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)

Good Diet, Bad Study

As the creator of the Zone Diet, I am a strong believer in the Mediterranean diet as a lifetime dietary program for good health. In fact, the Zone Diet can be considered to be the evolution of the Mediterranean diet as it provides even greater anti-inflammatory benefits. That being said, this week’s New England Journal of Medicine contained an article on using the Mediterranean diet with high-risk cardiovascular patients that got great press based on some really poor science1. Let’s get to the bad science first.

The researchers compared two “Mediterranean” diets (one with extra nuts and the other with extra olive oil) to a low-fat diet. Unfortunately, they were unable to get the subjects to follow a low-fat diet. If you are a follower of Dean Ornish, then a low-fat diet means less than 10% of your calories coming from fat. Using that definition of a low-fat diet, you have to throw out one-third of the subjects because they couldn’t reduce their fat intake below 37% of total calories. In fact, at the end of this five-year study, the percentages of protein, carbohydrate, and fat in the diets of all three groups were approximately the same. As a result, you are left with a study with two groups of subjects being compared to another group of subjects who really didn’t change their diet that much.

Even Dean Ornish pointed this out in his rebuttal blog in the Huffington Post to this study2. He wrote that if people had followed his low-fat diet, then the results would have been much different. Well, actually when high-risk cardiovascular patients did follow his diet in a study done 15 years ago, those on his low-fat diet had twice the deaths compared to those in the control group3. So maybe it’s a good thing that the low-fat group couldn’t follow the prescribed low-fat diet.

The reason for adverse effects of a low-fat, low-protein, very high-carbohydrate diet for cardiovascular patients is quite clear. Those subjects following his high-carbohydrate, low-fat, and low-protein diet developed insulin resistance as evidenced by a significant increase in their triglyceride-to-HDL ratio3. If you already have had a heart attack, then an increase in insulin resistance and the accompanying increase in inflammation are almost certain to push you over the edge.

If you really dig deeper into the supplemental material (Table S7 to be exact) of this article (as most journalists neglected to do), you are remarkably unimpressed by the changes in the diet over a five-year period except that the people who got free olive oil and free nuts were consuming more free olive oil and free nuts than those who were not getting free food.

Now, back to the clinical results — a strange brew of stroke, heart attack, and death. Usually when you include a lot of different clinical end points as your primary goal, it means you are not very confident about seeing any real striking clinical benefit. Stroke is primarily associated with high blood pressure, whereas heart attack is associated with the rupture of small vulnerable plaques leading to blockage of the coronary arteries. I personally like death as a clinical end point since you can’t cheat on its definition, thus making it harder to manipulate your statistics to prove your point.

So let’s look at the individual clinical endpoints. There was a reduction in strokes that was statistically significant. Unfortunately, there was no statistically significant reduction in either heart attacks or death. For such a large study, these clinical results are not too impressive. Maybe if the researchers had actually gotten the low-fat group to reduce their fat intake to less than 10% of calories (instead of going from 39% to 37% of calories), there might have been more deaths in that group, which would have made the other two Mediterranean diet groups look better.

Virtually every cardiovascular researcher knows that fatty acid composition of the plasma is an important factor in the prediction of future cardiovascular events. Unfortunately, the authors of the New England Journal of Medicine article apparently didn’t think so. Obviously, they measured one fatty acid (alpha linolenic acid) in Figure 5S (again buried deep in the supplemental material), but somehow forgot to report the other 34 fatty acids also found in the plasma. Two of the most important of these unreported fatty acids would have included arachidonic acid (AA) and eicosapentaenoic (EPA). The AA/EPA ratio in the blood is the best marker of cellular inflammation that drives heart disease4. You would think inclusion of information on this ratio (or at least providing the fatty acid levels) would be important since a far larger JELIS study demonstrated that the lowering of the AA/EPA ratio resulted in a significant reduction of cardiovascular events5.

