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.

References

  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.

References

  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)

“Biggest Loser” or best Zoner?

A few weeks ago I spoke at the American Society of Bariatric Physicians. Later in the day I heard an interesting lecture from the lead dietician for the TV series “The Biggest Loser”. In this lecture, she disclosed all the keys for successful weight loss in the individuals on the show.

The first was incredibly careful screening just like you would do for a clinical trial. This is to make sure you have incredibly motivated people, who aren’t depressed or have other existing medical conditions, such as heart disease. In other words, you stack the deck. Considering that after the first pilot show in 2004, there were 225,000 applications for the 2005 series, there is no problem in recruiting motivated people. Just to make sure the motivation is maintained, the contestants get paid while they are on the show in addition to the big payoff for the winner at the end of the series.

Next contestants are isolated in a “camp”. Consider this to be like a metabolic ward where they only have access to good food for the next 10 to 16 weeks. This means no white carbohydrates and no artificial sweeteners other than stevia and all the meals made for them.

According to the speaker, the real secret is that they are fed a Zonelike Diet with 45 percent of the calories coming carbohydrates (primarily non-starchy vegetables and fruits) with a very limited amount of whole grains, 30 percent of the calories from low-fat protein, and 25 percent from good fats, such as olive oil or nuts. The typical calorie intake for the females is 1,200 to 1,600 and for the males about 1,800-2,400. The typical 300-pound contestant will consume about 1,750 calories per day. Finally, you spread the balanced calories over three meals and two snacks during the day.

Of course, you never see the contestants eating their Zone meals and snacks or the dietician discussing nutrition with them because that makes for boring TV. So most of the time you see them being yelled at by their trainers. That makes for exciting TV. In fact. the more tears they shed by being intimidated, the better the ratings.

So what happens to them after they leave the show, no longer get paid, and are surrounded by their favorite foods? About 50 percent regain the lost weight. But the other 50 percent have found out that the Zone Diet isn’t that hard, and now they have a clear dietary plan for a lifetime without being yelled at by drill sergeant-like trainers.

Changing gene expression

I have often stated that the real power of the Zone Diet is to change gene expression, especially the expression of anti-inflammatory genes. What I never realized is how rapid gene expression could occur. Now, new research from Norway gives me the answer (1). It takes about 24 hours!

This pilot study is on the effect of diet on gene expression in healthy obese individuals. Interestingly, when the researchers calculated the estimated daily calorie requirements for these subjects necessary to maintain their weight, they were surprised that they were already eating 250 fewer calories per day than predicted to maintain their current weight. So much for the “fact” that obese individuals are fat because they eat more calories than they need to maintain their weight. In fact, this observation was confirmed in an earlier study in which the number of calories consumed by obese and lean individuals did not vary, but the obese individuals consumed fewer meals consisting of larger servings (2).

So what the Norwegian researchers did was simply maintain the same number of calories the subjects were already eating and change the macronutrient balance to be very close to the Zone Diet (30 percent carbohydrates, 30 percent protein, and 40 percent fat). Then the subjects consumed six meals containing about 460 calories evenly spaced throughout the day so that the total calories consumed at any one time was moderate. Just making those two simple dietary changes resulted in more than an eight-pound weight loss in 28 days. The levels of body fat didn’t change since the number of calories consumed was exactly the same as they were previously consuming. However, it appears that evenly spacing the meals and reducing the calorie size of the meals resulted in less insulin production and therefore less retained water.

Then they looked to see if they could find any changes in gene expression in both the fat cells and the blood with the dietary changes. Amazingly they found dramatic changes in only 24 hours. Of the 16,000 genes they could identify, about 60 percent remained unchanged in their expression, but 40 percent were either turned on (i.e., up-regulated) or turned down (i.e., down-regulated). Interestingly, the changes seen in the first 24 hours were held constant throughout the 28 days of the experiment.

Upon further analysis, the up-regulated genes corresponded to those that had anti-inflammatory properties, and the down-regulated genes were those associated with chronic disease conditions, such as diabetes and heart disease. Furthermore, since these changes in gene expression occurred within 24 hours of the dietary change, they could not be attributed to any change in body weight and fat loss.

Fortunately, I had the opportunity to have dinner with the lead author of the study to discuss her work while I was in Europe last week. She told me that she has expanded the number of subjects in several new trials, and the results remain the same. I also found out that she has been following my work for many years.

This type of study only confirms the power of genetic analysis to demonstrate how a highly structured diet with the correct macronutrient content can rapidly alter genetic expression and hence controls your future health. But the door swings both ways. An unbalanced diet will have just the opposite genetic effects. While I have always been impressed by the power of the Zone Diet, this new experimental data takes my respect for the Zone Diet to a new level of awe, even by me.

