Category Archives: Zone Diet

Obesity starts in the womb

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A new study from Harvard Medical School strongly suggests that childhood obesity begins in the mother’s womb (1). Specifically, the lower the EPA and DHA concentrations in either the mother’s diet or her umbilical cord attached to the fetus, the more likely the child will develop obesity by age 3.

It is well known from animal experiments that omega-6 fatty acids make the offspring fat, and omega-3 fatty acids make the offspring thin (2-4). This new study now confirms the same thing is happening in humans (1).

It has been demonstrated in animal models that it only takes three to four generations of a high omega-6 fatty acid intake to increase obesity in the offspring (5,6). I believe one of the driving forces for the increase in childhood obesity has been the dramatic increase in omega-6 fatty acids over the past 100 years (7). However, much of that omega-6 fatty acid increase has come from the massive increase in soybean oil consumption that started in the early 1970s. That 40-year period only represents about two generations of humans, which means it is quite likely there will be higher childhood obesity rates coming with the next generations as long as omega-6 fatty acid consumption stays elevated.

At the molecular level, the problem really starts when these excess omega-6 fatty acids are activated by ever-increasing insulin levels caused by refined carbohydrate consumption to create increased cellular inflammation. In my book “Toxic Fat“ I describe some of the political decisions and their metabolic consequences that have led to the epidemic increase of cellular inflammation that has resulted in the rapid deterioration of American health (8).

The bottom line is that this dramatic increase in omega-6 fatty acids in the diet of American mothers is causing trans-generation changes in our children due to fetal programming. This occurs in the womb and results in the final tuning of the genetic code of the fetus by changing the gene expression of the unborn child. This is called epigenetic programming and begins to explain why each succeeding generation of Americans is getting fatter and fatter (9).

Even more ominous warnings are animal studies that indicate the “reward” response (increased dopamine levels) induced by consuming junk food experienced by the mother can also be transferred to the next generation by fetal programming (10).

So what can you do about this growing genetic disaster? If you are contemplating having a child, then beginning to cut back on omega-6 fatty acids and eating more omega-3 fatty acids is a good starting point. The benefits include having a thinner and smarter child. If you already have children whose gene expression has already been altered by fetal programming, then you have to control their diet for a lifetime to prevent reverting to that altered gene expression. It’s not a pretty picture. Although you can’t escape the dietary consequences of fetal programming, you can minimize the damage by treating food as drug to manage increased cellular inflammation that is making us fatter, sicker and dumber.

References

  1. Donahue, SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gillman MW, and Oken E. “Prenatal fatty acid status and child adiposity at age 3y.” Amer J Clin Nutr 93: 780-788 (2011)
  2. Gaillard D, Negrel R, Lagarde M and Ailhaud G. “Requirement and role of arachidonic acid in the differentiation of pre-adipose cells.” Biochem J 257: 389-397 (1989)
  3. Kim HK, Della-Fera M, Lin J, and Baile CA. “Docosahexaenoic acid inhibits adipocyte differentiation and induces apoptosis in 3T3-L1 pre-adipocytes.” J Nutr 136: 2965-2969 (2006)
  4. Massiera F, Saint-Marc P, Seydoux J, Murata T, Kobayashi T, Narumiya S, Guesnet P, Amri EZ, Negrel R, and Ailhaud G. “Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?” J Lipid Res 44: 271-279 (2003)
  5. Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, and Rawlings RR. “Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century.” Am J Clin Nutr 93: 950-962 (2011)
  6. Hanbauer I, Rivero-Covelo I, Maloku E, Baca A, Hu Q, Hibbeln JR, and Davis JM. “The Decrease of n-3 Fatty Acid Energy Percentage in an Equicaloric Diet Fed to B6C3Fe Mice for Three Generations Elicits Obesity.” Cardiovasc Psychiatry Neurol: 2009, Article ID.867041 (2009)
  7. Massiera F, Barbry P, Guesnet P, Joly A, Luquet S, Moreilhon-Brest C, Mohsen-Kanson T, Amri EZ, and Ailhaud G. “A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations.” J Lipid Res 51: 2352-2361 (2010)
  8. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  9. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C, Rodford J, Slater-Jefferies J, Garratt E, Crozier SR, Emerald BS, Gale CR, Inskip HM, Cooper C, and Hanson MA. “Epigenetic gene promoter methylation at birth is associated with child’s later adiposity.” Diabetes 60: 1528-1534 (2011)
  10. Ong ZY and Muhlhausler BS. “Maternal “junk-food” feeding of rat dams alters food choices and development of the mesolimbic reward pathway in the offspring.” FASEB J 25: S1530-6860 (2011)

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.

