Obesity continues to climb

Last week the Robert Wood Johnson Foundation reported that more than 12 states now have adult obesity rates greater than 30 percent, and that one in three children are either overweight or obese. However, 16 years ago, no state in the United States had an adult obesity rate greater than 20 percent. So in less than a generation, adult obesity has skyrocketed. Yet at the same time, according to the Centers for Disease Control, the percentage of overweight people has remained fairly constant since 1960, while the percentage of obese individuals has increased significantly since 1980. What this suggests is that there is a genetic component that can be activated in those individuals predisposed to gain weight. Once activated, accumulation of excess fat accelerates.

I feel the driving force between this activation of genetic factors is the increasing inflammatory nature of the American diet. We know that it is elevated insulin levels that make us fat and keep us fat. But what really causes insulin to become elevated in the first place? The simple explanation is that it comes from eating excess carbohydrates. However, that is too simplistic an explanation since one-third of adult Americans who are thin are also eating excess carbohydrates.

A more comprehensive answer is it’s insulin resistance that causes elevated insulin levels. Insulin resistance is a consequence of disturbances in the body’s insulin-signaling pathways in the cell caused by cellular inflammation. My most recent book, “Toxic Fat,” goes into great detail on this subject (1). But simply stated, the more cellular inflammation you have in your cells, the greater the likelihood of insulin resistance. And if you are genetically prone to gain weight, increasing insulin resistance will really pack on the extra fat. More insidious is that insulin resistance also creates a “fat trap” through which incoming dietary calories are trapped in your fat cells and can’t be released to provide the necessary energy the body needs. This means you are constantly hungry.

If you are surrounded by cheap processed foods (rich in omega-6 fatty acids and refined carbohydrates), then you are going to quench that hunger with those foods that increase cellular inflammation to even greater levels. The end result is an increasing rise of obesity.

But the fastest growing segment of the overweight and obese population is not adults, but children under the age of 5, with 20 percent now either overweight or obese before entering kindergarten (2). You can’t blame school lunches for this because they are not in school yet. What you can blame is epigenetics (3). This is how the metabolic future of the child can be greatly determined in the womb by the inflammatory nature of the mother’s diet. When these children are born, their altered genetics make them sitting targets for a world full of inflammatory food. Unless you change the foundation of the food supply to become more anti-inflammatory (less omega-6 fatty acids and a lower glycemic load), then the future for these children is incredibly bleak.


  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Kim J, Peterson KE, Scanlon KS, Fitzmaurice GM, Must A, Oken E, Rifas-Shiman SL, Rich-Edwards JW, and Gillman MW. “Trends in overweight from 1980 through 2001 among preschool-aged children enrolled in a health maintenance organization. Obesity 14: 1107-1112 (2006)
  3. Lustig RH editor. “Obesity Before Birth.” Springer. New York (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.

Zone diet validation studies

Weight Loss

Any diet that restricts calories will result in equivalent weight loss. However, the same doesn’t hold true as to what the source of that weight loss is. Weight loss from either dehydration (such as ketogenic diets) or cannibalization of muscle and organ mass (such as low-protein diets) has no health benefits. Only when the weight loss source is from stored fat do you gain any health benefits. Here the Zone diet has been shown to be superior to all other diets in burning fat faster (1-4). It has been demonstrated that if a person has a high initial insulin response to a glucose challenge, then the Zone diet is also superior in weight loss (5,6). A recent study from the New England Journal of Medicine indicates that a diet composition similar to the Zone diet is superior to other compositions in preventing the regain of lost weight (7). This is probably caused by the increased satiety induced by the Zone diet compared to other diets (1,8,9).

Reduction of cellular inflammation

There is total agreement in the research literature that the Zone diet is superior in reducing cellular inflammation (10-12). Since cellular inflammation is the driving force for chronic disease, then this should be the ultimate goal of any diet. Call me crazy for thinking otherwise.

Heart disease

It is ironic that the Ornish diet is still considered one of the best diets for heart disease, since the published data indicates that twice as many people had fatal heart attacks on the Ornish diet compared to a control diet (13). This is definitely the case of don’t confuse me with the facts. On the other hand, diets with the same balance of protein, carbohydrate and fat as the Zone diet has have been shown to be superior in reducing cardiovascular risk factors, such as cholesterol and fasting insulin (14,15).


The first publication validating the benefits of the Zone diet in treating diabetes appeared in 1998 (16). Since that time there have been several other studies indicating the superiority of the Zone diet composition for reducing blood glucose levels (17-20). In 2005, the Joslin Diabetes Research Center at Harvard Medical School announced its new dietary guidelines for treating obesity and diabetes. These dietary guidelines were essentially identical to the Zone diet. Studies done at the Joslin Diabetes Research Center following those dietary guidelines confirm the efficacy of the Zone diet to reduce diabetic risk factors (21). If the Zone diet isn’t recommended for individuals with diabetes, then someone should tell Harvard.

