understanding these two hormones (which you could think of as the hormones of fat) will give you important insight into how the diet and lifestyle choices you make can help you achieve and maintain a healthy weight.

The hormone insulin, which is released by the pancreas in response to increased blood sugar, facilitates the transport of glucose into the cells of your body and signals to the liver to convert glucose into glycogen for storage.  When glycogen stores are maxed out, increased insulin levels stimulate conversion of glucose into triglycerides (fat) for long-term storage in adipocytes (fat cells) 1.  But beyond this important action for the metabolism of fuels, insulin has an additional role as an adiposity signal to the brain, i.e., it tells the brain whether or not you should eat and informs the brain about the energy status of your body.

The major stimulant of insulin secretion is an increase of blood glucose levels, as detected by the pancreas (blood glucose levels go up when you eat carbohydrates).  Circulating insulin enters the brain (proportionally to the amount that is circulating in the blood) where it binds to receptors in the hypothalamus region of the brain.  Although the exact details are unknown, it is understood that through this interaction with the central nervous system, insulin stimulates a decrease in food intake 2,3.  This makes some sense.  You eat, your blood sugar level rises, your body releases insulin to store all that glucose, and that increase in insulin tells your brain that you’ve got enough energy, thank you very much.  Importantly, the degree of glucose-stimulated insulin secretion by the pancreas is a direct function of body fat 4,5.  The more body fat, the more insulin is secreted both at a basal level and in response to feeding.  There is also a maximum amount of insulin that can actually cross the blood-brain barrier to stimulate satiety.  As the blood concentration of insulin increases beyond this level, no further signaling to the brain can occur.  Insulin resistance occurs when more insulin is required to maintain a normal level of blood glucose, and potentially when there is a decrease in insulin receptors in the brain, meaning that those high levels of circulating insulin don’t decrease appetite the way they are supposed to.

Fat storage cells, called adipocytes, produce the hormone leptin, which acts as a negative feedback control for adiposity (fatness).  Leptin is secreted by adipocytes (fat cells) in direct proportion to the amount of stored body fat, in particular, the amount of subcutaneous fat.  Similar to insulin, circulating leptin enters the brain where it binds to receptors (there are receptors for leptin in the hypothalamus but also several other areas of the brain).  Again, the exact details are unknown, but it is understood that leptin’s interaction with the brain stimulates a reduction in food intake and increasing energy expenditure 6.  This also makes some sense.  You have a good amount of fat stores, leptin is released and tells your brain that you have enough energy so you don’t need to eat anymore and hey, let’s get moving!  And analogous to insulin resistance, the body can also become leptin resistant, although this can happen from both obesity and overconsumption of energy 7 and by fasting or consuming too few calories and losing weight 8!  Uh, yeah.  Leptin is tricky.

It was initially believed that leptin’s dominant role was to tell the brain to stop eating.  However, recent studies have shown that it mediates the adaptation to fasting 8.  Fasting or consuming too few calories on a regular basis can lower sensitivity to leptin, which leads to increased hunger, cravings and lack of energy.  This has a very important implication in weight maintenance after weight loss since reduced leptin sensitivity is likely responsible for lowered metabolism and increased hunger, a combination that tends to lead to weight gain (why it’s so hard to keep weight off after going on a diet).  There is also a link between leptin and cortisol release, potentially explaining the cortisol spike that many people experience in response to intermittent fasting.  The many roles of leptin in the human body are still being studied.  It has also been implicated in the regulation of the reproductive, thyroid, growth hormone, and adrenal axes, independent of its role in energy balance.

To date, only the hormones leptin and insulin are known to act as adiposity signals 9.  The amount of leptin and insulin in the blood correlates with adiposity.  There are receptors in the brain for both insulin and leptin in areas of the brain known to be important in the control of food intake and energy balance.  Studies which have injected insulin or leptin show that this causes a reduction in food intake, whereas injection of antibodies to block insulin and leptin causes an increase in food intake.  Importantly, recent studies have demonstrated that insulin and leptin have additive effects when administered simultaneously 10.

What are the implications of this information for those who want to lose weight?  I think there are two major take home points here:

  1. Controlling insulin by avoiding high blood sugar is important for regulating hunger.
  2. Slow and steady wins the race in terms of weight loss and leptin sensitivity. 

I will be continuing to discuss many different hormones and the roles they play in health and weight loss over the next few months.  Leptin and insulin will feature prominently in these posts.

1. Click here for more information on insulin and its role in metabolism.

2. Begg DP and Woods SC. “The central insulin system and energy balance.” Handb Exp Pharmacol. 2012;(209):111-29.

3. Woods SC et al “Signals that regulate food intake and energy homeostasis”. Science. 1998 May 29;280(5368):1378-83.

4. Polonsky K S et al “Twenty-four-hour profiles and pulsatile patterns of insulin secretion in normal and obese subjects.” J Clin Invest. 1988 February; 81(2): 442–448.

5. Polonsky KS et al “Quantitative study of insulin secretion and clearance in normal and obese subjects.” J Clin Invest. 1988 Feb;81(2):435-41.

6. Ahima RS et al. “Leptin regulation of neuroendocrine systems.” Front Neuroendocrinol. 2000 Jul;21(3):263-307.

7. Enriori PJ et al “Leptin Resistance and Obesity” Obesity (2006) 14, 254S–258S; doi: 10.1038/oby.2006.319

8. Ahima RS.  “Revisiting leptin’s role in obesity and weight loss.” J Clin Invest. 2008 Jul;118(7):2380-3.

9. Benoit, SC. “Insulin and Leptin as Adiposity Signals” Recent Progress in Hormone Research 59:267-285 (2004) (link to the paper here)

10. Air EL et al “Insulin and leptin combine additively to reduce food intake and body weight in rats.” Endocrinology. 2002 Jun;143(6):2449-52. (link to the paper here)

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