A really dumb diet from France

After experiencing so many years of ridicule (now effectively past history) with the Zone diet, I never thought I would possibly criticize another new diet unless it was either dangerous or just plain foolish. The newest diet from France is both.

Called the Dukan diet, this program is a strange combination of the Atkins diet with a French twist. As usual, there are number of diet phases that have to be followed. The first one is downright dangerous as it recommends unlimited amounts of lean protein, 1½ tablespoons of oat bran and lots of water. The reason this phase is dangerous is because there are virtually no carbohydrates or fats to counterbalance the protein. My best estimate is in this first phase more than 90 percent of the total calories are coming from protein. This will overwhelm the liver's capacity to metabolize the excess protein leading to a condition known as “rabbit starvation” (1). This was a condition experienced by early Arctic explorers who only subsisted on lean protein. They quickly became dehydrated as the body desperately tried to excrete excess ammonia (the first breakdown product of protein) through the urine that could not be converted to urea by the liver. This leads to dehydration, diarrhea, nausea, low blood pressure and fatigue. At least on the Atkins diet there was a lot of fat coupled with the protein to help the liver metabolize the ammonia from the protein into urea that could be easily removed in the urine.

The dehydration from such a severely ketogenic diet explains the need for lots of water. As far as the oat bran, it contains virtually no carbohydrate, but lots of soluble fiber to help expand the stomach. Yes you will lose weight (primarily water) and insulin levels in the blood will drop dramatically, but you will reduce the elasticity of the blood vessels (2) and increase insulin resistance in the liver (3). The decrease in the elasticity of blood vessels increases the likelihood of a heart attack, (4) and the growing insulin resistance sets the stage for liver dysfunction that always promotes weight regain. This first phase is called the Attack Phase, I assume because it attacks your liver and your metabolism.

Phase 2 of this diet is just as wacky. Now you increase the oat bran to 2 tablespoons per day and have some vegetables every other day. This phase remains a highly ketogenic diet, meaning the liver and blood vessels are still in a metabolic mess. This is called the Cruise Phase. I guess this means you are cruising for a hard landing even though you are still losing weight.

If you last through the first two phases (about two months), you enter into the Consolidation Phase that is just as wacky as the Cruise Phase, but in the other direction. Now you can add non-starchy vegetables every day and a piece of fruit (I applaud these additions). But then why does this diet let the person start eating bread every day and rice and pasta twice a week plus two Porky Pig meals including dessert and wine (that's the French twist). It's like an insidious plot to demonstrate how quickly you will regain the lost weight, but now as newly synthesized fat. Of course, by following this Consolidation Phase, it is virtually guaranteed you will consolidate the lost weight into new stored fat.

Finally, there is the Stabilization Phase where you can eat anything you want (mac and cheese, fried chicken, etc.) as long as you eat only lean protein one day each week. Fat chance you will ever get there.

You probably won't die on the Dukan diet, but you will mess up your liver metabolism making it much more difficult to lose the resulting regain of fat mass on the Consolidation Phase.

I am frankly getting a cold sweat as I write this blog since I am sounding a lot like Dean Ornish yelling at Bob Atkins in the old days. But even Bob would say the Dukan diet is just plain stupid.

References

  1. Silsborough S and Mann N. “A review of issues of dietary protein intake in humans.” Int J Sports Nutr Exerc Metab 16: 129-152 (2006)
  2. Buscemi S, Verga S, Tranchina MR, Cottone S, and Cerasola G. “Effects of hypocaloric very-low-carbohydrate diet vs. Mediterranean diet on endothelial function in obese women.” Eur J Clin Invest 39: 339-347 (2009)
  3. Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D; Zhang XM, Samuel VT, and Shulman GI. “A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.” Am J Physiol Endocrinol Metab 299: E808-815 (2010)
  4. Yeboah J, Crouse JR, Hsu FC, Burke GL, and Herrington DM. “Brachial flow-mediated dilation predicts incident cardiovascular events in older adults.” J Am Coll Cardio 51: 997-1002 (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.

What is the Mediterranean diet?

The mediterranean dietToday we continually hear about the health benefits of following a Mediterranean diet. For example, a recent analysis of more than 50 published studies indicated that a Mediterranean diet would lead to a 30-percent reduction in metabolic syndrome (1). Since metabolic syndrome can be considered pre-diabetes, the public health implications are enormous. However, are we talking about the Spanish Mediterranean diet or the Italian, or the Moroccan, the Egyptian or the Lebanese versions? Here is the basic problem with all diets: Trying to define them correctly.

In order to compare one diet to another, each diet must ultimately be defined by its balance of the macronutrients (protein, carbohydrate and fat). This is because the macronutrient balance determines hormonal responses generated by that diet (2).

A Mediterranean diet can be considered to contain approximately 50 percent of the calories as carbohydrates, 20 percent of the calories as protein and 30 percent of the calories as fat. This is a higher protein-to-carbohydrate balance than is found in the usually recommended “healthy” diets for weight loss and cardiovascular health. As a result, this difference in the balance of the protein-to-carbohydrate ratio will generate different hormonal responses between the two types of diets, especially in terms of reducing insulin responses and controlling cellular inflammation.