Ease of use

The Zone diet simply requires balancing one-third of your plate with low-fat protein with the other two-thirds coming from fruits and vegetables (i.e. colorful carbohydrates). Then you add a dash (that’s a small amount) of heart-healthy monounsaturated fats. The Zone diet is based on a bell-shaped curve balancing low-fat protein and low-glycemic-index carbohydrates, not a particular magic number. If you balance the plate as described above using your hand and your eye, it will approximate 40 percent of the calories as carbohydrates, 30 percent of calories as protein, and 30 percent of the calories as fat. Furthermore, it was found in a recent Stanford University study that the Zone diet provided greater amounts of micronutrients on a calorie-restricted program than any other diet (22).

Eventually all dietary theories have to be analyzed in the crucible of experimentation to determine their validity. So far in the past 13 years since I wrote my first book, my concepts of anti-inflammatory nutrition still seem to be at the cutting edge.


  1. Skov AR, Toubro S, Ronn B, Holm L, and Astrup A. “Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity.” Int J Obes Relat Metab Disord 23: 528-536 (1999)
  2. 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)
  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. 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)
  5. Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, and Ludwig DS. “Effects of a low-glycemic-load vs low-fat diet in obese young adults: a randomized trial.” JAMA 297: 2092-2102 (2007)
  6. Pittas AG, Das SK, Hajduk CL, Golden J, Saltzman E, Stark PC, Greenberg AS, and Roberts SB. “A low-glycemic-load diet facilitates greater weight loss in overweight adults with high insulin secretion but not in overweight adults with low insulin secretion in the CALERIE Trial.” Diabetes Care 28: 2939-2941 (2005)
  7. 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)
  8. Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, Roberts SB, Agus MS, Swain JF, Larson CL, and Eckert EA. “Dietary high-glycemic-index foods, overeating, and obesity.” Pediatrics 103: E26 (1999)
  9. Agus MS, Swain JF, Larson CL, Eckert EA, and Ludwig DS. “Dietary composition and physiologic adaptations to energy restriction.” Am J Clin Nutr 71: 901-907 (2000)
  10. 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)
  11. 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)
  12. 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)
  13. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, and Brand RJ, “Intensive lifestyle changes for reversal of coronary heart disease.” JAMA 280: 2001-2007 (1998)
  14. Wolfe BM and Piche LA. “Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects.” Clin Invest Med 22: 140-1488 (1999)
  15. Dumesnil JG, Turgeon J, Tremblay A, Poirier P, Gilbert M, Gagnon L, St-Pierre S, Garneau C, Lemieux I, Pascot A, Bergeron J, and Despres JP. “Effect of a low-glycaemic index, low-fat, high-protein diet on the atherogenic metabolic risk profile of abdominally obese men.” Br J Nutr 86:557-568 (2001)
  16. Markovic TP, Campbell LV, Balasubramanian S, Jenkins AB, Fleury AC, Simons LA, and Chisholm DJ. “Beneficial effect on average lipid levels from energy restriction and fat loss in obese individuals with or without type 2 diabetes.” Diabetes Care 21: 695-700 (1998)
  17. Layman DK, Shiue H, Sather C, Erickson DJ, and Baum J. “Increased dietary protein modifies glucose and insulin homeostasis in adult women during weight loss.” J Nutr 133: 405-410 (2003)
  18. Gannon MC, Nuttall FQ, Saeed A, Jordan K, and Hoover H. “An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes.” Am J Clin Nutr 78: 734-741 (2003)
  19. Nuttall FQ, Gannon MC, Saeed A, Jordan K, and Hoover H. “The metabolic response of subjects with type 2 diabetes to a high-protein, weight-maintenance diet.” J Clin Endocrinol Metab 2003 88: 3577-3583 (2003)
  20. Gannon MC and Nuttall FQ. “Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition.” Nutr Metab (Lond) 3: 16 (2006)
  21. Hamdy O and Carver C. “The Why WAIT program: improving clinical outcomes through weight management in type 2 diabetes.” Curr Diab Rep 8: 413-420 (2008)
  22. Gardner CD, Kim S, Bersamin A, Dopler-Nelson M, Otten J, Oelrich B, and Cherin R. “Micronutrient quality of weight-loss diets that focus on macronutrients: results from the A TO Z study.” Am J Clin Nutr 92: 304-312 (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.

Ease off the fats during pregnancy

Obesity remains one of the primary headlines every day. But what you probably don’t know is the fastest growing segment of the obesity epidemic is children less than 4 years old. Approximately 20 percent are obese (1). Even more disturbing is the growth of obesity in children under the age of six months (2). You can’t blame school lunch programs for this youngest group, since they are too young to go to school, and you can’t blame lack of exercise since they can’t walk yet.

