The new “eat less” USDA Food Pyramid

For the first time in recent history the new USDA dietary guidelines finally reflect the realization that America has an obesity epidemic.

Five years ago, its dietary guidelines were best characterized as “eat more; exercise more”. After all, their constituency is not the American public but American agribusiness. Due to the constant fear of incurring the wrath of powerful food lobbies, the USDA dietary recommendations were virtually useless in preventing the spread of obesity and diabetes in America.

Now the Guidelines are somewhat helpful as they suggest that fruits and vegetables should occupy one-half your plate. Although that volume is not equal to the two-thirds of the plate that I have advocated for more than 15 years, at least it is a start. Unfortunately, the “eat-less” message is more deeply buried within the Guidelines.

This is because the “eat-less” message is a difficult one to digest for American agribusiness, whose revenue growth is based on “eat more”. Today agribusiness produces more than 4,000 calories per day for every American. For Americans to eat less, every sector of agribusiness (except the fruit and vegetable sector) has to make less money. In reality these new guidelines don't come out and actually say eat less of anything.

When the secretary of agriculture was asked if the guidelines might suggest something like eating less meat, his response was like asking President Clinton his definition of sex — it depends. (Well, that remark will drive comments for sure!). Obviously, he didn't want to offend the meat lobby.

The one segment of the agribusiness sector the USDA was willing to throw under the bus was the salt lobby due to the strong USDA message to eat less salt. Of course, the Salt Institute responded, “Obesity, not salt, is the main culprit in rising blood pressure rates”. The obvious implication is salt has no calories; therefore, the blame should be on those sectors of agribusiness that sell products that contain calories. Unfortunately, it is the responsibility of the USDA to promote those specific sectors.

If you are encouraged to increase the consumption of fruits and vegetables, eat more seafood (just forget about contamination), and replace dairy with soy protein, then what do you have to reduce in order to eat fewer calories? The usual suspects would be saturated fats, (which Harvard now tells us aren't so bad for heart disease), and sugar. Unfortunately, those recommendations are buried deep within the report. Without those ingredients it is difficult to make the tasty, cheap processed foods that drive the profits of agribusiness. This sounds very similar to our current budget crisis: No one wants to raise taxes, and no one wants to lower spending, although everyone wants to reduce the deficit.

Finally, the new guidelines contain the message that there is “no optimal proportion of macronutrients that can facilitate weight loss or assist in maintaining weight loss”. Maybe they should read the DIOGENES study published in the New England Journal of Medicine that came to an opposite conclusion (1). Of course, why let published nutritional science stand in the way of intuitive eating. I guess we will have to wait another five years for the next update of the USDA Guidelines.

References

  1. Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunesova M, Pihlsgard M, Stender S, Holst C, Saris WH, and Astrup A. “Diets with high or low-protein content and glycemic index for weight-loss maintenance.” N Engl J Med 363: 2102-2113 (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.

Coffee and diabetes: What’s the connection?

One of the great controversies in nutrition is the role of coffee and human health. On the one hand, coffee is the primary source of polyphenols in the American diet because of the lack of consumption of fruits and vegetables. On the other hand, coffee is rich in caffeine, an alkaloid that acts as a stimulant on the central nervous system and is known to be an addictive agent (1). In fact, Roland Griffiths, professor of Behavioral Biology at the John Hopkins School of Medicine (and my old college roommate), says, “Caffeine is the world’s most widely used mood-altering drug.” So the question remains is caffeine good for you?

No one knows for sure, but one interesting point has been made that it appears the more coffee you drink, the lower your risk for developing diabetes (2). In fact, if you drink more than four cups of coffee per day, you decrease your risk of diabetes by 50 percent. This new research demonstrates that coffee increases the levels of sex hormone-binding globlin (SHBG) in the blood. As I pointed out in my book “The Anti-Aging Zone,” SHBG plays an important role in sequestering the levels of estrogen and testosterone in the blood so that levels of these unbound sex hormones that can interact with their receptors are tightly regulated (3). Usually as insulin resistance increases, the levels of SHBG decrease in the blood (4). This can lead to an over-stimulation of the receptors by the unbound sex hormones resulting in increased risk for breast and prostate cancer development.

