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.

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.

References

  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.

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.

Is there an obesity gene?

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

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

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

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

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

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

References

  1. Small KS, Hedman AK, Grunberg E, Nica AC, Thorleissson G, Kong A, Thersteindottir U, Shin S-Y, Richards HB, soranzo N, Ahmadi KR, Lingren C, Stefansson K, Dermitzakis ET, Deloukas P, Spector TD, and Mcarthy MI. “Identification of an imprinted master trans regulator at the KLF14 locus related to multiple metabolic phenotypes.” Nature Genetics doi 10:1038/ng/833 (2011)
  2. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  3. Sears DD, Miles PD, Chapman J, Ofrecio JM, Almazan F, Thapar D, and Miller YI. “12/15-lipoxygenase is required for the early onset of high-fat, diet-induced adipose tissue inflammation and insulin resistance in mice.” PLoS One 4: e7250 (2009)
  4. Chakrabarti SK, Cole BK, Wen Y, Keller SR, and Nadler JL. “12/15-lipoxygenase products induce inflammation and impair insulin signaling in 3T3-L1 adipocytes.” Obesity 17: 1657-1663 (2009)
  5. Denys A, Hichami A, and Khan NA. “n-3 PUFAs modulate T-cell activation via protein kinase C-alpha and -epsilon and the NF-kappaB signaling pathway.” J Lipid Res 46: 752-758 (2005)
  6. Zwart SR, Pierson D, Mehta S, Gonda S, and Smith SM. “Capacity of omega-3 fatty acids or eicosapentaenoic acid to counteract weightlessness-induced bone loss by inhibiting NF-kappaB activation.” J Bone Miner Res 25: 1049-1057 (2010)
  7. Romier B, Van De Walle J, During A, Larondelle Y, Schneider YJ. “Modulation of signaling nuclear factor-kappaB activation pathway by polyphenols in human intestinal Caco-2 cells.” Br J Nutr 100: 542-551 (2008)
  8. Hotamisligil GS. “Inflammation and metabolic disorders.” Nature 444: 860-867 (2006)

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

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.

Obesity starts in the womb

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

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

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

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

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

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

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

References

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

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

Fetal programming: Gene transformation gone wild (Part II)

In part 1 of this blog, I discussed how dietary changes can alter gene expression and how those epigenetic changes can be mediated from one generation to the next by fetal programming. This is very clear from animal studies. One of the most frightening studies was published a few years ago (1). In this study, genetically identical mice were split into two colonies. For the next three generations they were fed exactly the same number of calories with exactly the same balance of protein, carbohydrate, and fat. The only difference was that one group had a diet rich in omega-6 fatty acids and low in omega-3 fatty acids, and the other had a better balance of omega-3 to omega-6 fatty acids. After three generations the mice fed the high omega-6 fatty acid diet were grossly obese.

In addition, the mice with high omega-6 fatty acids had fatty livers and enlarged hearts and kidneys, all indicative of major metabolic disturbances.

This also happens with the brain. It has been demonstrated that removing omega-3 fatty acids and replacing them with omega-6 fatty acids over three generations makes animals a lot dumber, probably due to significant reductions in neurotransmitters, like serotonin and dopamine (2-5). Not only are they dumber, but their offspring also show a strong preference for junk food. (6)

How could this happen in such a short period of time? The answer is fetal programming induced by increased cellular inflammation. If this cellular inflammation is maintained by an inflammatory diet, there will be a constant driving force to maintain these epigenetic effects from one generation to other.

The next question is how long does this epigenetic programming have to be continued until it becomes a permanent part of the gene structure. One indication might be found in the development of lactose intolerance in those populations who have been exposed to dairy products for thousands of years. Seventy percent of the world’s population can’t digest these dietary products because they have lost the ability to maintain the necessary enzyme production after weaning from mother’s breast milk. Those who have been constantly exposed to dairy products after weaning have developed an epigenetic programming that seems to be permanent.

These epigenetic changes in humans may take place in only one generation. This is the suggestion of a new article to be published in Diabetes that indicates more than 25 percent of the explanation for childhood obesity could be predicted by prenatal epigenetic changes at birth (7).

As long as our epidemic of cellular inflammation continues to be fueled by the Perfect Nutrition Storm, we can expect our children to continue to become fatter, sicker, and dumber (8).