Frankly, no child wants to be obese. In fact, their quality of life is similar to that of a child undergoing chemotherapy (3). Yet we are constantly reminded that they are obese because they lack personal responsibility, and they only have to “eat less and exercise more”. The fact that such interventions don’t seem to work is simply a minor detail (4-6).

As I mentioned in an earlier blog, the culprit may be fetal programming in the womb that is causing epigenetic changes in the fetus before birth. This has already been demonstrated in pregnant rats that were fed a high-fat diet from the first day of pregnancy (7). These rats were genetically bred to be obesity resistant so that extra fat in their diet didn’t increase the body weight of the mothers during pregnancy. However, the offspring of those mothers fed the high-fat diet had blood sugar levels that were nearly twice as high as compared to offspring coming from the pregnant rats being fed a normal-fat diet. This is an indication that they were born with insulin resistance.

When researchers looked for epigenetic markers that might distinguish the two groups of offspring, sure enough they found chemical markers in the genes that regulate glucose metabolism. Since these epigenetic markers on the genes are not easily removed, the offspring with them would face a lifetime of dietary challenge to counteract their new genetic pre-disposition to obesity and diabetes.

So let’s come back to the growing childhood obesity problem in the very young. It may be due to fetal programming caused by high levels of both saturated and omega-6 fatty acids in the prenatal diet. Both types of fatty acids will cause increased cellular inflammation that can affect gene expression. If that occurs in the fetus, then that may be enough to genetically alter their future for a lifetime, including a far greater risk of obesity and diabetes.


  1. Anderson SE and Whitaker RC. “Prevalence of Obesity Among US Preschool Children in Different Racial and Ethnic Groups.” Arch Pediatric Adolescent Med 163: 344-348 (2009)
  2. Kim J, Peterson KE, Scanlon KS, Fitzmaurice GM, Must A, Oaken E, Rifas-Shiman SL, Rich-Edwards JW, and Gillman MW. “Trends in overweight from 1980 through 2001 among preschool-aged children enrolled in a health maintenance organization.” Obesity 14: 1107-1112 (2006)
  3. Schwimmer JB, Burwinkle TM, and Varni JW. “Health-related quality of life of severely obese children and adolescents.” JAMA 289: 1813-1819 (2003)
  4. McGovern L, Johnson JN, Paulo R, Hettinger A, Singhal V, Kamath C, Erwin PJ, and Montori VM. “Clinical review: treatment of pediatric obesity: a systematic review and meta-analysis of randomized trials.” J Clin Endocrinol Metab 93: 4600-4605 (2008)
  5. Kamath CC, Vickers KS, Ehrlich A, McGovern L, Johnson J, Singhal V, Paulo R, Hettinger A, Erwin PJ, and Montori VM. “Clinical review: behavioral interventions to prevent childhood obesity: a systematic review and meta-analyses of randomized trials.” J Clin Endocrinol Metab 93: 4606-4615 (2008)
  6. Shaw K, Gennat H, O’Rourke P, and Del Mar C. “Exercise for overweight or obesity.” Cochrane Database Syst Rev 2006: CD003817 (2006)
  7. Strakovsky RS, Zhang X, Zhou D, and Pan YX. “Gestational high-fat diet programs hepatic phosphoenolpyruvate carboxykinase gene expression and histone modification in neonatal offspring rats.” J Physiol 589: 2707-2717 (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.

What are we really entitled to?

For the past year the future of the American economy has centered on the word “entitlement,” especially in terms of health care. But no one is quite certain about what the word means. Social Security is not really an entitlement because it is a forced savings program that promises you the money you put into an old-age fund will be given back to you when you need it, some time in your 60s. The fact that the government has been using that account as a piggy bank to fund itself without raising taxes and leaving behind government I.O.U.s in place of the funds is another matter. But you are definitely entitled to at least get back the money you put into it.

Medicare is a completely different matter. In this case, you put very little money into a fund (which is also heavily borrowed from by the government), and you expect to get a lot more back. In my view, you are entitled to get back the money you paid into Medicare, and anything more should be considered a gift from a rich uncle (Sam), who is no longer very rich.

In an attempt to resolve this problem, Congressman Paul Ryan came up with a plan that went nowhere but had at least some intellectual merit: You pay into the medical fund for old age, and you get back what you paid in (and a little more) at age 67. The most notable feature of this plan was getting an annual voucher for about $6,000 based on 2012 dollars to be applied for private health insurance premiums after age 67.