References

  1. Brattbakk H-R, Arbo I, Aagaard S, Lindseth I, de Soysa AK, Langaas M, Kulseng B, Lindberg, and Johansen B. “Balanced caloric macronutrient composition down regulates immunological gene expression in human blood cells-adipose tissue diverges.” OMICS 15: doi:1089/omi.2010.0124 (2011)
  2. Berg C, Lappas G, Wolk A, Strandhagen E, Toren K, Rosengren A, Rosengren A, Thelle D, and Lissner L. “Eating patterns and portion size associated with obesity in a Swedish population.” Appetite 52: 21-26 (2009)

Eat Less, Get Hungry

Telling an obese person simply to eat less rarely succeeds. Is it because they are weak-willed individuals or is there something more complex going on? New research indicates the latter. A new article in Cell Metabolism showed that during extreme calorie restriction, the levels of fatty acids begin to rapidly rise in the blood as the body begins breaking down stored fat for energy. These newly released fatty acids from the fat cells can then enter into the brain (the hypothalamus to be exact) and cause the self-digestion of cells in the hunger neurons (1). This self-digestion of the cells in the hunger neurons produces a rise in the very powerful hunger hormone (AgRP) from the same bundle of neurons. Not surprisingly, the urge to eat becomes almost overpowering. This begins to explain why very low calorie diets can cause rapid weight loss, but are rarely successful in keeping the weight off.

This is why very low calorie diets that promise quick weight loss invariably cause the rapid release of stored fatty acids that promotes constant hunger. This is clearly not a sustainable way to maintain long-term weight management.

Of course the question might be whether it is all fatty acids or just one that causes the problem of cellular death in the hunger neurons? I believe the answer comes back to the usual suspect, arachidonic acid (2). It has been known for 20 years that when you put obese individuals on a very low calorie diet there is a rapid increase in the levels of arachidonic acid levels in the blood (3). Arachidonic acid can easily cross the blood brain barrier and enter into the hypothalamus. Since arachidonic acid is a powerful promoter of cell death (4), increased concentrations inside the hypothalamus may be the primary accelerator of the death of the hunger neurons. Increased levels of arachidionic acid in the blood are also the underlying cause of insulin resistance because of its effect on the generation of cellular inflammation (2). So as you build up the levels of stored arachidonic acid in the fat cells, caused by the Perfect Nutritional Storm (2), you are almost ensuring constant hunger when you try to lose weight quickly by following very low calorie diets. To make matters even worse, as arachidonic acid levels also build up in the brain increasing the production of endocannabinoids (5). These are the hormones that give you the continual munchies (they are related to the active ingredient in marijuana).

So is there any good news in all of this research? Yes as long as you develop a lifetime dietary strategy for reducing arachidonic acid and the cellular inflammation it causes as well as following a reasonable low calorie diet that supplies adequate levels of fat to moderate the release of stored fatty acids from the fat cells. It means following an anti-inflammatory diet with adequate protein using low-glycemic load carbohydrates and fats very low in omega-6 fatty acids, but adequate in monounsaturated and omega-3 fats.

That’s why you never want to start any type of weight loss program without adding omega-3 fatty acids to counteract the released of stored arachidonic acid from the fat cells. Not only will these omega-3 fatty acids reduce the degradation of the hunger neurons thereby reducing the release of powerful hunger hormones during calorie restriction, but they will also inhibit the release of endocannabinoids in the brain (6). The combination of the two events will ensure weight loss without hunger and that’s sustainable.

References

  1. Kaushik S,Rodriguez-Navarro JA, Arias E, Kiffin R, Sahu S, Schwartz GJ, Cuervo AM, and Singh R. “Autophagy in hypothalamic AgRP neurons regulates food intake and energy balance.” Cell Metabolism 14: 173-183 (2011)
  2. Sears B. Toxic Fat. Thomas Nelson. Nashville, TN (2008)
  3. Phinney SD, Davis PG, Johnson SB, and Holman RT. “Obesity and weight loss alter serum polyunsaturated lipids in humans.” Amer J Clin Nutr 53: 831-838 (1991)
  4. Pompeia C, Lima T, and Curi R. “Arachidonic acid cytotoxicity: can arachidonic acid be a physiological mediator of cell death?” Cell Biochemistry and Function 21:97-104 (2003)
  5. Kim J, Li Y, and Watkins BA. “Endocannabinoid signaling and energy metabolism: A target for dietary intervention.” Nutrition 27: 624-632 (2011)
  6. Oda E. “n-3 Fatty acids and the endocannabinoid system.” Am J Clin Nutr 85: 919 (2007)

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

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).

Diabetes

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.

References

  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.

Where does fat go?

Many years ago I saw a great cartoon of farmer harvesting bales of fat on a tractor with the caption reading, “That’s where they grow fat”. Now let’s fast forward to our current obesity epidemic. The fastest and most popular (although costly) way to lose fat is to simply suck it out of the body. Plastic surgeons have been doing this for the past 40 years. Yet for some reason their patients keep coming back every 12 months needing a new liposuction touch-up, like taking your car in for an oil lube and tire change at your local garage. Maybe these patients simply have no willpower to keep the fat off.