This is important since it is excess insulin that makes you fat and keeps you fat, and it's cellular inflammation that makes you sick. Since insulin levels are determined by the protein-to-carbohydrate ratio, would more protein and less carbohydrate generate an even better response? Of course it would. That is why the Zone diet contains 40 percent of the calories as carbohydrates, 30 percent of the calories as protein, and 30 percent of the calories as fat. This improved protein-to-carbohydrate balance means lower insulin levels and less cellular inflammation.

Why stop there? Let's just continue reducing the carbohydrates. Now you get low-carbohydrate diets, like the Atkins diet. Unlike the Zone diet, carbohydrates are no longer the primary macronutrient in a true low-carbohydrate diet. Now the primary macronutrient is fat. Using these low-carbohydrate diets creates some real problems by generating an abnormal metabolic state known as ketosis. This occurs when you don't have enough carbohydrates (fewer than 20 percent of total calories) in the diet to metabolize fat completely to carbon dioxide and water. When that happens, your blood vessels lose their elastic nature, (3) increasing the risk of a heart attack (4). This is probably a consequence of lowering insulin too much as well as increasing inflammatory mediators (3). If you are trying to lose weight, increasing the likelihood of a heart attack is not a good idea. So it seems you need some carbohydrates, but not too few if your goal is to lose weight safely.

That's why people (as well as physicians and diet editors) get confused when they read articles in the New England Journal of Medicine talking about low-carbohydrate diets for weight loss when such diets actually contain 40 percent carbohydrates (5). To be correct, they should use the term “the Zone diet” instead of a “low-carbohydrate diet” to be correct. Despite the poor dietary description used in this article, the “low-carbohydrate” (aka the Zone) diet generated greater weight loss after two years, a greater reduction in the total cholesterol-to-HDL cholesterol (a marker of future cardiovascular risk), a greater decrease in triglycerides and a greater decrease in inflammatory markers when compared to a Mediterranean diet or the always-recommended low-fat diet (5). That's why you do controlled clinical trials instead of guessing what the best might be.

So if you want to lose weight and reduce your future heart disease risk, it seems prudent to follow the Zone diet and make most of your carbohydrates colorful ones (i.e., fruits and vegetables) and add olive oil and nuts for fat instead of using vegetable oils and saturated fats just as I recommended more than 15 years ago (2). Just call it the Mediterranean Zone diet. Now everyone is not only happy, but also they are finally using the proper diet terminology.

References

  1. Kastorini C-M, Milionis HJ, Esposito K, Giuglian D, Goudevnos JA, and Panagiotakos DB. “The effect of Mediterranean diet on metabolic syndrome and its components.” J Am Coll Cardiol 57: 1299-1313 (2011)
  2. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  3. Buscemi S, Verga S, Tranchina MR, Cottone S, and Cerasola G. “Effects of hypocaloric very-low-carbohydrate diet vs. Mediterranean diet on endothelial function in obese women.” Eur J Clin Invest 39: 339-347 (2009)
  4. Yeboah J, Crouse JR, Hsu FC, Burke GL, and Herrington DM. “Brachial flow-mediated dilation predicts incident cardiovascular events in older adults.” J Am Coll Cardio 51: 997-1002 (2008)
  5. Shai I, Schwarzfuchs D, Henkin Y, Shahaar DR, Witkow S, Greenberg I, Golan R, Fraser D, boltin A, Vardi H, Tangi-Roxental O, Zuk-Ramot R, Sarusi B, Fricner D, Schwartz Z, Sheiner E, Marko R, Katorza E, Thiery J, Fielder GM, Bluher M, Stumvoll M and Stamper MJ. “Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet.” N Engl J Med 359: 229-241 (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.

Blame weight gain on the brain

Many people claim they are addicted to food. That may not be too far from the truth.

Over millions of years of evolution, our brains have adapted to provide us a reward for successfully ingesting food. The hormone dopamine appears to be the key link in this reward process. But to complete the circuit, dopamine has to interact with its receptor. It has been known for many years that the ability of dopamine to combine with one of its receptors (the D2 dopamine receptor) is compromised in obese individuals compared to normal-weight individuals (1). This led to the hypothesis that obese individuals overeat as a way to compensate for the reduction in the dopamine reward circuits just as individuals with addictive behaviors (drugs, alcohol, gambling, etc.) do when their dopamine levels are low. It is also known that food restriction up-regulates the number of D2 receptors (2). This likely completes the reward circuit.

This effect of increasing D2 receptors is confirmed in obese patients who have undergone gastric bypass surgery that results in calorie restriction (3). This may explain why gastric bypass surgery is currently the only proven long-term solution of obesity. More recent studies with functional magnetic resonance imaging (fMRI) have indicated that unlike women with a stable weight where the mere visual image of palatable food increases the reward activity in the brain, that response is highly reduced in women who have gained weight in the past six months (4). This suggests that the dopamine reward circuits are compromised in women with recent weight gain, thus prompting a further increased risk for overeating in those individuals to increase dopamine output.

