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Dr. Sears' Blog

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Written By: Dr. Barry Sears Creator of the Zone Diet

Written by Dr. Barry Sears
on February 22, 2010

Most people think of the brain as the primary organ that does all of the information processing for the body. Actually, you have a second brain that is just as important. This second brain is your gastrointestinal (GI) tract that constantly senses dietary input and sends the resulting information to the brain to tell it when it can switch from seeking food to other activities, such as building cathedrals. This is why biological urges always overwhelm cognitive urges. Controlling these biological urges is not a matter of willpower but an integrated hormonal balancing mechanism. Try holding your breath for 25 minutes. It simply can’t be done not due to a lack of willpower, but because after about two minutes, the body’s need for a continual supply of oxygen overwhelms any other desire or course of action. The same is true of eating. It’s not a matter of willpower that controls appetite, but continual hormonal communication from the second brain as to whether or not there are adequate calories in the pipeline that can be ultimately converted to chemical energy to keep the body going.

There are hundreds of hormones released from your second brain to relay information on the body’s current food status. Two of the most important are PYY and GLP-1. These hormones are released from L-cells deep in the lower part of the GI tract. PYY is released in response to protein (1,2), and GLP-1 is released in response to carbohydrate (3). Both hormones are important because they also regulate satiety.

Both of these hormones are significantly increased after gastric bypass surgery (4,5), and this may account for the dramatic long-term benefits of the surgery on both weight loss and diabetes (6-8). The secret of the success of gastric bypass surgery may lie in the re-routing of the GI tract, which now brings a lot more protein and carbohydrate to their receptors found in L-cells that are located in the most distant parts of the GI tract. Apparently in obese individuals, much of the ingested protein and carbohydrate is broken down and absorbed much higher up in the GI tract. As a result, a relatively small amount of these macronutrients are sensed by the L-cells resulting in limited amounts of PYY and GLP-1 released from the GI tract to suppress hunger. As a consequence, obese individuals are constantly hungry.

This also begins to explain many of the seemingly contradictory reports on the benefit of low glycemic-load diets, like the Zone Diet, for weight loss (9, 10). The end result is to state that all diets are equally effective in weight loss since a “calorie is a calorie”, and if you restrict calories, the weight loss is identical. Of course, this simple thinking neglects genetic diversity. One study done by Harvard Medical School indicated that in genetically identical rats, weight gain is strongly correlated to the glycemic load of the diet (11). Based on this study, Harvard later conducted a clinical experiment putting overweight individuals on iso-caloric diets with differing glycemic loads for 18 months (12). If you just looked at the changes in weight, both diets were equally effective, indicating again that a “calorie is a calorie”. However, if the two groups are broken into high-initial-insulin responders versus low-initial-insulin responders, you find a very different picture emerging. For the high-insulin responders, their weight loss and long-term weight maintenance was considerably better on the low glycemic-load diet, just as it was with genetically identical rats. So this means that for those with a high initial insulin response to carbohydrates, a low glycemic-load diet, like the Zone Diet, would be their most appropriate choice, indicating a “calorie is not a calorie,” especially when you take into account genetics.

So how does this all science tie together in the real world? My hypothesis is that the fast insulin responders are simply digesting the protein and carbohydrate in a meal and absorbing it at a faster rate. This means carbohydrates enter into the bloodstream at a faster rate (i.e. high glycemic index) and fewer macronutrients (both protein and carbohydrate) are able to reach the lower part of the GI tract where the L-cells are located. This means that less PYY and GLP-1 will be secreted. As a result, there is less satiety, and they are likely to consume more calories. A low glycemic-load diet delays the absorption of carbohydrates, so that more GLP-1 is released from the L-cells. But you also have to slow down the absorption of protein so more PYY can be released. The type of protein that is broken down at the slowest rate is casein coming from milk. Other proteins, such a whey and soy, are rapidly broken down and absorbed in the upper regions of the GI track ensuring very little protein will ultimately reach the L-cells, causing an increase in PYY secretion.

So the ideal diet for those overweight individuals with a high initial insulin response may not only be a low glycemic-load diet (i.e. Zone Diet), but also a diet rich in casein. That’s why I am excited by the new generation of Zone Foods. They have a low glycemic load (similar to fruits) and are also rich in casein. The combination of the two factors may result in increased satiety because the delayed digestion and absorption means more of the initial carbohydrate and protein in the meal is reaching the L-cells, thus potentially releasing more GLP-1 and PYY.

If you aren’t hungry, then cutting back on calories is much easier, especially if you have a high initial insulin response to meals. This is the science behind the new Zone Foods. The science is complex, but the actual execution of that science is not, as long as you like to eat Zone bread, Zone pasta, and Zone pizza. New call-to-action


  1. Batterham RL; Heffron H; Kapoor S; Chivers JE; Chandarana K; Herzog H; Le Roux CW; Thomas EL; Bell JD; Withers DJ Critical role for peptide YY in protein-mediated satiation and body-weight regulation. Cell Metab 4: 223-233 (2006).
  2. Karra E; Chandarana K; Batterham RL. “The role of peptide YY in appetite regulation and obesity.” J Physiol 587: 19-25 (2009).
  3. Jang HJ, Kokrashvili Z, Theodorakis MJ, Carlson OD, Kim BJ, Zhou J, Kim HH, Xu X, Chan SL, Juhaszova M, Bernier M, Mosinger B, Margolskee RF, and Egan JM. “Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1.” Proc Natl Acad Sci U S A 104: 15069-15074 (2007).
  4. Holdstock C; Zethelius B, Sundbom M, Karlsson FA, and Eden Engstrom B. “Postprandial changes in gut regulatory peptides in gastric bypass patients.” Int J Obes (Lond) 32: 1640-1646 (2008).
  5. Morinigo R, Moize V, Musri M, Lacy AM, Navarro S, Marin JL, Delgado S, Casamitjana R, and Vidal J. “Glucagon-like peptide-1, peptide YY, hunger, and satiety after gastric bypass surgery in morbidly obese subjects.” J Clin Endocrinol Metab 91: 1735-1740 (2006).
  6. Laferrere B, Teixeira J, McGinty J, Tran H, Egger JR, Colarusso A, Kovack B, Bawa B, Koshy N, Lee H, and Yapp K. “Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with type 2 diabetes.” J Clin Endocrinol Metab 93: 2479-2485 (2008).
  7. le Roux CW, Welbourn R, Werling M, Osborne A, Kokkinos A, Laurenius A, Lonroth H, Fandriks L, Ghatei MA; Bloom SR. “Gut hormones as mediators of appetite and weight loss after Roux-en-Y gastric bypass. Ann Surg 246: 780-785 (2007).
  8. White S, Brooks E, Jurikova L, and Stubbs RS. “Long-term outcomes after gastric bypass.” Obes Surg 15: 155-163 (2005).
  9. Dansinger ML, Gleason JA, Griffith JL, Selker HP, and Schaefer EJ “Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial.” JAMA 293: 43-53 (2005).
  10. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, Kraemer HC, and King AC. “Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial.” JAMA 297: 969-977 (2007).
  11. Pawlak DB, Kushner JA, and Ludwig DS. “Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals.” Lancet 364: 778-785 (2004).
  12. Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, and Ludwig DS. “Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial.” JAMA 297: 2092-2102 (2007).

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