At the current Medicare tax rate, the only way to pay in more than $6,000 into proposed trust fund on an annual basis is if you make more than $200,000 per year. Since there aren’t too many Americans making that type of salary, it’s your rich uncle who must make up the difference. Even if you were making $200,000 per year for 40 years and only planned to live another 15 years after retirement, it is still a pretty good deal, as it is forced savings for health-care insurance in the future. Any overpayment on your part will only help those who are not lucky enough to make $200,000 a year for 40 years. Unfortunately, this proposal was politically dead on arrival

The real problem with any health-care entitlement program was pointed out in a well-reasoned article in the May 19th issue of The New Republic — you can’t cure chronic disease, you can only manage it (1). In addition, new research analyses of the current state of Americans in old age indicates that we aren’t doing a very good job of managing chronic diseases (2). Although Americans are living longer, the length of life with chronic disease and loss of functional mobility (i.e. independent living) have rapidly increased since 1998. We are living longer because the elderly are essentially on life support generated by increasingly more expensive drugs that only marginally extend the lives of the very sick. We are not going to cure heart disease, cancer, stroke, and definitely not Alzheimer’s. The best we can do is to help manage their outcomes. Unfortunately, these are also diseases of the elderly, and the cost of increasing each year of life after 65 has risen from about $50,000 in the 1970s to nearly $150,000 in the 1990s. This could possibly be justified if the rich uncle were still rich.

The solution according to the authors of the New Republic article is redirecting the money that we can spend to maximize expenditures on public health care (prevention and elongation of independent living) as opposed to “curing” elderly with chronic disease that usually results in the decreased quality of life (1). The primary beneficiaries of this shift in medical thinking should be children followed by working adults, with the lowest health-care priority going to those over age 80. It sounds harsh, but that is exactly how socialized medicine works in Europe.

So what do you do to protect yourself in the future, especially if you are nearing 65? My suggestion is to start aggressively reducing cellular inflammation by following an anti-inflammatory diet and lifestyle. That’s the only thing you are really entitled to and that will also be the only thing your “rich” uncle can realistically pay for in the future.


  1. Callahan D and Nuland S. “The quagmire: how American medicine is destroying itself.” The New Republic. May 19, 2011
  2. Crimmins EM and Beltran-Sanchez H. “Mortality and morbidity trends: is there compression of morbidity?” J Gerontol B Physchol Soc Sci 66: 75-86 (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.

Getting closer to the Zone all the time

Last week the USDA announced its newest version of how Americans should eat. For the first time in more than 20 years, the USDA apparently stopped acting as the marketing arm of agribusiness by using a food pyramid (presented in 1992) and worse yet some abstract concept of an “eat-more, exercise-more” idea (presented in 2005). Now the USDA has turned to a plate format, which I have used for years. For comparison, you can see that the Zone diet recommendations are still a lot easier to understand than even the new and improved USDA recommendations as shown below:

The USDA proposes that half your plate (I’ll assume at every meal that you want to control the glycemic load of the meal) should be composed of vegetables and fruits. This is much closer to my Zone recommendation of filling 2/3 of the plate at each meal with vegetables and fruits. Both plates give a volume size to protein (and I’ll assume it is a low-fat protein source). The Zone plate appears to have a higher amount of low-fat protein consisting of 1/3 the plate instead of a quarter as found in the USDA plate. Of course if you add in the strange circle outside the plate that represents milk or cheese (both protein sources) back onto the plate, then you would probably get to about 1/3 the plate volume as low-fat protein.

Finally, what about whole grains on the USDA plate? From a glycemic-load viewpoint, whole grains have nearly the same impact on insulin response as refined grains, so you really don’t gain anything hormonally from having them in your diet. However, if you are at your ideal percentage of body fat, have no chronic disease, perform at peak levels, and are always happy and even-keeled emotionally, only then should you think about adding some whole grains to your diet. (Keep in mind that real whole grains are usually only found in storage bins or in the frozen product section of the supermarket, not in the processed food aisles.) But if you begin to gain weight, develop indications of a chronic disease, or don’t perform physically, mentally, and emotionally on a consistent basis, then take the whole grains out of your diet and go back to my classic Zone plate.

The one thing not mentioned in the USDA guidelines is the role of fat. On the Zone plate, I always say add a dash (that’s a small amount), but that dash of fat should be very low in omega-6 and saturated fats as both can accelerate cellular inflammation. I guess the USDA hasn’t had time to grapple with that more complex dietary concept. Perhaps they will another five years from now. But you don’t have to wait for their next guideline revision. Just follow the dietary guidelines on the Zone plate the best you can at every meal and snack. If you do, then you have done everything possible to maintain your wellness (as measured by your ability to manage cellular inflammation) for as long as possible. I guarantee you that will be the only real health-care reform program that you can count on in the future.

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 new wrinkle in the cholesterol story

One of the great marketing successes of the pharmaceutical industry has been the linkage between LDL cholesterol levels and heart disease. In essence, the message, “if your LDL cholesterol is high, you are going to die,” is powerful. Unfortunately, the data state otherwise.