Fish oil and fat loss

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I have often said, “It takes fat to burn fat”. As I describe in my book “Toxic Fat,” increased cellular inflammation in the fat cells turns them into “fat traps” (1). This means that fat cells become increasingly compromised in their ability to release stored fat for conversion into chemical energy needed to allow you to move around and survive. As a result, you get fatter, and you are constantly tired and hungry.

One of the best ways to reduce cellular inflammation in the fat cells is by increasing your intake of omega-3 fatty acids. This was demonstrated in a recent article that indicated supplementing a calorie-restricted diet with 1.5 grams of EPA and DHA per day resulted in more than two pounds of additional weight loss compared to the control group in a eight-week period (2).

How omega-3 fatty acids help to ”burn fat faster” is most likely related to their ability to reduce cellular inflammation in the fat cells (3,4) and to increase the levels of adiponectin (5). Both mechanisms will help relax a “fat trap” that has been activated by cellular inflammation.

However, there is a cautionary note. This is because omega-3 fatty acids are very prone to oxidation once they enter the body. This is especially true relative to the enhanced oxidation of the LDL particles (6-9).

This means that to get the full benefits any fish oil supplementation, you have to increase your intake of polyphenols to protect the omega-3 fatty acids from oxidation. How much? I recommend at least 8,000 additional ORAC units for every 2.5 grams of EPA and DHA that you add to your diet. That's about 10 servings per day of fruits and vegetables, which should be no problem if you are following the Zone diet. If not, then consider taking a good polyphenol supplement.

Once you add both extra fish oil and polyphenols to a calorie-restricted diet, you will burn fat faster without any concern about increased oxidation in the body that can lead to accelerated aging.

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, and Martinez JA. “Randomized trial of weight-loss diets for young adults varying in fish and fish oil content.” Int J Obes 31: 1560-1566 (2007)
  3. Huber J, Loffler M, Bilban M, Reimers M, Kadl A, Todoric J, Zeyda M, Geyeregger R, Schreiner M, Weichhart T, Leitinger N, Waldhausl W, and Stulnig TM. “Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids.” Int J Obes 31: 1004-1013 (2007)
  4. Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhausl W, and Stulnig TM. “Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids.” Diabetologia 49: 2109-2119 (2006)
  5. Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, and Jebb SA. “Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women.” Int J Obes 30: 1535-1544 (2006)
  6. Pedersen H, Petersen M, Major-Pedersen A, Jensen T, Nielsen NS, Lauridsen ST, and Marckmann P. “Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes.” Eur J Clin Nutr 57: 713-720 (2003)
  7. Turini ME, Crozier GL, Donnet-Hughes A, and Richelle MA. “Short-term fish oil supplementation improved innate immunity, but increased ex vivo oxidation of LDL in man–a pilot study.” Eur J Nutr 40: 56-65 (2001)
  8. Stalenhoef AF, de Graaf J, Wittekoek ME, Bredie SJ, Demacker PN, and Kastelein JJ. “The effect of concentrated n-3 fatty acids versus gemfibrozil on plasma lipoproteins, low-density lipoprotein heterogeneity and oxidizability in patients with hypertriglyceridemia.” Atherosclerosis 153: 129-138 (2000)
  9. Finnegan YE. Minihane AM, Leigh-Firbank EC, Kew S, Meijer GW, Muggli R, Calder PC, and Williams CM. “Plant- and marine-derived n-3 polyunsaturated fatty acids have differential effects on fasting and postprandial blood lipid concentrations and on the susceptibility of LDL to oxidative modification in moderately hyperlipidemic subjects.” Am J Clin Nutr 77: 783-795 (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 new obesity suspect

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The number of overweight and obese has been remarkably stable for the past several years at about two-thirds of the adult population. This strongly suggests that these Americans are genetically prone to gain weight under the right dietary circumstances. Yet a greater number of adults are moving from a classification of being simply overweight to being labeled as obese. This is a strong indication that those who are genetically predisposed to weight gain are becoming fatter. According to the Centers for Disease Control, only three states in 2007 had more than 30 percent of the adult population classified as obese. In only two years, the number of states that have more than 30 percent obesity in adult populations had increased to nine. That’s a 300 percent increase in two years!

