Why doesn’t exercise and diet reduce heart disease for diabetics?

That’s a good question after the June 24 issue of the New England Journal of Medicine reported on the failure of long-term diet and exercise to reduce heart disease in diabetics1. It had been known from earlier and shorter studies that diet and exercise in diabetics appeared to generate a decreased risk of cardiovascular disease. This is important since heart disease remains the number-one killer of Americans, and people with diabetes are two to four times more likely to develop heart disease. Since diabetes is becoming epidemic, this would suggest that heart disease should soon begin to escalate. But for exercise and diet have any benefits in any condition, they have to been continued forever. That is the motivation for this 13-year study that started with the best of intentions. However, last year the study was terminated at 10 years since it was clear that there were no cardiovascular benefits. Now that the study details have been published, it is clear why it failed.

First, all of the success of diet and exercise started to evaporate after the first year. Remember, the people who enter these studies are highly motivated with a terrible future awaiting them. So why would they seemingly throw away all the initial benefits of weight loss and reduction of blood sugar? Part of the reason can be explained by why most diet program fail: Willpower can only take you so far if your hormones are working against you. The end result is you are constantly hungry and always tired.

The amount of calories the subjects of this study consumed was low (between 1,200 and 1,800 calories per day), but the diet was a high-carbohydrate diet (that induces low blood sugar due to hyperinsulinemia). The diet was coupled with lots of exercise (that also lowers blood sugar). This is an almost surefire prescription to be constantly hungry and tired. As a result, compliance wanes.

On the other hand, if you are never hungry, then compliance is better. That was the case with another 13-year study of diabetic patients who had gastric bypass surgery. For these patients, there was a significant reduction in cardiovascular events2. The reason is probably hormonal. If you lose weight by diet and exercise, your levels of the hunger hormone ghrelin increases with no change in the levels of your satiety hormone, PYY. Just the opposite happens with gastric bypass surgery. Ghrelin doesn’t change, but PYY increases3. The result is that you are not hungry, and therefor your lifestyle compliance improves.

Of course, giving every diabetic gastric bypass surgery makes little sense. Giving them new, more powerful diabetic drugs with equally powerful side effects (like heart attacks) also makes no sense.

There may be third way: Functional foods that can increase PYY levels. But these have to be tasty (like pasta and rice) and convenient (only 90 seconds to make) since you have to take them the rest of your life. That’s the project I have been working on for the past six years. These new Zone meals may be the answer, as they appear to reduce hunger without causing fatigue while eating the foods you like to eat. Zone meals are low-tech medicine with potentially high-tech results and are coming soon.


  1. Wing RR et al. “Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes.” NEJM DOI:10.1056/NEJMoa 1212914 (2013)
  2. Romeo S et al. “Cardiovascular events after bariatric surgery in obese subjects with type 2 diabetes.” Diabetes Care 35: 3613-2617 (2012)
  3. Olivan B et al. “Effect of weight loss by diet or gastric bypass surgery on peptide YY3-36 (PYY) levels.” Ann Surg 249: 948-953 (2009)

Harvard explains why people regain weight with the Atkins diet

A study from Harvard Medical School explains that even though people can lose weight on a ketogenic diet, all lost weight usually rapidly returns.

Ketogenic diets have been recommended for decades for rapid weight loss. The most famous is the Atkins diet. Ketogenic diets are based on high-protein and very low-carbohydrate intake. For the past 40 years such diets have been routinely used in America for weight loss, yet America remains in the midst of a growing epidemic of obesity. While ketogenic diets can induce initial weight loss, all lost weight usually rapidly returns, resulting in more weight (and even more fat) than when the person started the ketogenic diet.

For many years it was thought that such weight regain was due to poor dietary compliance. Now Harvard Medical School in an article in the June 27, 2012, issue of the Journal of the American Medical Association shows the reason for weight regain is more ominous than simple dietary non-compliance. In carefully controlled studies Harvard researchers demonstrated that on a ketogenic diet the levels of the hormone cortisol increase by 18%, and the levels of active thyroid hormone (T3) control metabolism decrease by 12% (1).

The effect of increased cortisol is to cause rapid fat accumulation, as any patient who has ever used prescription cortisol-like drugs knows. It also causes depression of the immune system, loss of memory, and thinning of the skin. These are also hallmarks of the acceleration of the aging process. Furthermore, the lowering of the active form of the thyroid hormone slows down the metabolism, making even seemingly small increases in calorie intake result in increased body fat accumulation. Besides setting you up to regain all the lost weight, the Atkins diet apparently also increases the rate of aging.