So does this mean that the obese patient with a disrupted dopamine reward system has no hope of overcoming these powerful neurological deficits? Not necessarily. There are a number of dietary interventions to increase the levels of dopamine and its receptors. The first is calorie restriction, which is only possible if you aren’t hungry. The usual culprit that triggers constant hunger is a disruption of hormonal communication of hunger and satiety signals in the brain. It has been shown that following a strict Zone diet can quickly restore the desired balance that leads to greater satiety (5-7). The probable mechanism is the reduction of cellular inflammation by an anti-inflammatory diet (8-10).

Another dietary intervention is high-dose fish oil that has been demonstrated to both increase dopamine and dopamine receptors in animals (11,12). This would explain why high-dose fish oil has been found useful in the treatment of ADHD, a condition characterized by low dopamine levels (13). Finally, high-dose fish oil can reduce the synthesis of endocannabinoids in the brain that are powerful stimulators of hunger (14).

I often say that if you are fat, it may not be your fault. The blame can be placed on your genes and recent changes in the human food supply that are changing their expression, especially in the dopamine reward system. However, once you know what causes the problem, you have the potential to correct it. If you are apparently addicted to food, the answer may very well lie in an anti-inflammatory diet coupled with high-dose fish oil.

References

  1. Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, and Fowler JS. “Brain dopamine and obesity.” Lancet 357: 354-357 (2001)
  2. Thanos PK, Michaelides M, Piyis YK, Wang GJ, and Volkow ND. “Food restriction markedly increases dopamine D2 receptor (D2R) in a rat model of obesity as assessed with in-vivo muPET imaging and in-vitro autoradiography.” Synapse 62: 50-61 (2008)
  3. Steele KE, Prokopowicz GP, Schweitzer MA, Magunsuon TH, Lidor AO, Kuwabawa H, Kumar A, Brasic J, and Wong DF. “Alterations of central dopamine receptors before and after gastric bypass surgery.” Obes Surg 20: 369-374 (2010)
  4. Stice E, Yokum S, Blum K, and Bohon C. “Weight gain is associated with reduced striatal response to palatable food.” J Neurosci 30 :13105-13109 (2010)
  5. 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)
  6. Agus MS, Swain JF, Larson CL, Eckert EA, and Ludwig DS. “Dietary composition and physiologic adaptations to energy restriction.” Am J Clin Nutr 71: 901-7 (2000)
  7. Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahren B, and Lindeberg S. “A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart disease.” Nutr Metab 7:85 (2010)
  8. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effects of a low glycemic-load diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA 292: 2482-2490 (2004)
  9. Pittas AG, Roberts SB, Das SK, Gilhooly CH, Saltzman E, Golden J, Stark PC, and Greenberg AS. “The effects of the dietary glycemic load on type 2 diabetes risk factors during weight loss.” Obesity 14: 2200-2209 (2006)
  10. Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, and Sears B. “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006)
  11. Chalon S, Delion-Vancassel S, Belzung C, Guilloteau D, Leguisquet AM, Besnard JC, and Durand G. “Dietary fish oil affects monoaminergic neurotransmission and behavior in rats.“ J Nutr 128: 2512-2519 (1998)
  12. Chalon S. “Omega-3 fatty acids and monoamine neurotransmission. Prostaglandins Leukot Essent Fatty Acids 75: 259-269 (2006)
  13. Sorgi PJ, Hallowell EM, Hutchins HL, and Sears B. “Effects of an open-label pilot study with high-dose EPA/DHA concentrates on plasma phospholipids and behavior in children with attention deficit hyperactivity disorder.” Nutr J 6: 16 (2007)
  14. Watanabe S, Doshi M, and Hamazaki T. “n-3 Polyunsaturated fatty acid (PUFA) deficiency elevates and n-3 PUFA enrichment reduces brain 2-arachidonylglycerol level in mice.” Prostaglandin Leukot Essent Fatty Acids 69:51–59 (2003)

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.

A short history of the human food supply

The real goal of nutrition is the management of cellular inflammation. Increased cellular inflammation makes us fat, sick, and dumb (how about overweight, ill, and less intelligent). Strictly speaking, diets are defined by their macronutrient balance. This is because that balance determines the resulting hormonal responses. This doesn’t mean you can ignore the impact of various food ingredients on the generation of cellular inflammation.

This is why I categorize food ingredients into three major classes depending on when they were introduced into the human diet. The more ancient the food ingredients, the less damaging inflammatory impact they will have on turning genes off and on (i.e. gene expression). This is because the greater the period of time our genes have co-evolved with a given food ingredient, the more our body knows how to handle them. Unfortunately, human genes change slowly, but changes in our food supply can happen very rapidly.

With that as a background, let me describe the three major categories of food ingredients, especially in terms of their introduction to the human diet.