What in the coffee actually causes the increase in SHBG is unknown, but what is known is that once you decaffeinate the coffee, all its benefits on the elevation of SHBG levels and any reduction in risk for diabetes disappear.

It is highly unlikely that caffeine by itself is beneficial for reducing type 2 diabetes, since there were no benefits related to drinking tea or to total daily caffeine intake (2). Perhaps some other compound that was also extracted with the caffeine may play a role in the reduction of type 2 diabetes.

So what really happens when you decaffeinate coffee? First, you soak the beans in water to remove the caffeine and flavors as well as the polyphenols. Then you treat the water with organic solvents (methylene chloride or ethyl acetate) to remove the caffeine (as well as many of the polyphenols and much of the flavor). Then (assuming you have removed all of the organic solvent), you add back the treated water extract to the beans to hopefully reabsorb some of the flavors back into them. Obviously, not all the flavors or polyphenols return since the resulting taste is far less robust than the original coffee bean.

So it seems to me that exploring what else has been extracted in addition to the caffeine may lead to new dietary treatments for diabetes. Whether that will be done is highly unlikely. Instead of waiting for such experiments, you might as well follow the best treatment for preventing diabetes, which is following the anti inflammatory diet for a lifetime. That is how you control cellular inflammation, which is the driving force for development of type 2 diabetes (5,6).

References

1. Juliano LM and Griffiths RR. “A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features.” Psychopharmacology 176: 1-29 (2004)

2. Goto A, Song Y, Chen BH, Manson JE, Buring JE, and Liu S. “Coffee and caffeine consumption in relation to sex hormone-binding globulin and risk of type 2 diabetes in postmenopausal women.” Diabetes 60: 269-275 (2011)

3. Sears B. “The Anti-Aging Zone.” Regan Books. New York, NY (1999)

4. Akin F, Bastemir M, and Alkis E. “Effect of insulin sensitivity on SHBG levels in premenopausal versus postmenopausal obese women.” Adv Ther 24: 1210-1220 (2007)

5. Sears B. “Anti-inflammatory diets for obesity and diabetes.” J Coll Amer Nutr 28: 482S-491S (2009)

6. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

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.

Try the team approach to nutrition

One of the problems with nutrition is that it is too complex for simple thinking. Unlike drugs, which are designed to inhibit a particular target enzyme, nutrients often work in combinations like a team operating at the genetic level. When you try to apply drug-like thinking (i.e. one compound has to do all the work) to nutrient research, then the results are often underwhelming. Nowhere is this clearer than when we look at how nutrients interact to control body weight.

Weight gain can be best understood as a defect in both metabolism (the conversion of dietary energy into chemical energy) and storage (the stockpiling of excess dietary intake). This involves a four-way conversation between the brain, the gut, the liver and the adipose tissue. The only way these various organs can communicate with each other is via hormones. The gut sends signals to the brain when to stop eating. If the brain receives those signals loud and clear, your desire for food decreases (i.e. satiety). Finally, the food that has been ingested is either converted by the liver into suitable metabolites that can either be used for generating chemical energy (i.e. ATP) or stored (primarily in the fat cells) for future use. When it all works together, it runs smoothly. When it doesn’t work well, you end up gaining more body fat accelerating the pathway toward chronic disease.

One of the key hormones in this complex communication process is adiponectin. Apidonectin is an anti-inflammatory hormone made by the fat cells that is essential for reducing insulin resistance and preventing lipotoxicity (1). In other words, it is at the center of this complex hormonal communication system to help keep body weight in check and slow the development of chronic disease. Great, but how do you increase adiponectin?

First, there is no drug that can do it, but there are nutrients that can. One approach is to consume more omega-3 fatty acids (1). High levels of omega-3 fatty acids activate a genetic transcription factor that causes the increased production of adiponectin. But it takes a lot of high purity omega-3 oil to turn on that gene transcription factor. Now there appears to be another way: Taking polyphenols (2). The polyphenols don’t increase the activity of the genetic transcription factor, but they do facilitate the assembly of adiponectin into its most active form. Of course, if you don’t have enough omega-3 fatty acids in the diet, you can’t produce the necessary adiponectin building blocks to be assembled. When you combine the two (high purity omega-3 oil and polyphenols), then you don’t need to use as much of either one for the desired end result (3).