However, many people seem willing to continue to try such ketogenic diets in hopes of losing weight quickly. Yet highly controlled studies I published in the world’s most prestigious nutrition journal in world more than six years ago demonstrated that is simply not a true statement (2). In this study either a ketogenic diet (the Atkins diet) or a non-ketogenic diet (the Zone Diet) were compared in obese individuals. For the first six weeks all meals for both groups were prepared in a metabolic kitchen at Arizona State University (in essence treating subjects like lab rats). Both diets contained an equal number of calories.

When it came to weight loss, the subjects following the Zone Diet actually lost slightly more weight than as those on the ketogenic diet during the initial six-week period as shown in Figure 1.

Figure 1. Weight Loss (Zone Diet in open circles, Atkins diet in black squares)

Relative to fat loss on the non-ketogenic Zone Diet, their loss of body fat was again superior to the Atkins diet as shown in Figure 2. Fat loss is far more important than weight loss since all the health benefits from weight loss come from the loss of excess body fat; not from the loss of retained water or loss of muscle mass.

Figure 2. Fat Loss (Zone Diet in open circles, Atkins diet in black squares)

When the subjects continued on the respective diets for another four weeks (but now preparing meals on their own), those subjects on the non-ketogenic Zone Diet continued to lose even more weight and body fat, whereas those on the ketogenic Atkins diet did not. They had reached a plateau. The new research from Harvard Medical explains why.

One of the major problems in following a calorie-restricted diet is lack of energy. In this same study, the subjects on the Zone Diet demonstrated improved daily energy compared to those on the Atkins diet. In another publication using the same subjects, we also demonstrated that those subjects following the Zone Diet had greater performance in endurance testing compared to those following the ketogenic Atkins diet (3).

Figure 3. Energy levels (Zone Diet in open circles, Atkins diet in black squares)

For the past 40 years, ketogenic diets (like the Atkins diet) have failed to treat obesity in America. That is why one relies upon science, not hype, to determine which is the best diet to lose weight (and really body fat), keep it off, and increase energy. Continuing research from Harvard Medical School since 1999 demonstrates that the Zone Diet is the best dietary program to accomplish both goals (1,4-7). And the one thing Harvard will always tell you is that they are never wrong.


  1. Ebbeling CB, Swain JF, Feldman HA, Wong WA, Hachey DL, Garcia-Logo E, and Ludwig DD. “Effects of dietary composition on energy expenditure during weight loss maintenance.” JAMA 307: 267-2634 (2012)
  2. Johnston, C.S., Tjonn, S., Swan, P.D., White A., Hutchins H., and Sears B. “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006)
  3. White AM, Johnston CS, Swan PD, Tjonn SL, and Sears B. “Blood ketones are directly related to fatigue and perceived effort during exercise in overweight adults adhering to low-carbohydrate diets for weight loss: A pilot study.” J Am Diet Assoc 107: 1792-1796 (2007)
  4. Ludwig, DS, Majzoub AJ, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB. “High glycemic index foods, overeating, and obesity.” Pediatrics 103: e26 (1999)
  5. Agus MSD, Swain JF, Larson CL, Eckert EA, and Ludwig DS. “Dietary composition and physiologic adaptations to energy restriction.” Am J Clin Nutr 71:901–907 (2000)
  6. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effect of low-glycemic diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA. 292: 2482-2490 (2004)
  7. 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”. JAMA 297: 2092-2102 (2007)

Preventing obesity through prenatal nutrition

It is obvious that pediatric obesity is a growing problem. However, compared to adult obesity, it is a relatively new problem. In a new article to be published in the Journal of Adolescent Health, it is pointed out that while childhood obesity has increased some 300 percent since 1960, most of that increase only began in the mid 1990s (1). This is well after the beginning of the climb of adult obesity, which started in the 1980s. Why the lag time? I believe it may have been caused by the amplification of any genetic predisposition to obesity by prenatal programming in the womb. That means you had to have obese mothers whose own hormonal changes and diet were altering the fetal programming of their children, thus amplifying their likelihood for obesity after birth.

This possibility makes sense based on results from another recent article that demonstrates that the lower the omega-3 fatty acid status in the mother, the more likely the child would be obese by the age of 3 (2). In this particular study, researchers found that by age 3 about 10 percent of the children were already obese. What they also analyzed was even though virtually all the women were consuming very low levels of omega-3 fatty acids during pregnancy, the higher the levels of the omega-3 fatty acids in mother’s diet, or her blood, and especially in the blood from the umbilical cord to the fetus, the lower the levels of obesity in the child three years later after birth.