It was known in the mid 1990s that oxidized LDL was the primary suspect in the development of atherosclerotic lesions; not natural, non-oxidized LDL. But it was also at this time that the first statin studies began to appear, and that gave the pharmaceutical industry a patented drug to “prevent” heart disease (2). It was such a good story to tell and an even better one to sell. Unfortunately, as I pointed out in an earlier blog, it has never held up well against unbiased scrutiny, especially in patients with high cholesterol levels but without any heart disease.

Part of the reason lies in the data. Shown below is the correlation of LDL cholesterol to heart disease

You can see from this data that there is a higher percentage of cardiovascular disease patients with high LDL cholesterol levels compared with very low levels, but not that much. This explains why about half the people who die from heart disease have normal LDL cholesterol levels (less than 130 mg/dl). It also means that high LDL cholesterol is not a very good predictor of heart disease.

On the other hand, a very different picture emerges if you look at the levels of oxidized LDL levels as shown below.

Even without a background in statistics you can see a very striking relationship in the prediction of heart disease with increasing levels of oxidized LDL levels.

So why don’t physicians use oxidized LDL levels as an indicator of heart disease risk? First, the test is much more difficult to do than a simple cholesterol test. Second, it ruins a great story that is easy to communicate to the patient. Third, the best way of reducing oxidized LDL levels is natural anti-oxidants, such as polyphenols, that have no patent protection (3,4). Reducing LDL cholesterol is simple. Just take a statin drug for the rest of your life. Reducing oxidized LDL cholesterol requires having plenty of antioxidants in your diet with polyphenols the most powerful.

Now there is another new entry into the LDL story. This is “super-sticky” LDL. In an online pre-publication, it was demonstrated that this new type of LDL particle may be even worse than oxidized cholesterol in promoting the development of heart disease (5). This “super-sticky” LDL comes from the formation of advanced glycosylation end products (AGEs). I described this formation of protein-carbohydrate linkages as an integral part of the aging process in my book, “The Anti-Aging Zone,” published more than a decade ago (6).

The best way to reduce the production of “super-sticky” LDL is to reduce blood sugar levels. This helps explain why individuals with diabetes are two to three times more likely to develop heart disease. The best way to reduce elevated blood sugar is the Zone diet. That’s why the latest dietary recommendations for the treatment of diabetes by the Joslin Diabetes Research Center at Harvard Medical School are essentially identical to the Zone diet.

Heart disease remains the number-one cause of death in America. Unfortunately, it is more complex than “taking a statin a day to keep death away”.


  1. Maor I and Aviram M. “Oxidized low-density lipoprotein leads to macrophage accumulation of unesterified cholesterol as a result of lysosomal trapping of the lipoprotein hydrolyzed cholesterol ester.” J Lipid Res 35: 803-819 (1994)
  2. Simvastatin Study Group. “Randomized trial of cholesterol lowering in 4,444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).” Lancet 344: 1383-1389 (1994)
  3. Shafiee M, Carbonneau MA, Urban N, Descomps B, and Leger CL. “Grape and grape seed extract capacities at protecting LDL against oxidation generated by Cu2+, AAPH or SIN-1 and at decreasing superoxide THP-1 cell production.” Free Radic Res 37: 573-584 (2003) (ISSN: 1071-5762)
  4. Chen CY, Yi L, Jin X, Mi MT, Zhang T, Ling WH, and Yu B. “Delphinidin attenuates stress injury induced by oxidized low-density lipoprotein in human umbilical vein endothelial cells.” Chem Biol Interact 183: 105-112 (2010)
  5. Rabbani N, Godfrey L, Xue M, Shaheen F, Geoffrion M, Milne R, and Thornalley PJ. “Glycation of LDL by methylglyoxal increases arterial atherogenicity.” Diabetes 60 doi:10.2337/db09-1455 (2011)
  6. Sears B. “The Anti-Aging Zone.” Regan Press. New York, NY (1999)

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.

No excuses, eat your breakfast

Everyone knows that breakfast should be the most important meal of the day. Unfortunately, no one seems to have time to consume a real breakfast. If they do, then it’s usually a high-carbohydrate quasi-dessert that is so portable that they can eat it in the car. Although our world is becoming time-compressed, our biological rhythms are not. While you sleep, your body is literally digesting itself to provide energy for the brain. Much of this energy comes from digesting muscle mass to make glucose as the supplies of stored carbohydrate in the liver are rapidly depleted during the night forcing the body to start digesting muscle to supply enough glucose to the brain. Rebuilding lost muscle mass demands protein replenishment upon waking, and you aren’t going to get achieve that goal by eating a typical breakfast cereal and definitely not by drinking a cup of coffee as a stimulant.

It has been known for some time there is a strong relationship between skipping breakfast and obesity and subsequent establishment of poor dietary habits (1,2). Furthermore, the higher the protein content of the breakfast, the greater the satiety. That increase in satiety is correlated with increased PYY (the satiety hormone) levels in the blood (3). It was also demonstrated more than 10 years ago that giving a higher-protein breakfast meal to overweight adolescents resulted in significant appetite suppression. This lack of hunger is correlated with dramatic changes in the levels of insulin and glucagon in the blood (4).