In contrast to this poorly executed study, there exists a far more powerful study conducted nearly 20 years ago on the benefits of a stricter Mediterranean diet. This is was the Lyon Diet Heart Study6. The primary clinical difference between this new study and older Lyon Diet Heart Study is that the Lyon Diet Heart Study generated a 65% reduction in overall cardiovascular mortality, a complete reduction in cardiac sudden death, and 44% reduction in all-cause mortality6,7. Those are clinical end points to get excited about. On the other hand, this New England Journal of Medicine article showed no impact on mortality. The only striking difference between the two groups in the Lyon Diet Heart Study was the restriction of omega-6 fatty acids in the experimental group. You find omega-6 fatty acids in vegetable oils like corn, safflower, and sunflower oils. They accomplished this dietary change by giving the subjects in the experimental groups margarines rich in omega-3 fats and trans fats. Although there was a dramatic decrease in death between the two groups in the Lyon Diet Heart Study, there were no differences in weight, BMI, blood pressure, cholesterol (good and bad), and blood lipids between the two groups. In other words, all the usual suspects in heart disease were eliminated. The only differences between the two groups were in the fatty acids, both linoleic acid and the AA/EPA ratio. If you again go back to bowels of the recent New England Journal article (in supplemental Table S7), you find out that the levels of linoleic acid (an omega-6 fatty acid) as analyzed from dietary records of the subjects was between 5 and 6% in both of the Mediterranean diets. In the Lyon Diet Heart Study, the investigators were able to reduce to the linoleic levels to 3.6%, which is similar to levels found in the Japanese (actually Okinawans), who have the lowest cardiovascular mortality in the developed world (8). The subjects in the control group of the Lyon Diet Heart Study had a nearly 50% higher level of linoleic acid in their blood compared to the experimental group8. However, those subjects following the “Mediterranean” diets in the new study had even higher levels of linoleic acid than those in the control group of the Lyon Diet Heart Study. That is the most likely reason there wasn’t any change in cardiovascular mortality or overall mortality in the New England Journal of Medicine study. Unlike this more “modern” study, the Lyon researchers further demonstrated that the AA/EPA ratio was reduced by some 30% (from 9 to 6.2) in the active group compared to the control group, and this resulted in a 65% reduction of cardiovascular death.

Bottom line, unless you dramatically reduce omega-6 intake by reducing your consumption of vegetable oils (such as corn, soy and safflower oils), you will not get clear-cut clinical results (like reduction in death) no matter how much hype the media give to the research.

As I said earlier, the Zone Diet can be considered to be the evolution of the Mediterranean diet because it represents a superior dietary program to control inflammation, the true underlying cause of heart disease. This is because the Zone Diet dramatically reduces white carbohydrates (pasta, bread, rice, and potatoes) and replaces them with increased amounts of colorful carbohydrates (vegetables and fruits). Unlike the New England Journal of Medicine article where the subjects were consuming about 5 servings a day of vegetables and fruits, the Zone Diet recommends 10 servings per day. Rather than keeping the linoleic acid content at 6% of the calories (the American Heart Association recommends 10-15%) or even at the 3.6% level as in the Lyon Diet Heart Study, the Zone Diet recommends fewer than 2% of total calories should consist of linoleic acid. Like the JELIS study, the Zone Diet recommends extra supplemental of omega-3 fatty acids to reduce the AA/EPA ratio to 1.5 or less.

Although the jury may still be out on the Mediterranean diet (especially after this poorly executed study) for the primary prevention of heart disease, the data from secondary prevention studies (5-7) strongly suggest that the Zone Diet may be the dietary approach you want to follow if reducing mortality is your personal clinical end point.

References

  1. Estuch R et al. “Primary prevention of cardiovascular disease with a Mediterranean diet.” N Engl J Med 368: doi10.1056/NEJMoa1200303 (2013)
  2. Ornish D. “Does a Mediterranean diet really beat a low-fat for health?” HuffPost Healthy Living Feb 25 (2013)
  3. Ornish D et al. “Intensive lifestyle changes for reversal of coronary heart disease.” JAMA 280: 2001-2007 (1998)
  4. Sears B. The Anti-Inflammation Zone. Regan Books. New York, NY (2005)
  5. Yokoyama M et al. “Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomized open-label, blinded endpoint analysis.” Lancet 369: 1090-1098 (2007)
  6. de Lorgeril et al. “Mediterranean alpha-linolenic-rich diet in secondary prevention of coronary heart disease.” Lancet 343: 1454-1459 (1994)
  7. de Lorgeril et al. “Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction.” Circulation 99: 779-785 (1999)
  8. Kagawa Y et al. “Eicosapolyenoic acids of serum lipids of Japanese islanders with low incidence of cardiovascular disease.” J Nutr Sci Vitaminol 28: 441-453 (1982)

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.

