Give your second brain a chance

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.

References

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)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Think before taking that next bite

The Mediterranean diet emphasizes consumption of fruits, vegetables, fish, olive oil, and legumes with limited intakes of dairy, meat and saturated fats. The benefits of the Mediterranean diet are well known from reducing heart disease and diabetes, to improving cholesterol levels, blood pressure, and weight control. A new study may add to the growing list of benefits to include diseases of the brain, specifically dementia (1, 2). In a study to be presented at the American Academy of Neurology in April, researchers followed 712 participants for approximately six years, placing them into three groups based on how closely they adhered to the Mediterranean diet. At the study’s end, each participant underwent an MRI to detect the number of infarcts, areas of the brain with obstructions in the flow of blood. Compared to those who only moderately followed the diet, participants who strictly followed the Mediterranean diet had a 36 percent decreased risk of having an infarct. Although obstructions in blood flow to the brain may not have resulted in outward symptoms, the brain scan could detect the damage from these obstructions or clots, which are known to play a role in future cognitive decline and dementia.

The Zone Diet is the evolution of the Mediterranean diet, featuring low-fat protein, lots of non-starchy, fibrous vegetables, fruit and monounsaturated fat. The difference is the Zone Diet minimizes the consumption of grains.

References
1) Mediterranean diet may help prevent dementia, study says. Available at:
http://www.cnn.com/2010/HEALTH/02/08/mediterranean.diet.brain/index.html. Accessed: 2/9/2010.
2) Mediterranean Diet May Be Key To Avoiding Stroke, Dementia. Available at:
http://abcnews.go.com/Health/AlzheimersNews/mediterranean-diet-hold-key-avoiding-stroke-dementia/story?id=9780494. Accessed: 2/9/2010.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

An update on our origins

About eight years ago I wrote a section in “The OmegaRx Zone” on the origins of our species. At the time it was becoming known that genetically every human on the face of the earth had extremely similar genes. In fact, the size of that genetic pool was only about 1,000 individuals. I wrote that one of the factors that let this small group of our ancestors conquer the world may have come from the fact that they blundered onto eating “brain food” in the form of large amounts of omega-3 fatty acids.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Examining sloth and gluttony at the genetic level

The common refrain for treating obesity is simply “eat less and exercise more”. With obesity rates increasing, how is it possible that so many Americans seem to be unable to follow such simple instructions? The answer may lie in our genes.

Nothing contained in this blog is intend to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Ways to prevent vegetable overload

Many times I get questions from Zoners who are aghast at all the favorable carbohydrates they think they have to consume at each meal.

Here’s an example:

“I’m a little bit confused about vegetable portion sizes. You say that 4 cups of mushrooms equals one block, 2 green peppers equal one block, 10 cups of spinach equal one block, and 1 ½ cucumbers equal 1 block. Really?!!

“That would mean that for lunch or dinner I would eat 4 cups of mushrooms, 2 full green peppers, 10 cups of spinach, and more than an entire cucumber? That seems impossible (and very undesirable)…Sorry to bother you with such a basic question, but the portions–at least for the vegetables–seem really insane.”

I also have been asked this question:

“Are you telling me I have to have 12 cups of broccoli at one meal? You’ve got to be kidding…10 cups of lettuce?”

It’s true four cups of broccoli equal one block. But nobody wants to eat that much broccoli or even chop that much broccoli for each meal.

Also, treat lettuce as a freebie. The amount of lettuce used in a side salad certainly won’t budge your block count.

Let’s say you used 4 cups of broccoli for one block. It could be cooked in 1cup tomato sauce (2 blocks) with nine chopped olives (3 blocks) and topped with 3 ounces of chicken. That would make a meal for a typical woman. A man might want to add a small piece of fruit, another ounce of chicken and three more olives.

Black beans, kidney beans, hummus and chickpeas also weigh in at ¼ cup equaling a block.

A great three-bean salad could be made from ¼ cup each of chickpeas, kidney beans and black beans.

And don’t forget lentils. About ¼ cup cooked equals one block. (Check the label.) They make a good addition to soups and stews.

You can also add 1 cup of berries to complete your meal.

Use the Food Block Guide here at zonediet.com and check out the hundreds of recipes.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

High purity omega-3 oil may be alternative to anti-psychotic drugs

The risks of anti-psychotic medications are well documented especially in young adults making safer alternatives highly desired. A study published this month in the Archives of General Psychiatry shows promise for individuals with psychotic disorders, such as schizophrenia (1).

In a double-blind, placebo-controlled trial (the gold standard), 81 individuals 13-25 years of age were randomized to receive either supplementation with omega-3 fatty acids or a placebo. In order to be eligible for inclusion, individuals had to meet one or more of three well-defined and validated groups of risk factors. This may include hallucinations, suspiciousness, conceptual disorganization and genetic risk. Individuals with these risk factors have a 40 percent greater likelihood of becoming psychotic within a 12-month period of time.

The goal of this study was to determine if supplementation with omega-3 fatty acids could reduce an individual’s risk of progressing to a psychotic disorder despite having these risk factors. It is thought that a dysfunction in fatty acid metabolism may underlie schizophrenia, and that supplementation may help to counteract this (1). This trial took place over 12 weeks with follow-up at six and 12 months. At 12 months, 27.5 percent (11 of 40) of individuals in the placebo group had converted to having a psychotic disorder (10 with a form of schizophrenia and one bipolar) whereas only 4.9 percent (two of 41) of those in the omega 3 fatty acid group presented with a disorder (two with a form of schizophrenia).

Although more research is needed, and the results of this trial may only be generalized to the age group studied, the implications of this trial are huge as omega 3 fatty acids are a safe and inexpensive alternative to anti-psychotic medications.

Reference:
1. Amminger PG, Schäfer MR, Papageorgiou K, Klier CM, Cotton SM, Harrigan SM, Mackinnon A, McGorry PD, Berger GE. Long-Chain-3 Fatty Acids for Indicated Prevention of Psychotic Disorders: A Randomized, Placebo-Controlled Trial. Arch Gen Psychiatry. 2010;67(2):146-154.

Statins for everyone?

We are led to believe that statins are the greatest drugs the pharmaceutical industry has ever developed. It is true that they are the most profitable drugs ever developed, but they only reduce cardiovascular mortality by about 20 percent compared to a placebo. This means that about 80 percent of the people taking statins to reduce elevated cholesterol will see no impact on their mortality from heart disease. Furthermore, nearly 50 percent of individuals who have heart attacks also have normal cholesterol levels. So much for the major marketing message sent to Americans that cholesterol causes heart disease.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.