Now a new study pre-published electronically indicates that a high-protein breakfast also dramatically alters brain function (5). Overweight adolescents who normally skipped breakfast were either given nothing for breakfast, a carbohydrate-rich breakfast, or a protein-rich breakfast for six days. On the seventh day of each breakfast cycle, they had a fMRI scan of their brains while being shown pictures of various palatable foods on a screen. After consuming the higher-protein breakfast for six days, there was far less activation in the regions of brain associated with food motivation and reward when shown the pictures of highly desirable foods.

One surprising observation from this study is the primary reason given by the overweight adolescent subjects for skipping breakfast was not that they were trying to lose weight, but they just lacked the time or were not feeling hungry upon waking. The lack of time in the morning is understandable because adolescents don’t get enough sleep anyway. However, the lack of hunger is probably due to the rise of hormonal levels early in the morning to rouse someone out of sleep. This acts like a powerful stimulant (and if you need more, then drink coffee). But the lack of breakfast means eating more snacks with higher calories throughout the day. Bottom line, even if you aren’t hungry at breakfast, just eat it anyway. But make sure it has adequate levels of protein if you want to lose weight.


  1. Deshmukh-Taskar PR, Nicklas TA, O’Neil CE, Keast DR, Radcliffe JD, and Cho S.
    “The relationship of breakfast skipping and type of breakfast consumption with nutrient intake and weight status in children and adolescents: the National Health and Nutrition Examination Survey 1999-2006.” J Am Diet Assoc 110: 869-878 (2010)
  2. Sjoberg A, Hallberg L, Hoglund D, and Hulthen L. “Meal pattern, food choice, nutrient intake and lifestyle factors in The Goteborg Adolescence Study.” Eur J Clin Nutr 57: 1569-1578 (2003)
  3. Leidy HJ and Racki EM. “The addition of a protein-rich breakfast and its effects on acute appetite control and food intake in ‘breakfast-skipping’ adolescents.” Int J Obes 34: 1125-1133 (2010)
  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. Leidy HJ, Lepping RJ, Savage CR, and Harris CT. “Neural responses to visual food stimuli after a normal vs. higher-protein breakfast in breakfast-skipping teens.” Obesity doi 10.1038./oby.2011.108 (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.

The demise of the Mediterranean diet?

This week is Mediterranean diet week. Unfortunately after 2,000 years, no one really knows what the Mediterranean diet actually consists of. Is it the Italian, Spanish, Moroccan, Egyptian, Greek or Lebanese Mediterranean diet? Each diet is very different from each other. What is clear is that people in the Mediterranean region are becoming fatter and less healthy (1).

Part of the reason for the demise of the benefits of a “Mediterranean diet” is the time it takes to prepare a quality meal. It takes time to purchase fresh vegetables. It takes even more time to prepare them. In a world without globalization, you have a lot more time. Now you are competing with every human on the face of the globe for a job, and the result is time-compression. The first casualty of this time-compression effect of globalization is the inability to cook and consume good food containing high-quality food ingredients. Another sinister aspect of globalization is the reduction in the number of food ingredients being used by the general population. In particular, those food ingredients are the least expensive, have an extended shelf life and can be made into very inexpensive, convenient, and portable (not requiring a knife or fork to eat) processed foods. The only food ingredients that meet those requirements are cheap refined grains and cheap refined vegetable oils. And the low-cost producer of these food ingredients is not China, but the United States.

Fruits and vegetables are really expensive unless you grow them yourself. With urbanization of the Mediterranean region, most people now rely on processed foods and restaurants for their meals. Not surprisingly, is the consumption of cheap, refined grains and vegetable oils, which in the past were alien components to the Mediterranean diet (regardless of the location). Now they have replaced vegetables, fruits and olive oil (the primary food ingredients of a Mediterranean diet) because they are cheaper. For example, vegetables and fruits are now 400 times more expensive for the same number of calories as cheap, refined grains imported from America. Corn oil from America is now five times cheaper than olive oil produced in the Mediterranean region.

The people in the Mediterranean regions are eating the same foods that have produced the Perfect Nutritional Storm in America. This explains why 75 percent of Greeks are now overweight or obese and more than half the populations of Italy, Spain and Portugal are now overweight or obese. They are making the right economic choices (cheap food), but the wrong health choices (an increasingly inflammatory diet).