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.

References

  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.

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.

References

  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.

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.

References

  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.

Ward off the common cold with exercise

There is nothing like fall in New England — the crisp air on your face, the changes in foliage and all the fun activities like apple and pumpkin picking.  Even though the calendar says the season lasts three months, the end of daylight savings in my mind signals the beginning of winter.  I think it’s the combination of the cold air and driving home in the dark that makes me feel this way.  With the change in season comes the rise in sniffles, sneezes and coughs; but before you run out for your supply of Vitamin C or the newest remedy to ward off a cold, you may want to look no further than your activity level.

According to the British Journal of Sports Medicine, individuals who reported five days or more of aerobic exercise per week compared to those who were sedentary (less than 1 day/week of activity) were 43 percent less likely to have an upper respiratory tract infection (URTI) (1).  The investigators studied 1,002 adults aged 18-85 over 12 weeks during the autumn and winter of 2008.  Individuals reported their aerobic level and used a 10-point scale to assess the level of physical fitness.

The authors took into account other factors that may have confounded the results (e.g., lifestyle, diet and stress) in their analyses.  In addition, they found that people’s perception of how fit they felt and the amount of activity performed lessened the severity of URTI and symptoms by 32-41 percent.

More intriguing is another recent paper (2) in which rats that like to exercise, were bred with similar exercise-loving rats for 11 generations.  These were compared to rats that didn’t like to run who were bred with other exercise-hating rats for 11 generations.  The super rats could not only run more distance than their coach potato cousins, but several groups of genes were up-regulated.

1).   D.C. Nieman, Henson D.A., Austin M.D et al. Upper respiratory tract infection is reduced in physically fit and active adults. Brit J Sports Med doi:10.1136/bjsm.2010.077875.

2)  R. Kivela, M. Silvennoinen, M. Lehit et al.  Gene expression centroids that link with low intrinsic exercise capacity and complex disease risk.  FESEB J 24: 4565-4574 (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.

Omega-3 fatty acids may reduce breast cancer risk

The list just keeps growing for the benefits of omega-3 fatty acids and overall health. The newest to the list is breast cancer. A study just published in the journal of Cancer Epidemiology, Biomarkers & Prevention surveyed approximately 35,000 postmenopausal women, ages 50 to 76, for their use of various specialty supplements (1). The 24-page summary took into account past and present use of supplements as well as frequency (days/week) and duration (year). Individuals taking high purity omega-3 oil had a 32 percent reduced risk of developing breast cancer, whereas other supplements typically taken to reduce menopausal symptoms (e.g., black cohosh, dong quai, soy, or St. John’s wort) had no association. Although further research needs to be conducted, this again adds to the growing body of evidence on the benefits of omega-3s for disease prevention.

Of this survey didn’t answer the question about if they had taken more, would they have seen even better results? This is because cancer like all chronic diseases is driven by silent inflammation coming from increasing levels of Toxic Fat (i.e., arachidonic acid). High purity omega-3 oil dilutes Toxic Fat, but only a strict anti inflammatory diet can actually reduce Toxic Fat. Follow an anti-inflammatory program consisting of a strict anti inflammatory diet, ultra-refined high purity omega-3 oil concentrates and anti-inflammatory polyphenols to reduce the driving force for virtually all chronic disease.
1. Brasky TM, Lampe JW, Potter JD, Patterson RE, White E. Specialty supplements and breast cancer risk in the VITamins And Lifestyle (VITAL) Cohort. Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1696-708.

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.