Paleolithic Ingredients

This category includes food ingredients that were available more than 10,000 years ago. Our best evidence is that humans first appeared as a new species in Southern Africa about 200,000 years ago (1). For the next 190,000 years, food ingredients of the human diet consisted of animal protein (grass-fed only), fish, animal and fish fats, fruits, vegetables, and nuts. I call these Paleolithic ingredients. This means for the first 95 percent of our existence as a species, these were the only food ingredients that genes were exposed to. As a result of 190,000 years of co-existence with our genes, these food ingredients have the least inflammatory potential on our genes.

Our best estimate of the macronutrient composition of the typical Paleolithic diet some 10-15,000 years ago was 25-28 percent protein, 40 percent carbohydrate, 32-35 percent fat with a very high intake of EPA and DHA (about 6 grams per day) and a 1:1 ratio of omega-6 to omega-3 fats (2). This is basically the composition of the anti inflammatory diet (3-5). If you use only Paleolithic ingredients, then you are almost forced to follow an anti inflammatory diet. The food ingredients are more restrictive, but the increased anti-inflammatory benefits are well worth it.

Mediterranean Ingredients

The second group of food ingredients represents those food choices that were available 2,000 years ago. We started playing Russian roulette with our genes 10,000 years ago as we started to introduce a wide variety of new food ingredients into the human diet. First and foremost was the introduction of grains, but not all at the same time. Wheat and barley were introduced about 10,000 years ago with rice and corn coming about 3,000 years later. Relative latecomers to the grain game were rye (about 5,000 years ago) and oats (about 3,000 years ago).

At almost the same time came the first real use of biotechnology. This was the discovery that if you fermented grains, you could produce alcohol. Alcohol is definitely not a food ingredient that our genes were prepared for (and frankly our genes still aren’t). I think it only took mankind about 10 years to learn how to produce alcohol, which probably makes the first appearance of beer occurring some 9,990 years ago. Wine was a relatively late arrival appearing about 4,000 years ago. With the domestication of animals (some 8,000 years ago) came the production of milk and dairy products. About 5,000 years ago, legumes (beans) were also introduced. Legumes tend to be rich in many anti-nutrients (such as lectins) that must be inactivated by fermentation or boiling. Needless to say, these anti-nutrients are not the best food ingredients to be exposed to.

I call this second group of food ingredients Mediterranean ingredients since they are the hallmark of what is commonly referred to as a “Mediterranean diet” (even though the diets as determined by macronutrient balance in different parts of the Mediterranean region are dramatically different). Those cultures in the Mediterranean region have had the time to genetically adapt to many of these new ingredients since all of these ingredients existed about 2,000 years ago.

Unfortunately, many others on the planet aren’t quite as fortunate. That’s why we have lactose intolerance, alcohol-related pathologies, celiac disease, and many adverse reactions to legumes that have not been properly detoxified. As a result these Mediterranean ingredients would have greater potential to induce increased levels of cellular inflammation than Paleolithic ingredients. However, at least they were better than the most recent group, which I term as, the “Do-You-Feel-Genetically-Lucky” group.

Do-You-Feel-Genetically-Lucky Ingredients

Unfortunately, these are the food ingredients that are currently playing havoc with our genes, especially our inflammatory genes. You eat these ingredients only at your own genetic risk. The first of these was refined sugar. Although first made 1,400 years ago, it didn’t experience a widespread introduction until about 300 years ago. With the advent of the Industrial Revolution came the production of refined grains. Products made from refined grains had a much longer shelf life, were easier to eat (especially important if you had poor teeth), and could be mass-produced (like breakfast cereals).

However, in my opinion the most dangerous food ingredient introduced in the past 200,000 years has been the widespread introduction of refined vegetable oils rich in omega-6 fatty acids. These are now the cheapest source of calories in the world. They have become ubiquitous in the American diet and are spreading worldwide like a virus. The reason for my concern is that omega-6 fatty acids are the building blocks for powerful inflammatory hormones known as eicosanoids. When increasing levels of omega-6 fatty acids in the diet were combined with the increased insulin generated by sugar and other refined carbohydrates, it spawned a massive increase in cellular inflammation worldwide in the past 40 years starting first in America (6). It is this Perfect Nutritional Storm that is rapidly destroying the fabric of the American health- care system.

The bottom line is that the macronutrient balance of the diet will generate incredibly powerful hormonal responses that can be your greatest ally or enemy in controlling cellular inflammation. Unless you feel incredibly lucky, try to stick with the food ingredients that give your genes the best chance to express themselves.

References

  1. Wells S. “The Journey of Man: A Genetic Odyssey.” Random House. New York, NY (2004)
  2. Kuipers RS, Luxwolda MF, Dijck-Brouwer DA, Eaton SB, Crawford MA, Cordain L, and Muskiet FA. “Estimated macronutrient and fatty acid intakes from an East African Paleolithic diet.” Br J Nutr 104: 1666-1687 (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.” Thomas Nelson. Nashville, TN (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.

When is a diet not a diet?

One of the major problems in nutrition is the lack of rigor in describing diets. The first problem is that the root of the word diet comes from the ancient Greek phrase “way of life”. A diet is not a short-term plan to fit into a swimsuit, but rather it is a way of life to reach a lifetime goal, like a longer and better life. If your goal is less grand like simply to lose weight, then to lose that weight and keep it off, you had better maintain that diet for the rest of your life. From that perspective, a diet like the Grapefruit diet doesn’t make much sense.