Even if you were to go back to the original Mediterranean diet (circa Roman times), it is apparently still not the best diet for health. This was demonstrated in a recent publication that compared the Mediterranean diet (50 percent calories as carbohydrates, 20 percent calories as protein, and 30 percent of calories as fat) to a diet that contained 40 percent carbohydrates, 30 percent protein, and 30 percent fat in a cross-over study. The higher protein, lower carbohydrate diet was more satiating and had better clinical results, especially in hormonal responses, than a real Mediterranean diet (2). Besides having a different macronutrient ratio, the other diet was extremely limited in grains and dairy products compared to the Mediterranean diet.

So if you want to follow a diet that is the evolution of the Mediterranean diet, then make it a diet that is higher in low-fat protein, lower in carbohydrates (but rich in vegetables and fruits) and low in omega-6 fats. Sure sounds like the Zone diet, but call me crazy (3).


  1. Ciezaldlo A. “Does the Mediterranean diet even exist?” New York Times April 1, 2011
  2. 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)
  3. Sears B. “The Zone.” Regan Books. New York, NY (1995)

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.

Is there an obesity gene?

When I first heard about the discovery of a potential obesity gene on the news, I ignored it. After all, a gene only codes for a single protein, and there are about 25,000 genes of which nearly 1,000 seem to be associated with obesity. Nonetheless, I decided to read the research paper in its pre-publication form (1). Even though it is an incredibly scientifically dense paper, rich in genetic jargon, it finally did it begin to make sense.

The protein for which the gene in question codes is called a transcription factor. Transcription factors are the key players in the process of transferring hormonal signals from the surface of the cell to ultimately generate the gene expression of new proteins. As I explained in my book, “Toxic Fat,” nuclear factor-κB (NF-κB) is the transcription factor that turns on the genetic expression of more proteins that leads to cellular inflammation (2).

The transcription factor in this article, known as KLF14, seems to be related to turning on the metabolic responses that lead to insulin resistance, obesity and metabolic syndrome.

Transcription factors have been around for hundreds of millions of years, and they have been highly conserved by evolution because they work so effectively to fine tune gene expression. This might be expected since they are the key players in turning genes “off” and “on” inside the cell. Since they have been around for a long time, this also means that there are natural compounds (usually nutrients) that are instrumental in controlling their activity. For NF-kB (the master regulatory switch for inflammation), it is known that leukotrienes derived from arachidonic acid activate this transcription factor (3,4), whereas omega-3 fatty acids and polyphenols inhibit its activation (5-7). It is very likely the same nutrients may do the same for the activity of the KLF14 transcription factor. From an evolutionary point of view this makes common sense since in less developed organisms (like the fruit fly), the control of fat, metabolism and immunity are found in a single organ known as fat bodies (8).

As I have pointed out in my books, increased cellular inflammation is the first step toward metabolic dysfunction. This is why any decrease in nutrients like omega-3 and polyphenols or any corresponding increase in nutrients like arachidonic acid may be common nutrient control points that dramatically influence our future health. Obviously, as the balance of these nutrients change, their effects on various transcription factors will amplify their impact on gene expression.

A more ominous implication from this study is that the gene mutations that gave rise to increased insulin resistance came only from the mother. This may be the link to understand how fetal programming transmits epigenetic information from one generation to the next. The combination of fetal programming with radical changes in the human diet may well prove to be a deadly combination for our future health and longevity.


  1. Small KS, Hedman AK, Grunberg E, Nica AC, Thorleissson G, Kong A, Thersteindottir U, Shin S-Y, Richards HB, soranzo N, Ahmadi KR, Lingren C, Stefansson K, Dermitzakis ET, Deloukas P, Spector TD, and Mcarthy MI. “Identification of an imprinted master trans regulator at the KLF14 locus related to multiple metabolic phenotypes.” Nature Genetics doi 10:1038/ng/833 (2011)
  2. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  3. Sears DD, Miles PD, Chapman J, Ofrecio JM, Almazan F, Thapar D, and Miller YI. “12/15-lipoxygenase is required for the early onset of high-fat, diet-induced adipose tissue inflammation and insulin resistance in mice.” PLoS One 4: e7250 (2009)
  4. Chakrabarti SK, Cole BK, Wen Y, Keller SR, and Nadler JL. “12/15-lipoxygenase products induce inflammation and impair insulin signaling in 3T3-L1 adipocytes.” Obesity 17: 1657-1663 (2009)
  5. Denys A, Hichami A, and Khan NA. “n-3 PUFAs modulate T-cell activation via protein kinase C-alpha and -epsilon and the NF-kappaB signaling pathway.” J Lipid Res 46: 752-758 (2005)
  6. Zwart SR, Pierson D, Mehta S, Gonda S, and Smith SM. “Capacity of omega-3 fatty acids or eicosapentaenoic acid to counteract weightlessness-induced bone loss by inhibiting NF-kappaB activation.” J Bone Miner Res 25: 1049-1057 (2010)
  7. Romier B, Van De Walle J, During A, Larondelle Y, Schneider YJ. “Modulation of signaling nuclear factor-kappaB activation pathway by polyphenols in human intestinal Caco-2 cells.” Br J Nutr 100: 542-551 (2008)
  8. Hotamisligil GS. “Inflammation and metabolic disorders.” Nature 444: 860-867 (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 dangers of over-analyzing too much data in prostate study

In the last week there has been a constant buzz about an online pre-publication of a new research article that suggests that high concentrations of omega-3 fatty acids promote aggressive prostate cancer (1). Well, that really isn’t the case, in spite of the press reports. That’s why you have to carefully read the article before jumping to conclusions.