Of course, lower levels of omega-3 fatty acids usually indicate higher levels of omega-6 fatty acids, giving rise to an unbalanced ratio of omega-3 to omega-6 fatty acids. This is why the highest correlation with increased childhood obesity was found with an increasing ratio of arachidonic acid to EPA and DHA in the blood of the mother and also in the umbilical cord of the fetus. This makes perfect sense since it is known from animal studies that the higher the omega-6 to omega-3 ratio in the diet of the mother, the greater the obesity in the offspring (3-5).

So if you want to begin to decrease childhood obesity, it is probably best to start in the womb of the mother with appropriate prenatal nutrition using appropriate levels of omega-3 fatty acids. This would prevent the fetal programming of the unborn child that would lead to rapid accumulation of excess body fat after birth. I think this makes a lot more sense than telling obese children to “eat less and exercise more” after their genetic expression has been altered in the womb. And if this makes sense, then doesn’t it also strongly suggest that feeding children more omega-3 and less omega-6 fatty acids after birth will silence the activation of ancient genes that make them fat and keep them fat (6).


  1. Lee H, Lee D, Guo G, and Harris KM. “Trends in body mass index in adolescence and young adulthood in the United States: 1959-2002.” J Adolescent Heath DOI:10.1016/jadolheath2011.04.019 (2011)
  2. Donahue SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gilman MW, and Oken E. “Prenatal fatty acid status and child adiposity at age 3.” Am J Clin Nutr 93: 780-788 (2011)
  3. Korotkova M, Gabrielsson BG, Holmang, A, Larrson BM, Hanson LA, and Strandvik B. “Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids.” Am J Physiol Regul Integr Comp Physiol 288: R575-579 (2005)
  4. Ailhaud G, Guesnet P, and Cannane SC. “An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?” Br J Nutr 100: 461-470 (2008)
  5. Massiera L, Barbry P, Guesnet P, Joly A, Luquet S, Moreihon-Brest C, Moshen-Kanson T, Amri E-Z, 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)
  6. Massiera Saint-Marc P, Seydoux J, Murata T, Kobayshi T, Narumiya S, Guesnet P, Amri E-Z, Negrel R, and Alhaud G. “Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?’ J Lipid Res 44: 271-279 (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.

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.

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.

Mythologies in treatment of childhood obesity

childhood obesityWe all know that obese children tend to be inactive. This leads to the “obvious” conclusion that the solution to childhood obesity is simply more exercise. But what if that conclusion is totally wrong?

There is no mistaking that obesity and lack of physical activity are linked. But which comes first? The answer appears to be obesity (1). A study published online in the Archives of Disease in Childhood followed young children over a four-year period carefully measuring their physical activity with accelerometers to measure physical activity for seven consecutive days as well as their percentage of body fat using DEXA scans. What they found was that physical inactivity was not related to the increased accumulation of body fat, rather they found that increased body fat was the cause of decreasing physical activity. This is also the situation with adults (2-5).

So why do so many researchers believe that inactivity leads to fatness? Because it just has to be the answer. This belief persists in spite of numerous studies that demonstrate that increased physical activity has little impact on reducing childhood obesity (6). This is a classic case of don't confuse me with the facts, since in my heart I know I am right.

This is not to say that exercise has no benefits in obese children. In fact, the same authors had published an earlier study indicating that while intense exercise had little impact on fat loss, there is a significant benefit in reducing insulin resistance (7).

The implications of this study in children are immense. In essence, increasing public expenditures to increase physical activity will not address the childhood obesity epidemic no matter how much money you throw at the problem. Instead you have to focus on reducing calorie intake. However, this decrease in calorie consumption is not going to be accomplished by increased willpower, but by increasing satiety (lack of hunger) in obese children.

As I pointed out in my most recent book, “Toxic Fat,” if you want to increase satiety, you must reduce cellular inflammation in the brain (8). That is best accomplished by a combination of an anti-inflammatory diet coupled with high-dose fish oil.

Of course, as an alternative, you could always consider gastric bypass surgery.