The second problem is the lack of precision in defining a diet. My definition of a diet is based on the macronutrient balance that ultimately determines hormonal responses. From this perspective, there are really only four diets based on the glycemic load, assuming that each diet contains the same number of calories.

Diet Common Name
Very low glycemic-load diet Ketogenic (i.e. Atkins diet)
Low glycemic-load diet Non-ketogenic (i.e. Zone Diet)
High glycemic-load diet American Heart (or Diabetes or Cancer, etc.) Association diet
Very high glycemic-load diet Strict vegetarian (i.e. Ornish diet)

Assuming these diets have an equal number of calories, you can then rank them in terms of the total amount of calories coming from protein, carbohydrates and fat as shown below:

Diet Macronutrient Composition
Very low glycemic-load diet 30% P, 10% C, and 60% F
Low glycemic-load diet 30% P, 40% C, and 30% F
High glycemic-load diet 15% P, 55% C, and 30% F
Very high glycemic-load diet 10% P, 80% C, and 10% F

You can see that depending on the macronutrient composition of the diet you choose to follow, it will generate very different hormonal responses. A ketogenic diet will induce increased cortisol levels that make you fat and keep you fat. High-glycemic diets induce excess insulin levels that make you fat and keep you fat. It’s only a low-glycemic diet that has been shown to burn fat faster (1) as well as maintain weight loss most effectively (2).

That’s why unless you define a diet carefully in terms of macronutrient balance, you can’t ever undertake any meaningful nutritional research to validate whether or not it achieves its stated goal. This is why most diet studies produce such conflicting results.

The wild card is which food ingredients you choose for a particular diet. This is where much of the confusion emerges as people throw around arbitrary terms like a Paleolithic diet or a Mediterranean diet. What the heck is a Mediterranean diet? Is it the diet from Morocco, Lebanon, Italy, or Spain? What you can do, however, is to review the food ingredients found in these diets.

For example, Paleolithic food ingredients would consist only of fruits, vegetables, nuts, grass-fed beef, eggs, and fish. A pretty limited group of foods to choose from, but it was all that was available to man 10,000 years ago. Mediterranean food ingredients include all of those in the Paleolithic group but now adding whole grains, alcohol, legumes, and dairy products. These were the dietary choices available about 2,000 years ago — a more diverse number of food choices for a particular diet, but now with a greater potential for generating inflammatory responses. Finally, there are the “Do-You-Feel-Lucky” food ingredients. This includes very recent additions to the human diet, such as sugar, refined carbohydrates and vegetable oils. These are food ingredients that make processed foods possible. However, they carry with them the greatest potential to increase cellular inflammation. Remember, it is increased cellular inflammation that makes you fat, sick, and dumb.

So if you want to be correct about the use of the word diet, then you should use the right terms. It could be an anti inflammatory diet using only Paleolithic food ingredients (i.e. a Paleo Zone Diet), or an anti inflammatory diet using only Mediterranean food ingredients (i.e. a Mediterranean Zone Diet), or even an anti inflammatory diet using the “Do-You-Feel-Lucky” food ingredients. This designation includes the most recent additions (sugar, refined carbohydrates, and vegetable oils) that have the greatest impact on inducing cellular inflammation, regardless of the macronutrient balance. Ultimately important are the hormonal responses of the macronutrient balance of the diet (especially after avoiding the worst offenders in the “Do-You-Feel-Lucky” group). The more restrictive your choices for food ingredients for any diet, the better the hormonal outcome for that particular diet. In particular, the primary clinical outcome for the anti inflammatory diet is the life-long management of cellular inflammation. And for that clinical parameter, the clinical research has found the anti inflammatory diet to be the clear winner regardless of the food ingredients selected (3-5).

References

  1. Layman DK, Evans EM, Erickson D, Seyler J, Weber J,; Bagshaw D, Griel A, Psota T, and Kris-Etherton P. “A moderate-protein diet produces sustained weight loss and long-term changes in body composition and blood lipids in obese adults.” J Nutr 139: 514-521 (2009)
  2. 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)
  3. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effects of a low glycemic-load diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA 292: 2482-2490 (2004)
  4. Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, and Sears B. “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006)
  5. Pittas AG, Roberts SB, Das SK, Gilhooly CH, Saltzman E, Golden J, Stark PC, and Greenberg AS. “The effects of the dietary glycemic load on type 2 diabetes risk factors during weight loss.” Obesity 14: 2200-2209 (2006)

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.

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.

Lights off for weight loss

I have often said that weight loss is a lot more complicated than simply “eating less and exercising more”. New research indicates how much more complicated weight gain is due to circadian rhythms. Our brain and virtually all of our cells are programmed to run on a 24-hour cycle to help us optimize future events (like sleep and eating) that are essential for life. In fact, even fungi have these biological clocks. There is a central clock in the brain that responds to light and dark by releasing the hormone melatonin. Melatonin, as well as other hormones, prepares the individual cells in different organs for an anticipated stimulus that allows those organs to rapidly respond with the greatest efficiency. The adipose tissue is one of those organs. This is why the uptake and release of fatty acids by the adipose tissue has a strong circadian rhythm (1). One hormone that is exclusively released by the fat cells is leptin. Both leptin and ghrelin (the hunger hormone released from the gut) are also under circadian control (2).