That’s how nutrition really works. You have to use a team nutrient approach to alter genetic expression. A lot more complicated than giving a single drug, but of course without the inherent side effects.

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Neschen S, Morino K, Rossbacher JC, Pongratz RL, Cline GW, Sono S, Gillum M, and Shulman GI. “Fish oil regulates adiponectin secretion by a peroxisome proliferator-activated receptor-gamma-dependent mechanism in mice.” Diabetes 55: 924-928 (2006)
  3. Wang Q, Liu M, Liu X, Dong LQ, Glickman RD, Slage TJ, Zhou Z, and Liu F. “Up-regulation of adiponectin by resveratrol.” J Biol Chem 286: 60-66 (2011)
  4. Shirai N and Suzuki H. “Effects of simultaneous intakes of fish oil and green tea extracts on plasma, glucose, insulin, C-peptide, and adiponectin and on liver lipid concentrations in mice fed low- and high-fat diets.” Ann Nutr Metab 52: 241-249 (2008)

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.

Want to lose Weight? Eat like our Paleolithic ancestors

A recent article appeared in the British Journal of Nutrition that gives an updated estimate of what diet (i.e. Paleolithic) our ancestors may have eaten during the time from their first appearance in Africa some 200,000 years ago until they started leaving Africa 100,000 years later (1). This is important because this type of diet until 10,000 years ago (with the advent of agriculture) was the nutritional foundation through which our genes evolved. Since our diet and gene expression are intimately tied together (2), understanding the dietary forces that molded how our genes respond to diet is important. This is particularly true since nutritional science has many conflicting interactions that make the study of a single nutrient often result in conflicting data. One such example is the study of insulin responses induced by the diet without studying the impact of fatty acid composition on insulin secretion and vice versa. This is why the study of Paleolithic nutrition provides a template to ask questions to optimize our current diet. In fact, I actually I stated this on page 99 of my first book, “The Zone” (3).

So what are the newest updates on the composition of the Paleolithic diet of our African ancestors? It appears the protein content was between 25 and 29 percent, the carbohydrates were about 40 percent and the total fat was about 30-36 percent. If that sounds familiar to the 30 percent protein, 40 percent carbohydrate, and 30 percent fat ratio in the anti inflammatory diet, it should. Essentially the newest estimate of the Paleolithic diet of our human ancestors in Africa is the anti inflammatory diet.

Equally important, it was estimated that the intake of long-chain omega-3 fatty acids (EPA and DHA) was about 6 grams per day. This is similar to my recommendations in “The OmegaRx Zone,” published in 2002 (4). The dietary ratio of arachidonic acid (AA) to EPA was also estimated in this article and was found to be about 2. Since the dietary intake of these fatty acids would be reflected in the blood, then we can assume the AA/EPA ratio in Paleolithic man was about 2. This AA/EPA ratio is again strikingly similar to the recommendations in my various books about what the best AA/EPA ratio should be for optimal control of the cellular inflammation, which leads to the acceleration of chronic disease (4-6).

When you follow the Paleolithic diet (a.k.a. the anti inflammatory diet), you find almost instantaneous changes in hormonal responses (7, 8) and improved glycemic control (8,9) before there is any weight loss. And if you continue to follow it, you not only lose weight, but also burn fat faster (11-14).

Was I just taking lucky guesses on my recommendations for the anti inflammatory diet over the past 15 years? I would like to think they were not lucky guesses, but based on insight coming from my background in drug delivery technology that strives for a therapeutic zone for optimal results. The lucky part was having the perseverance to stay true to those insights. On the other hand, it is always nice to get validation even 15 years after the fact.