  1. Metcalf BS, Hosking J, Jeffery AN, Voss LD, Henley W, and Wilkin TJ. “Fatness leads to inactivity, but inactivity does not lead to fatness.” Arch Dis Chil doi:10.1136/adc.2009.175927
  2. Bak H, Petersen L, and Sorensen TI. “Physical activity in relation to development and maintenance of obesity in men with and without juvenile onset obesity.” Int J Obes Relate Metabl Disord 28: 99-104 (2004)
  3. Petersen L, Schnorhr, and Sorensen TI. “Longitudinal study of the long-term relation between physical activity and obesity in adults.” Int J Obes Relate Metabl Disord 28: 105-112 (2004)
  4. Mortensen LH, Siegler Ic, Barefoot JC, Gronbaek M, and Sorensen TI. “Prospective associations between sedentary lifestyle and BMI in midlife.” Obesity 14: 1462-1471 (2006)
  5. Ekelund U, Brage S, Besson H, Sharp S, and Wareham NJ. “Time spent being sedentary and weight gain in healthy adults.” Am J Clin Nutr 88: 612-617 (2008)
  6. Wareham NJ, van Sluijs EM, and Ekelund U. “Physical activity and obesity prevention: a review of the current evidence.” Proc Nutr Soc 64: 229-247 (2005)
  7. Metcalf BS, Voss LD, Hosking J, Jeffery AN, and Wilkin TJ. “Physical activity at the government-recommended level and obesity-related outcomes.” Arch Dis Child93: 772-777 (2008)
  8. 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.

New food trends may be dysfunctional

dysfunctional food trendsAs our obesity epidemic gets worse and the general health of Americans continues to decline, people are always searching for new food trends to make us thinner, happier and smarter.

The leading contenders for the next new thing are functional foods. Frankly, these are simply processed foods with added dietary supplements to make you more likely to purchase them compared to the competition on the same shelf. Of course, this means the functional food can’t be too much more expensive than its competitor (and ideally the same price) without affecting the taste of the product. As an afterthought, it might even have some health benefit for you.

Frankly, there are only two functional foods that have been truly successful over the years. The first is Gatorade. Originally developed to reduce minerals lost during exercise, the original Gatorade tasted terrible. So they simply added some sugar to make it taste better and called it a sports drink. Gatorade is basically a Coke or a Pepsi with minerals, but you feel better about yourself when you guzzle down those carbohydrates. The other commercial success was Tropicana Orange Juice with Calcium. The makers of Tropicana didn’t ask you to pay a premium for this functional food since it was exactly the same price as Tropicana Orange Juice without calcium. That’s why the sales of this functional food dramatically increased. Who doesn’t want something extra (and it might even be healthy) for free?

It’s been a long time since any new functional foods tried to break into the market. The two most recent have been POM and Activia yogurt. POM contains polyphenols from the pomegranate seed. That’s good because polyphenols are excellent anti-oxidants and potentially good anti-inflammatory chemicals. But like the minerals in Gatorade, they taste terrible. So when you purchase a bottle of POM, what you are getting is a mass of added sugar. I guarantee you that the intake of these polyphenols in POM is not worth the extra sugar.

Another “new” source of polyphenols we hear about comes from chocolate, which is now being promoted as the new super-fruit (1). Like all polyphenols, the polyphenols found in chocolate are intensely bitter. That’s why no one likes to eat unsweetened Baker’s Chocolate even though it is polyphenol-rich. But if you add a lot of sugar to it, then it tastes great. In fact, it’s a candy bar. Again like most functional foods, these polyphenol functional foods represent one step forward in that you are consuming more polyphenols, but two steps backwards for consuming too much sugar.

Tasting bad is something that has really prevented yogurt sales from taking off in America. The solution was simple. Add more sweetness, usually in the form of fruit plus extra sugar. Finally, natural yogurt became acceptable. But to turn it into a functional food, Dannon decided to add more probiotics to its already sugar-sweetened yogurt and call it Activia, promoting it to help soothe an angry digestive system. In December 2010 the Federal Trade Commission stepped in and hit Dannon with a $21-million fine for false advertising (2). Not only were the levels of probiotics in Activia too low to be of any health benefit, but Dannon was also making drug-claims on a food to boot. Not surprisingly, the FTC is also after POM for similar misleading claims (3). Darned those regulators. They take all the fun out of marketing functional foods.

The list goes on and on. Whether it is vitamin waters, or micro-encapsulated fish oil, vitamin D, etc., trying to put bad-tasting nutritional supplements that have some proven benefits into foods and charge the consumer a higher price is never going to work. To prevent the poor taste, you have to microencapsulate the supplement to make it sound high-tech, (they call it nanotechnology) and this costs a lot of money. Adding the bad-tasting nutritional supplement without the microencapsulation to a food makes it taste worse (unless you are adding a lot of sugar at the same time, of course eroding all the potential health benefits of the supplement). Finally, the consumer will only buy this new functional food if it is the same price as what they usually purchase.

So what’s the next new thing in functional foods? In my opinion, it is returning to the concept of cooking for yourself in your own kitchen using food ingredients you buy on the periphery of the supermarket, and then taking the nutritional supplements that have proven efficacy (like fish oil and polyphenols) at the therapeutic level to produce real health benefits. Now you have real functional foods that finally work at a lower cost than you would pay for in the supermarket.