The bottom line is that as our light/dark cycles are becoming more distorted, the hormones that affect our appetite are also being adversely affected. It is known that sleep-deprived individuals are more inflamed (3) as well as have abnormalities in glucose metabolism (4).

New research indicates that increased light during the normal sleeping cycle for mice increases their weight and their fat mass (5). Most disturbing is that you only need a very dim light on during their normal sleep cycle to increase weight gain in the animals. The more intense the light during their normal sleep cycle, the greater the weight gain.

This is also true for humans, as discussed in an online pre-publication release that will be published in the March 2011 issue of the Journal of Endocrinology and Metabolism (6). In this study, subjects were exposed to dim lighting (about one-half the intensity of a typical office light) for eight hours prior to bedtime; then the release of melatonin would be completely suppressed for about 90 minutes after they started sleeping. Just like the mice, if the light was on, even dimly, while they were sleeping, their melatonin levels were depressed by about 50 percent. The less melatonin you release during sleep, the more body fat you accumulate.

This leads to an interesting thought. It is known that increased television viewing and prolonged computer use leads to increased weight gain. It has always been assumed that this was because the person was not exercising. This new data strongly suggests it is not a lack of physical activity that is the problem, but the disturbances in circadian rhythms that may be the underlying problem. It’s hard to exercise in the dark, but you sure can sleep better and get thinner in the process if you keep the lights off.

References

1. Bray MS and Young ME. “Circadian rhythms in the development of obesity: potential role for the circadian clock within the adipocyte.” Obesity Rev 8: 169-181 (2006)

2. Karla SP, Bagnasco M, Otukonyong EE, Dube MG, and Kalra PS. Rhythmic, reciprocal ghrelin and leptin signaling: new insight in the development of obesity.” Regulatory Peptides 111: 1-11 (2003)

3. Vgontzas AN, Papanicolaou DA, Bixler EO, Kales A, Tyson K, and Chrousos GP. “Elevation of plasma cytokines in disorders of excessive daytime sleepiness.” J Clin Endocrinol Metab 82: 1313-1316 (1997)

4. Spiegel K, Leproult R, and Van Cauter E. “Impact of sleep debt on metabolic and endocrine function.” Lancet 354: 1435-1439 (1999)

5. Fonken LK, Workman, JL, Walton JC, Weil ZM, Morris JS, Haim A, and Nelson RJ. “Light at night increases body mass by shifting the time of food intake.” Proc Natl Acad Sci USA 107: 18664-18669 (2010)

6. Gooley JJ, Chamberlain K, Smith KA, Shalsa SBS, Rajaatnam SMW, van Reen E, Zeitzer JM, Czeisler CA, and Lockley SW. “Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans.” J Clin Endocrino Metabol doi:10.1210/jc.2010-2098

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.

Another good reason to eat your fruits and vegetables

Your grandmother always told you, you couldn’t leave the table until you ate all your vegetables. She was giving you the essence of reducing your chances of dying from cardiovascular disease.

The trouble with testing any dietary hypothesis (even Grandma’s advice on vegetables) is the complexity of understanding nutrition. Unlike drugs, which are based on linear thinking (one drug affects one enzyme and that treats you), nutrition is based on non-linear thinking. That means nutrition is more like a three-dimensional chess match. Whenever you change one component (i.e. amount of fat) in the diet, there will be unintended changes as something else is automatically changed as a consequence (like either an increase in dietary protein or carbohydrate to make up the difference of the reduction of dietary fat). This secondary dietary change may totally obscure what you are trying to study. This explains why so many dietary studies appear to produce such wishy-washy results. To try to get around this constant dilemma, investigators often do extremely large epidemiological studies, using people who are initially disease-free and ask how an exposure to some dietary variable affects the development of a particular disease or more importantly death from a particular disease. These are called prospective cohort studies.

As you might imagine, there are very few of these studies since they require a very large number of subjects, and if the outcome is death, then they have to be followed for a very long time. This also means that these studies are extremely expensive. In a soon-to-be-published article in the European Heart Journal is a massive prospective cohort study (with more than 300,000 subjects and based upon an average of eight years of follow-up) that suggested if you ate more fruits and vegetables, your likelihood of dying of heart disease was reduced by 22 percent (1).

How much is more fruits and vegetables? It is about eight servings per day, and it appeared to be a dose-response effect. For each serving of fruits or vegetables, the risk of death from heart disease goes down by 4 percent. Bottom line, the more fruits and vegetables you eat, the greater the reduction in cardiovascular death.