References
1. Kuipers RS, Luxwolda MF, Dijck-Brouwer DJA, Eaton SB, Crawford, MA, Cordain L, and Muskiet FAJ. “Estimate macronutrient and fatty acid intakes from an East African paleolithic diet.” British J Nutr 104: 1666-1687 (2010)
2. Sears B and Ricordi C. “Anti-Inflammatory nutrition as a pharmacological approach to treat obesity.” J Obesity published online September 30, 2010. doi: 10.1155/2011/431985. (2010)
3. Sears B. “The Zone.” Regan Books. New York, NY (1995)
4. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
5. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)
6. Sears B. “Toxic Fat.” Nelson Publishing. Nashville, TN (2008)
7. Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB. “High-glycemic-index foods, overeating, and obesity.” Pediatrics 103: E26 (1999)
8. Markovic TP, Jenkins AB, Campbell LV, Furler SM, Kragen EW, and Chisholm DJ. “The determinants of glycemic responses to diet restriction and weight loss in obesity and NIDDM.” Diabetes Care 21: 687-694 (1998)
9. Lindberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjorstrom K, and Ahren B. “A Paleolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease.” Diabetologia 50: 1795-1807 (2007)
10. Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, and Sebastian A. “Metabolic and physiologic improvements from consuming a Paleolithic, hunter-gatherer type diet.” Eur J Clin Nutr 63: 947-955 (2009)
11. Osterdahl M. Kocturk T. Koochek A, and Wandell PE. “Effects of a short-term intervention with a Paleolithic diet in healthy volunteers.” Eur J Clin Nutr 62: 682-685 (2008)
12. Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, and Christou DD. “A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women.” J Nutr 133: 411-417 (2003)
13. Lasker DA, Evans EM, and Layman DK, “Moderate carbohydrate, moderate protein weight loss diet reduces cardiovascular disease risk compared to high-carbohydrate, low-protein diet in obese adults. A randomized clinical trial.” Nutrition and Metabolism 5: 30 (2008)
14. Fontani G, Corradeschi F, Felici A, Alfatti F, Bugarini R, Fiaschi AI, Cerretani D, Montorfano G, Rizzo AM and Berra B. “Blood profiles, body fat and mood state in healthy subjects on different diets supplemented with omega-3 polyunsaturated fatty acids.” Eur J Clin Invest 35: 499-507 (2005)

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.

Simple dietary changes ease diabetes risk

Since 1980 the number of individuals with diabetes in the United States has nearly tripled to an astonishing 17 million (1), leading physicians, researchers and pharmaceutical companies on the hunt for the most effective treatment options. A recent publication in Diabetes Care studied approximately 400 non-diabetic individuals at high cardiovascular risk and randomized them to one of three diets: Low-fat, Mediterranean with nuts, and Mediterranean with olive oil (2). Individuals were educated on the various diets but did not have to follow a certain calorie allotment or physical activity plan. After four years, the number of individuals with diabetes was 10.1 percent in the Mediterranean with olive oil group, 11 percent in the Mediterranean with nuts group and 17.9 percent in the low-fat group. Collectively when compared to the low-fat group, those following a Mediterranean diet were 52 percent less likely to develop diabetes. These results show the significant impact that simple dietary changes can have on diabetes risk reduction without having to dramatically change caloric intake or activity levels.

1. Diabetes Data and Trends. Available at: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed: 10/14/2010

2. Salas-Salvadó J, Bulló M, Babio N, Martínez-González MA, Ibarrola-Jurado N, Basora J, Estruch R, Covas MI, Corella D, Arós F, Ruiz-Gutiérrez V, Ros E; For the PREDIMED Study investigators. Reduction in the Incidence of Type 2-Diabetes with the Mediterranean Diet: Results of the PREDIMED-Reus Nutrition Intervention Randomized Trial. Diabetes Care. 2010 Oct 13. [Epub ahead of print]

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.

For losing weight, exercise is good; diet is better

Here’s standard quote: “Losing weight can improve health and reduce many of the risk factors related to diabetes and heart disease.” Unfortunately, that’s not true. The correct statement is “losing excess body fat can improve health and reduce many of the risk factors related to diabetes and heart disease.”

It may seem like a minor difference, but it makes a world of difference. Weight loss could be due to water loss or cannibalization of lean body mass (muscles and organs), neither of which will lead to any health benefits.

If you want to reduce excess body fat, you have to lower insulin levels. How do you control that on a consistent basis? Remember the 80/20 rule. That means 80 percent of your insulin control will come from following a strict anti inflammatory diet, and 20 percent will come from increased physical activity.

This means the best exercise program can be undone by the wrong diet. Physical exercise has many important benefits, such as reducing the likelihood of diabetes and heart disease, improving sense of self-worth and hanging out with like-minded individuals.

Unfortunately, initial weight loss is not one of those benefits since research has demonstrated that exercise increases one’s appetite. This is why following a strict anti inflammatory diet is imperative if you are trying to lose weight by increasing your exercise. Another helpful hint is to increase your high purity omega-3 oil intake, as it has been demonstrated that fat loss is significantly increased when high purity omega-3 oil is used in combination with exercise.