Now, that’s a radical new food trend that just might work.


1. Crozier SJ, Preston AG, Hurst JW, Payne MJ, Mann J, Hainly L, and Miller DL. “Cacao seeds are a ‘super fruit’: A comparative analysis of various fruit powders and products.” Chem Central J 5:5 (2011)

2. Horovitz B. “Dannon’s Activia, DanActive health claims draw $21M fine.” USA Today. December 15, 2010

3. Wyatt E. “Regulators Call Health Claims in Pom Juice Ads Deceptive.” New York Times. September 27, 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.

Pass the polyphenols

Considering that virtually nothing was written about the health benefits of polyphenols before 1995, it continues to amaze me the amount of health benefits this group of nutrients generates. This is primarily due to our growing understanding of how these phytochemicals interact with the most primitive parts of our immune system that have been conserved through millions of years of evolution.

Three new studies add to this growing knowledge. In the January 2011 issue of the American Journal of Clinical Nutrition, it was reported that eating one serving a week of blueberries could reduce the risk of developing hypertension by 10 percent (1). Since a serving size of fruit is defined as ½ cup, that serving size contains about 65 grams of blueberries. Put that into more precise molecular terms, this serving size would provide about 4,000 ORAC units or about the same amount of ORAC units as a glass of wine. The researchers speculated that there was a subclass of polyphenols (which includes delphinidins) that appear to be responsible for most of the effects. So if eating one serving of blueberries (½ cup) once a week is good for reducing the risk of hypertension, guess what the benefits of eating 1 cup of blueberries every day might be? The answer is probably a lot.

Speaking of red wine, in the second study in Biochemical and Biophysical Research Communications researchers found that giving high levels of isolated polyphenols from red wine demonstrated that exercise endurance in older rats could be significantly enhanced. Very good news for old folks like me. They hypothesized the effects may be directly related to “turning on” genes that increase the production of anti-oxidant enzymes (2). The only catch is that the amount of red wine polyphenols required to reach these benefits would equate to drinking about 20-30 glasses of red wine per day.

The final study in Medicine & Science in Sports and Exercise demonstrates that cherry juice rich in polyphenols reduces muscle damage induced by intensive exercise in trained athletes. This reduction in muscle damage was correlated with decreased levels of inflammatory cytokines (3). The reduction of cytokine expression is one of the known anti-inflammatory benefits of increased polyphenol intake.

Three pretty diverse studies, yet it makes perfect sense if you understand how polyphenols work. Polyphenols inhibit the overproduction of inflammatory compounds made by the most ancient part of the immune system that we share with plants. The only trick is taking enough of these polyphenols. To get about 8,000 ORAC units every day requires eating about a cup of blueberries (lots of carbohydrates) or two glasses of red wine (lots of alcohol), or half a bar of very dark chocolate (lots of fat) or 0.3 g of highly purified polyphenol powder in a small capsule (with no carbohydrates, no alcohol, and no saturated fat). And if you are taking extra high purity omega-3 oil, exercising harder, or have an inflammatory disease, you will probably need even more polyphenols. It doesn’t matter where the polyphenols come from as long as you get enough. That’s why you eat lots of colorful carbohydrates on an anti inflammatory diet.


  1. Cassidy A, O’Reilly EJ, Kay C, Sampson L, Franz M, Forman J, Curhan G, and Rimm EB. “Habitual intake of flavonoid subclasses and incident hypertension in adults.” Am J Clin Nutr 93: 338-347 (2011)
  2. Dal-Ros S, Zoll J, Lang AL, Auger C, Keller N, Bronner C, Geny B, Schini-Kerth VB. “Chronic intake of red wine polyphenols by young rats prevents aging-induced endothelial dysfunction and decline in physical performance: Role of NADPH oxidase.” Biochem Biophys Res Commun 404: 743-749 (2011)
  3. Bowtell JL, Sumners DP, Dyer A, Fox P, and Mileva KN. “Montmorency cherry juice reduces muscle damage caused by intensive strength exercise”. Med Sci Sports Exerc 43: online ahead of print doi: 10.1249/MSS.obo13e31820e5adc (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 new “eat less” USDA Food Pyramid

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

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

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

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

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

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

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

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


  1. Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunesova M, Pihlsgard M, Stender S, Holst C, Saris WH, and Astrup A. “Diets with high or low-protein content and glycemic index for weight-loss maintenance.” N Engl J Med 363: 2102-2113 (2010)

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

Lights off for weight loss

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

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

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

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

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


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

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

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

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

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

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

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