Since you have to eat, why not eat right if your goal is reducing the risk of death from heart disease. If you are eating more fruits and vegetables, then something must be removed from the diet if the calories are to remain constant. The most logical choice would be reducing grains and starches as you increase fruits and vegetables. In the process, you reduce the glycemic load of the diet and reduce production of insulin. This will not only reduce your risk of dying from heart disease, but also help you lose excess body fat (2)

Notice that I keep emphasizing the words death and dying. The prevailing “wisdom” in the cardiovascular community is that it doesn’t matter what you eat as long as you reduce cholesterol levels. And since increased fruits and vegetables consumption has little impact on cholesterol levels, we are told that if you really want to reduce the risk of dying from heart disease, it’s imperative that you must take a statin drug for the rest of your life. Unfortunately, the research data doesn’t support such optimism. For example, if subjects are studied who have no heart disease (these are called primary prevention studies), then taking statin drugs has no impact on reducing their all-cause mortality (3). In other words, any reduction in cardiovascular death was offset by increases of death from other causes. Not such a good deal if your goal is reducing death whatever the cause. Another group of researchers came to the conclusion after analyzing a number of published trials using statin drugs for the primary prevention of developing heart disease, that there was no compelling reason for their use (4). Since the vast majority of the people taking statin drugs have no established heart disease, this would mean the continued prescription of these drugs comes close to health-care fraud.

But what if you already have heart disease? What is the best way to reduce the risk of dying from it? To answer that question, you undertake secondary prevention studies using death (it’s very easy to measure) as your clinical endpoint. In secondary prevention studies, statins will reduce cardiovascular mortality by about 20 percent in people who already have established heart disease. But if you really want to reduce the likelihood of dying from existing heart disease (like by 70 percent), then you not only have to have the patients increase their intake of fruits and vegetables, but also remove much of the omega-6 fatty acids from the diet and replace them with omega-3 fats (5).

If you do both of these dietary changes (replace grains and starches with more fruits and vegetables as well as replace omega-6 fats with omega-3 fats), then you are essentially following the anti inflammatory diet. That’s how you live longer whether you have heart disease or not.

References

1. Crowe FL, Roddam AW, Key TJ, et al. “Fruit and vegetable intake and mortality form ischaemic heart disease.” Eur Heart Journal 32: doi 10.1093 (2011)

2. Sears B. “The Zone.” Regan Books. New York, NY (1995)

3. Ray KK, Seshsai SRK, Erqou S, Sever P, Jukema JW, Ford I, and Sattar NS. “Statins and all-cause morality in high-risk primary prevention.” Arch Intern Med 170: 1024-1031 (2010)

4. Taylor F, Ward K, Moore THM, Burke M, Davey-Smith G, Casas JP, and Ebrahim S. “Statins for the primary prevention of cardiovascular disease.” The Cochrane Library Issue 1 (2011)

5. de Lorgeril M, Renaud S, Mamelle N, Salen P, Martin JL, Monjaud I, Guidollet J, Touboul P, and Delaye J. “Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease.” Lancet 343: 1454-1459 (1994)

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.

Increased satiety: The real secret to weight loss

Satiety is defined as lack of hunger. If you aren’t hungry, then cutting back calories is easy. Unfortunately, Americans seem to be hungrier than ever. This is not caused by a lack of willpower but due to hormonal imbalances in the hypothalamus that tell the brain to either seek more food or spend time on more productive activities. So the real question is not what is the best diet for weight loss, but what is the best diet for satiety?

the anti inflammatory diet has been clinically shown to burn fat faster than standard, recommended diets (1-3) as well as decreasing hunger compared to standard, recommended diets (4,5). But then whoever said that standard, recommended diets (like the USDA Food Pyramid) are good? A better comparison might be the anti inflammatory diet versus a Mediterranean diet.

I have often said that the anti inflammatory diet should be considered as the evolution of the Mediterranean diet because of its enhanced hormonal control. So where is the data for my contention?

The first randomized controlled research appeared in 2007 using patients with existing heart disease (6). In this study, while both groups lost weight, it was only the group on a Paleolithic diet that had any benefits in glucose reduction. So what’s a Paleolithic diet? In this study it was one that supplied 40 percent of the calories as low-glycemic-load carbohydrates, 28 percent of the calories as low-fat protein, and 28 percent from fat (the remaining calories came from alcohol, which didn’t exist in Paleolithic times). That sounds exactly like the anti inflammatory diet to me, so I will simply call it that. On the other hand, the Mediterranean diet was lower in protein (20 percent) and higher in carbohydrates (50 percent) as well as containing far more cereals and dairy products than the anti inflammatory diet.

The interesting thing that came out of this initial study was that patients on the anti inflammatory diet were apparently eating fewer calories, but with greater satiety. So they repeated the study again with another set of cardiovascular patients, except they measured leptin levels this time. The results were exactly the same (7), that is the anti inflammatory diet was more satiating per calorie, and there was also a greater reduction in leptin levels. This makes perfect sense since improved glycemic control seen in the first comparison study (6) would have been a consequence of reducing insulin resistance. The decrease in the leptin levels in the second study (7) would have been a consequence of the reduction of leptin resistance. The most likely cause of this hormone resistance would be the anti-inflammatory benefits of the anti inflammatory diet because it decreases cellular inflammation. It’s cellular inflammation that disrupts hormonal signaling efficiency and causes hormone resistance.