On the other hand, after you reach your weight goals, the balance of diet and exercise to maintain your weight shifts to a 50/50 balance. Now exercise becomes an ideal way to maintain your weight as long as you continue to control insulin through the anti inflammatory diet.

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.

Sleep…it does a body good

It shouldn’t come as a surprise to most people that a recent sleep poll reported a discrepancy between the number of hours people said they needed to sleep to function properly and the actual amount they reported getting. Only about one-third of respondents were getting enough sleep (1). What people may not be aware of is that not clocking enough hours each night might be putting your health at risk. A recent study published in the Journal of Clinical Endocrinology and Metabolism showed that even a partial night’s rest over a single night induces insulin resistance (2). Nine healthy individuals were studied after a night of normal sleep (up to 8.5 hours) and a night of partial sleep (4 hours duration). In those with only 4 hours of sleep there was a significant decline in glucose disposal suggesting decreased insulin sensitivity (2). Insulin is a key hormone involved in blood glucose control. When insulin is secreted by the pancreas, it allows for glucose to be drawn into your cells to be used for energy. If insulin resistance is present, cells don’t respond to this hormone, so more insulin is needed in order for glucose to get into your cells. It’s when the levels of insulin and glucose build up in the body that it puts individuals at greater risk for disease, especially type II diabetes and heart disease (3). Time to get those Zzzzzzzzzzzzzzzz’s!

1. 2010 Sleep in America Poll. Available at:
http://www.sleepfoundation.org/sites/default/files/nsaw/NSF%20Sleep%20in%20%20America%20Poll%20-%20Summary%20of%20Findings%20.pdf
Accessed: May 11, 2010.

2. Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA. A Single Night of Partial Sleep Deprivation Induces Insulin Resistance in Multiple Metabolic Pathways in Healthy Subjects. J Clin Endocrinol Metab. 2010 Apr 6. [Epub ahead of print]

3. Insulin Resistance and Pre-diabetes. Available at: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/#what. Accessed: May 11, 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.

What’s the buzz about magnesium?

Magnesium is a mineral that is inching its way into the spotlight. About 50 percent of the magnesium in our bodies is located in our bone, and the other half is found inside our cells and tissues (1). So what’s the big deal? Well in addition to maintaining muscle and nerve function, regulating heart rhythm, bone health and supporting our immune system, it also helps control blood sugar levels, blood pressure, energy metabolism and protein synthesis (2). This means it may play a role in diseases like hypertension, diabetes and even cardiovascular disease, although more research is needed. It has even been shown to help individuals with asthma based on its anti-inflammatory and bronchodilating effects (3) and a recent animal study shows promise with regards to its memory boosting properties (4).

Despite all the benefits attributed to magnesium, the increase in processed and refined food intake in the United States has led to a decrease in magnesium consumption through the years. So how can you make sure you’re getting enough? The best sources of magnesium include leafy greens, nuts and unrefined grains, such as oatmeal. Meats, starches and milk include some magnesium but are not the best sources. For women over the age of 30 the recommended daily intake is 320mg/day and for men 420mg/day (1). Women, you can meet your requirements with 1 ounce of almonds (80mg), 1 cup frozen spinach (150mg), 1 cup oatmeal (55mg) and 1 cup of yogurt (45mg). Men add 3oz. of halibut (90mg) to this and you’ve met your daily requirements too!

1) Magnesium: Available at: http://www.nap.edu/openbook.php?record_id=5776&page=190. Accessed: February 22, 2010.
2) Magnesium. Available at: http://dietary-supplements.info.nih.gov/factsheets/magnesium.asp. Accessed: February 22, 2010.
3) Bichara MD, Goldman RD. Magnesium for treatment of asthma in children. Can Fam Physician. 2009 Sep;55(9):887-9.
4) Slutsky I, Abumaria N, Wu LJ, Huang C, Zhang L, Li B, Zhao X, Govindarajan A, Zhao MG, Zhuo M, Tonegawa S, Liu G. Enhancement of Learning and Memory by Elevating Brain Magnesium. Neuron. 2010 Jan 28;65(2):165-177.

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.

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.