Now a new study in an online pre-publication article (1) indicates liposuction recipients may not be so “weak-willed” after all. After one year compared to a control group (who were promised discount prices for their liposuction if they would agree to wait for the outcome of the study), the females who had liposuction had no change in their body weight or their percentage of body fat 12 months after the operation. All the fat that had been removed by liposuction had returned. More ominously, the new fat appeared in the wrong places. Initially, it was taken from the hips, and 12 months later it reappeared on the abdomen. In essence, the liposuction had transformed the patients from a pear shape (with few long-term cardiovascular consequences) to an apple shape (with greater long-term cardiovascular consequences). While there was no short-term deterioration in their metabolic markers suggestive of future diabetes or heart disease, the change in the body shape is still an ominous predictor for their future health.

Why the body would grow new fat cells in different parts of the body is still a mystery. But it does indicate the body’s ability to defend itself against rapid fat loss. Fat loss must be a slow, continuous process to avoid activating these “fat-defending” systems. It is impossible to lose more than one pound of fat per week. You can lose a lot more weight, but that difference in weight loss primarily comes from either water loss or loss of muscle mass. This is why you see large of amounts of weight loss during the first week or two of any quick weight-loss diet (primarily water loss) followed by a much slower weight loss (now consisting of fat loss but at a much slower rate).

This is also why it is much easier to lose a lot of weight on shows like “The Biggest Loser” but very difficult to lose the last 10-15 pounds of excess weight (which is usually stored body fat). Apparently, it is only through the slow, steady loss of body fat that there isn’t any activation of the hormonal signals that activate the formation of new fat cells in other parts of the body to restore fat levels. Liposuction is rapid fat loss, and hence those hormonal signals are activated, which leads to the increased production of new fat cells in different parts of the body. People don’t like to hear this, but unfortunately it is the truth.

What drives fat gain is cellular inflammation that creates insulin resistance, as I explain in my book “Toxic Fat” (2). To lose excess body fat, you must first reduce cellular inflammation. That can only be done by an anti-inflammatory diet. There is no secret about it. What you must do is eat adequate protein at every meal, primarily eat colorful vegetables as carbohydrate choices, and avoid the intake of excess omega-6 (i.e., vegetable oils) fats and saturated fats by primarily using monounsaturated and omega-3 fats. You have to do this for a lifetime. Of course, if you do, then you will become thinner, healthier, and smarter.

The alternative is to turn yourself from a pear into an apple with liposuction.

References

  1. Hernandex TL, Kittelson JM, Law CK, Ketch LL, Stob NR, Linstrom RC, Scherziner A, Stamm ER, and Eckel RH. “Fat redistribution following section lepectomy: defense of body fat and patterns of restoration.” Obesity doi:1038/oby.2011.64
  2. 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.

Fish oil and fat loss

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.

Omega-3 fatty acids and blood pressure

Blood Pressure CuffIt was recognized many years ago that fish oil has a dose-dependent effect on lowering blood pressure (1). So how does it do it? There are a lot of different ways.

The first is the ability of the omega-3 fatty acids in fish oil to alter the levels of a group of hormones known as eicosanoids (2,3). These are the hormones that cause blood vessels to contract, thereby increasing the pressure needed to pump blood through the arteries. The omega-3 fatty acids, especially eicosapentaenoic acid (EPA), inhibit both the synthesis and release of the omega-6 fatty acid arachidonic acid (AA) that is the molecular building block necessary to produce those eicosanoids that cause constriction of blood vessels.

The second way that fish oil helps reduce blood pressure is to accelerate weight loss. When you lose excess weight, blood pressure invariably decreases. A recent trial has indicated that when you add fish oil to a calorie-restricted diet, there is greater weight loss (4). This study was followed by an additional trial that indicated when adding fish oil to a weight-reduction diet, there was a further effect on lowering blood pressure (5). So how does fish oil help you lose excess weight? The answer lies in the ability of the omega-3 fatty acids in fish oil to reduce cellular inflammation in the fat cells (6). It's that cellular inflammation that makes you fat and keeps you fat. Reducing that cellular inflammation in the fat cells is the key to weight loss.

Finally another cause of increased blood pressure is increased stress. It was shown in 2003 that high levels of fish oil reduce the rise of blood pressure induced by mental stress (7).

Of course, the best way to reduce blood pressure is to follow an anti-inflammatory diet rich in omega-3 fatty acids. That means a diet rich in fruits and vegetables with adequate levels of low-fat protein and low levels of omega-6 and saturated fats. It's also commonly known as the Zone diet.

References:

  1. Morris MC, Sacks F, and Rosner B. “Does fish oil lower blood pressure? A meta-analysis of controlled trials.” Circulation 88: 523-533 (1993)
  2. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  3. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  4. 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)
  5. Ramel A, Martinez JA, Kiely M, Bandarra NM, and Thorsdottir I. “Moderate consumption of fatty fish reduces diastolic blood pressure in overweight and obese European young adults during energy restriction.” Nutrition 26: 168-174 (2010)
  6. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  7. Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, and Tappy L. “Fish oil prevents the adrenal activation elicited by mental stress in healthy men.” Diabetes Metab 29: 289-295 (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.

What is the Mediterranean diet?

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

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

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

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

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

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

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

References

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

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