References

  1. Hanbauer I, Rivero-Covelo I, Maloku E, Baca A, Hu Q, Hibbeln JR, and Davis JM. “The Decrease of n-3 Fatty Acid Energy Percentage in an Equicaloric Diet Fed to B6C3Fe Mice for Three Generations Elicits Obesity.” Cardiovasc Psychiatry Neurol: 2009, Article ID.867041 (2009)
  2. Chalon S, Delion-Vancassel S, Belzung C,,Guilloteau D, Leguisquet AM, Besnard JC, and Durand G. “Dietary fish oil affects monoaminergic neurotransmission and behavior in rats.” J Nutr 128: 2512-2519 (1998)
  3. Zimmer L, Delpal S, Guilloteau D, Aioun J, Durand G, and Chalon S. “Chronic n-3 polyunsaturated fatty acid deficiency alters dopamine vesicle density in the rat frontal cortex.” Neurosci Lett 284: 25-28 (2000)
  4. Moriguchi T, Greiner RS, and Salem N. “Behavioral deficits associated with dietary induction of decreased brain docosahexaenoic acid concentration.” J Neurochem 75: 2563-2573 (2000)
  5. Chalon S. “Omega-3 fatty acids and monoamine neurotransmission.” Prostaglandins Leukot Essent Fatty Acids 75: 259-269 (2006)
  6. Ong ZY and Muhlhausler BS. “Maternal “junk-food” feeding of rat dams alters food choices and development of the mesolimbic reward pathway in the offspring.” FASEB J 25: S1530-6860 (2011)
  7. Godfrey KM, Sheppard A, Gluckman PD, Lillycrop KA, Burdge GC, McLean C, Rodford J, Slater-Jefferies J, Garratt E, Crozier SR, Emerald BS, Gale CR, Inskip HM, Cooper C, and Hanson MA. “Epigenetic gene promoter methylation at birth is associated with child’s later adiposity.” Diabetes 60: doi: 10.2337/db10-0979 (2011)
  8. Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD, and Hanson MA. “Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease.” Pediatr Res 61: 5R-10R (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.

Fetal programming: Gene transformation gone wild (Part I)

Normally genes change very slowly through mutation. Most mutations are harmful and hence provide no survival advantage to the organism. This is why there is a less than a 2 percent difference between our genes and those of a chimpanzee, even though we became a separate species more than six million years ago. What distinguishes mankind is not the number of genes (corn has twice as many genes as humans), but the speed at which our genes can be turned on and off. This is because of the presence of gene transcription factors that can be activated or inhibited by nutrients. The effect of nutrients on gene expression is known as nutrigenomics.

Because of mankind’s rapid gene switching abilities, gene expression can be influenced significantly by the diet. Due to the speed at which new food ingredients are being introduced into the human diet, these types of nutrigenomic interactions can create radical changes in gene expression in a very short period of time. Normally what a person eats should only affect their gene expression during their lifetime. But is it possible that these changes in genetic expression can be transferred to the next generation?

We can see how genetic engineering (i.e. cross-breeding) can rapidly change the size and shape of dogs, flowers, vegetables and fruits. The genes in each of these species don’t change, but changes in gene expression induced by crossbreeding can persist from one generation to the next, especially if they are constantly reinforced. This is known as epigenetics.

Somehow we don’t think this type of epigenetic change can happen to us, but it does as a result of fetal programming. The prenatal period in the womb is the time that a child’s genes are most susceptible to epigenetic programming. Epigenetic programming can be amplified by the ongoing dietary effects on gene transcription factors (i.e. nutrigenomics) taking place in the mother. The result is the imprinting of epigenetic changes on the genes of the developing fetus that can alter the metabolic future of the child (1).

Examples of how this type of epigenetic programming influences future metabolic effects has been demonstrated under the conditions of famine, which generate increased obesity and cardiovascular disease in the next generation (2). This is also true of children who were exposed to excess calories or elevated levels of glucose while they were developing in the womb (3,4). Likewise hypertension (i.e. pre-eclampsia) during pregnancy increases the risk of stroke as adults if the fetus is exposed to the high blood pressure in the womb (5) as well as the increased risk of adult obesity if the fetus is exposed to gestational diabetes in the mother (6).

Bottom line: The dietary and metabolic environment the fetus is exposed to in the womb can echo through the rest of his or her life. In part II of this blog, I will explore how the Perfect Nutritional Storm, described in my book “Toxic Fat” (7) has been making Americans fatter, sicker and dumber for the last three generations.

References

  1. Kussman M, Krause L, and Siffert W. “Nutrigenomics: where are we with genetic and epigenic markers for disposition and susceptibility?” Nutrition Rev 68: S38-S47 (2010)
  2. Painter RC, Roseboom TJ, and Bleker OP. “Prenatal exposure to the Dutch famine and disease in later life.” Reprod Toxicol 20: 345-352 (2005)
  3. Singhal A. “Early nutrition and long-term cardiovascular health.” Nutrition Rev 64: S44-S49 (2006)
  4. Boney CM, Verma A, Tucker R, and Bovh BR. “Metabolic syndrome in childhood: associated with birth weight, maternal obesity, and gestational diabetes mellitus.” Pediatrics 115: e290-e296 (2005)
  5. Kajantie E, Eriksson JG, Osmond C, Thornburg K, and Barker DJP. “Pre-eclampsia is associated with increased risk of stroke in the adult offspring.” Stroke 40: 1176-1180 (2009)
  6. Lawlor DA, Pichtenstein P, and Langstrom N. “Association of maternal diabetes mellitus in pregnancy with offspring adiposity into early adulthood.” Circulation 123: 258-265 (2011)
  7. 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.

A new obesity suspect

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

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

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

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

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

References:

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

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

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.