So here we have two randomized controlled studies (6,7) that indicate the superiority of the anti inflammatory diet compared to Mediterranean diet relative to reducing hormone resistance as well providing greater satiety with fewer calories, just as demonstrated in earlier studies when the anti inflammatory diet was compared to standard recommended diets (4,5). It is increased satiety that is ultimately how you lose weight and keep it off. The anti inflammatory diet appears the easiest way to reach that goal.

References

1. 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)

2. 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)

3. 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)

4. 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)

5. Agus MSD, Swain JF, Larson CL, Eckert E, and Ludwig DS. “Dietary composition and physiological adaptations to energy restriction.” Am J Clin Nutr 71: 901-907 (2000)

6. Lindberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K and Ahren B. “A Paleolithic diet improves glucose tolerance more than a Mediterrean-like diet in individuals with ischaemic heart disease.” Diabetologia 50: 1795-1807 (2007)

7. Jonsson T, Granfeldt Y, Erlanson-Albertsson, Ahren B, and Lindeber S. “A Paleolithic diet is more satiating per calorie than a Mediterrean-like diet in individuals with ischemic heart disease.” Nutrition & Metabolism 7:85 (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.

Why the Atkins diet doesn’t work and never will

The goal of any diet is to help you lose excess weight and keep it off. The first part is relatively easy to achieve; the second part is incredibly difficult to maintain. Any diet that restricts calories will do the first part, but invariably the lost weight returns. This is definitely the situation for the Atkins diet. I knew Bob Atkins well, and the only answer he had as to why people regain weight on his diet was that they are addicted to carbohydrates. Frankly, I never bought into that explanation from Bob any more than I believed the reasoning of the advocates for low-fat diets saying the failure to maintain weight loss is because people are addicted to fat. To paraphrase former President Clinton, “It’s the hormones, stupid.”

In most cases what really causes weight regain is cellular inflammation induced by hormonal imbalance. This is why any diet that uses the word “low” or “high” to describe itself will induce hormonal imbalance, and therefore ultimately fail. Low-fat diets are generally high-carbohydrate diets. High levels of carbohydrates will increase the production of insulin, which is the hormone that makes you fat and keeps you fat. This increase in insulin will generate increased cellular inflammation that increases the likelihood for weight regain (1). On the other hand, the Atkins diet is a low-carbohydrate diet that is also a high-fat diet. If those fats on the Atkins diet are rich in saturated and omega-6 fats (which they usually are), then their presence will also increase cellular inflammation (1). This increase in cellular inflammation (by either type of diet) disrupts hormonal signaling patterns (especially for insulin signaling) that generate increased insulin resistance. This was shown in one of my earlier research articles that demonstrated that under carefully controlled clinical conditions, following the Atkins diet shows significant increases in cellular inflammation compared to those subjects following the Zone Diet (2). In addition, there was decreased endurance capacity of the subjects on the Atkins diet compared to those on the Zone Diet (3).

The differences are probably due to the fact that the  anti inflammatory diet is a diet that is moderate in protein, carbohydrate and fat. It’s this type of dietary moderation of macronutrients that generates hormonal balance.Now new data from Yale Medical School indicates that a ketogenic (i.e. Atkins) diet may even have worse health implications than simply weight regain (4). In this study, it was demonstrated that although indicators of insulin resistance in the blood may be decreased on a ketogenic diet, insulin resistance in the liver was dramatically increased. Since the liver is the central processing organ for controlling metabolism, this would suggest that long-term use of the Atkins diet would cause metabolic problems leading to accumulation of excess fat. Adding even more fuel to this hormonal fire is another study that demonstrated that a ketogenic diet leads to increased production of cortisol (another hormone that makes you fat and keeps you fat) in the fat cells (5). Any increase in cortisol increases insulin resistance in that particular organ.

So it appears that ketogenic diets (like the Atkins diet) may initially reduce insulin levels in the blood, but increase insulin resistance in organs, such as the liver and the adipose tissue. The bottom line: Any initial weight loss with the Atkins diet is a false hope since it causes insulin resistance in various organs that ultimately cause the regain of any lost weight as excess fat. That’s a very bad prescription.

References:
1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
2. Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, and Sears B. “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006)
3. White AM, Johnston CS, Swan PD, Tjonn SL, and Sears B. “Blood ketones are directly related to fatigue and perceived effort during exercise in overweight adults adhering to low-carbohydrate diets for weight loss: a pilot study.” J Am Diet Assoc 107: 1792-1796 (2007)

4. Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D, Zhang XM, Samuel VT, and Shulman GI. “A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.” Am J Physiol Endocrinol Metab 299: E808-815 (2010)
5. Stimson RH, Johnstone AM, Homer NZ, Wake DJ, Morton NM, Andrew R, Lobley GE, and Walker BR. “Dietary macronutrient content alters cortisol metabolism independently of body weight changes in obese men.” J Clin Endocrinol Metab 92: 4480-4484 (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.