One new suspect in our growing obesity crisis may be caffeinated coffee. It has been known for a long time that a high-fat meal increases blood sugar as well as maintains high levels of triglycerides (1). A new study from the University of Guelph found that consuming a high-fat meal increased blood sugar by more than 30 percent when giving a standard glucose tolerance test five hours later (2). Adding the equivalent of two cups of coffee more than doubled this increase in blood-sugar levels five hours after a high-fat meal.

The implication is that a constant diet of high-fat foods and a lot of coffee will accelerate the development of insulin resistance. When this occurs, the pancreas is forced to release more insulin to help reduce blood sugar levels. Unfortunately, it is excess insulin that makes you fat and keeps you fat.

The controversy over caffeine has continued for more than 100 years. The first instance occurred in a trial in the early part of the 20th century at which the U.S. government sued Coca-Cola for adulterating a food by adding caffeine to a soft drink. (Fortunately for Coca-Cola, the company had removed the coca extracts containing cocaine several years earlier). In a trial similar to the Scopes trial on evolution that would be held 15 years later in the same court system, the testimony was highly charged on both sides. The local judge dismissed the case, but the government continued it for many years in various appeals courts until the case was settled with a no-contest plea (3).

Now a new call for limits on caffeine was presented in a recent article in the Journal of the American Medical Association (4). Maybe with more research we will find that caffeine may be another factor for those who are genetically predisposed to gain weight to become fatter than ever.

References:

  1. Tushuizen ME, Nieuwland R, Scheffer PG, Sturk A, Heine RJ, and Diamant M. “Two consecutive high-fat meals affect endothelial-dependent vasodilation, oxidative stress and cellular microparticles in healthy men.” J Thromb Haemost 4: 1003-1010 (2006)
  2. Beaudoin MS, Robinson LE, and Graham TE. “An oral lipid challenge and acute intake of caffeinated coffee additively decrease glucose tolerance in healthy men.” J Nutrition 141: 574-581 (2011)
  3. Carpenter M. “A century later, jury’s still out on caffeine limits.” New York Times. March 28, 2011
  4. Arria A and O’Brien MC. “The ‘high’ risk of energy drinks.” JAMA 305: 600-601 (2011)

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.

New solution or simply admitting failure?

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SurgeryLast week the International Diabetes Federation (IDF) announced that gastric bypass surgery is a cost-effective treatment for type 2 diabetes. This marks the first time in modern medicine that cutting out normal tissue is now considered good medicine. It also indicates the pathetic state of medical science for the treatment of diabetes.

Make no mistake: Type 2 diabetes is now a pandemic, affecting approximately 300 million people worldwide. This is projected to increase to some 450 million people worldwide by 2030. Since diabetes is one of the most costly chronic disease conditions, it is the most likely to break the financial backbone of health-care systems in every advanced country.

The typical gastric bypass surgery costs from $15,000 to $24,000. Just for argument's sake, let's assume it is $20,000 for each surgery. Since some 26 million people in the United States have type 2 diabetes, then a mere $520 billion dollars spent on gastric bypass surgery would solve our growing epidemic. Obviously we don't have that type of money floating in the health-care system.

Furthermore, the 10-year failure rate is relatively high for this type of surgery (1). For example, 20 percent of patients who were initially obese (BMI >50 percent) could not maintain their long-term BMI below 35 percent (the definition of morbidly obese). This failure rate rises to 58 percent for those whose initial BMI was greater than 50.

The key feature as to why gastric bypass surgery works is the almost immediate suppression of hunger, mediated by improved release of hormones from the gut (i.e. PYY) that go directly to the brain to tell the patient to stop eating. Over time it would appear that this initial enhancement of PYY release is being compromised. As a result, those patients regain the lost weight.

So maybe gastric bypass is not the best long-term solution (and definitely not a cost-effective one in those patients that regain much of their lost weight) for solving the current epidemic of diabetes. So what's the alternative? One solution would be an anti-inflammatory diet that supplies adequate protein to stimulate PYY release as well as control the levels of cellular inflammation in the pancreas, the underlying reason why insufficient insulin levels are secreted in the first place (2).

Call me crazy, but this dietary approach appears far more cost-effective.

References

  1. Christou NV, Look D, and MacLean LD. “Weight gain after short- and long-limb gastric bypass in patients followed for longer than 10 years.” Ann Surg 244: 734-740 (2006)
  2. Donath MY,Boni-Schnetzler M, Ellingsgaard H, and Ehses JA. “Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.” Physiology 24: 325-331 (2009)

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 really dumb diet from France

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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?

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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

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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

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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?

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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

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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.