Prostate cancer, like all cancers, is driven by cellular inflammation. The level of cellular inflammation is defined by the AA/EPA ratio of isolated serum phospholipids. When you analyze the data correctly in that article, you find that there was no difference in the AA/EPA ratio between the low-aggressive, high- aggressive, or control group. In fact, all the groups had the same elevated AA/EPA ratio of 18.8. Since I like to have individuals try to maintain an AA/EPA ratio of less than 3, all of these groups could be considered to be inflamed.

Not surprisingly, when you look at either EPA or AA levels separately in each group, they are identical. It’s only when you look at the DHA levels, do you see a small difference statistically, but it’s meaningless clinically. There was a 2.5 percent increase in the DHA levels in the high-aggressive group compared to the control group. In the paper, authors state their error in measuring DHA is ± 2.4 percent. Call me crazy, but I don’t see the big difference between the reported results and their error measurements. To further cloud the results, the authors also find that the levels of trans-fatty acids are lower in the aggressive prostate cancer patients than the controls. So I guess if you wanted to take their data at face value, DHA makes prostate cancer more aggressive and trans-fatty acids found in junk foods make prostate cancer less aggressive.

I believe this is simply a case of over-interpretation of massive amounts of collected data. If you get enough data points, you can always make some type of correlation, but that’s all it is. At some point you also have to allow common sense to enter the final analysis.

Nonetheless, let’s say their data might be correct. How could excess DHA increase the aggressiveness of any cancer? Well, it might decrease the levels of dihomo gamma linolenic acid (DGLA) as I have explained in many of my books (2-5). DGLA is the building block for a powerful group of anti-inflammatory eicosanoids, and its formation is inhibited by DHA. Depressing DGLA levels would reduce the body’s ability to hold back the inflammation that drives the tumor. Unfortunately, with all the data they accumulated, they forgot to publish the changes in the DGLA levels in the various groups. Oops.

So even if there were not any changes in the AA/EPA ratio between groups, a depression of DGLA levels in the aggressive prostate cancer group would easily explain the clinical observation. Unfortunately, that interpretation requires an extensive background in understanding eicosanoid biochemistry, which is not easily found in academic clinical-research centers.

This is not the first time that the potential benefits of DHA are in question. In the largest cardiovascular intervention study ever done, it was demonstrated that adding high levels of EPA to the diet of Japanese patients with high cholesterol levels (who already with a very low AA/EPA ratio of 1.6), dramatically decreased their likelihood of future cardiovascular events (6). This reduction was only correlated with increases in EPA levels as well as with a decrease in the AA/EPA ratio from an already low 1.6 to an even lower 0.8 (7). The levels of DHA in these patients had no significance for predicting future cardiovascular events.

Likewise other studies using DHA alone to treatment post-partum depression, improve neurological functioning of children or treating Alzheimer’s have also been found to be negative (8,9).

It’s not that DHA is bad, it just doesn’t do much to reduce cellular inflammation. DHA does a lot of other useful things, but reducing cellular inflammation in not one of them.


  1. Brasky TM, Till C, White E, Neuhouser ML, Song X, Goodman P, Thompson IM, King EB, Albanes D, and Kristal AR. “Serum phospholipid fatty acids and prostate cancer risk.” Amer J Epidem 173: doi 10:1093/aje/kwr9027 (2011)
  2. Sears, B. “The Zone.” Regan Books. New York, NY (1995)
  3. Sears, B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  4. Sears, B. “The Anti-inflammation Zone.” Regan Books. New York, NY (2005)
  5. Sears, B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  6. Matsuzaki M, Yokoyama M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, and Matsuzawa Y. “Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated patients with coronary artery disease.” Circ J 73:1283-1290 (2009)
  7. Itakura H, Yokoyama M, Matsuzaki M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, and Matsuzawa Y. “Relationships between Plasma Fatty Acid Composition and Coronary Artery Disease.” J Atheroscler Thromb 18:99-107 (2011)
  8. Makrides M, Gibson RA, McPhee AJ, Yelland L, Quinlivan J, and Ryan P. “Effect of DHA supplementation during pregnancy on maternal depression and neurodevelopment of young children: a randomized controlled trial.” JAMA 304; 1675-1683 (2010)
  9. Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, and Aisen PS. “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.” JAMA 304: 1903-1911 (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.