Obesity continues to climb

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

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

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

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

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

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Kim J, Peterson KE, Scanlon KS, Fitzmaurice GM, Must A, Oken E, Rifas-Shiman SL, Rich-Edwards JW, and Gillman MW. “Trends in overweight from 1980 through 2001 among preschool-aged children enrolled in a health maintenance organization. Obesity 14: 1107-1112 (2006)
  3. Lustig RH editor. “Obesity Before Birth.” Springer. New York (2011)


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

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.

Getting closer to the Zone all the time

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

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

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

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

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

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.

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.

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.

New solution or simply admitting failure?

SurgeryLast week the International Diabetes Federation (IDF) announced that gastric bypass surgery is a cost-effective treatment for type 2 diabetes. This marks the first time in modern medicine that cutting out normal tissue is now considered good medicine. It also indicates the pathetic state of medical science for the treatment of diabetes.

Make no mistake: Type 2 diabetes is now a pandemic, affecting approximately 300 million people worldwide. This is projected to increase to some 450 million people worldwide by 2030. Since diabetes is one of the most costly chronic disease conditions, it is the most likely to break the financial backbone of health-care systems in every advanced country.

The typical gastric bypass surgery costs from $15,000 to $24,000. Just for argument's sake, let's assume it is $20,000 for each surgery. Since some 26 million people in the United States have type 2 diabetes, then a mere $520 billion dollars spent on gastric bypass surgery would solve our growing epidemic. Obviously we don't have that type of money floating in the health-care system.

Furthermore, the 10-year failure rate is relatively high for this type of surgery (1). For example, 20 percent of patients who were initially obese (BMI >50 percent) could not maintain their long-term BMI below 35 percent (the definition of morbidly obese). This failure rate rises to 58 percent for those whose initial BMI was greater than 50.

The key feature as to why gastric bypass surgery works is the almost immediate suppression of hunger, mediated by improved release of hormones from the gut (i.e. PYY) that go directly to the brain to tell the patient to stop eating. Over time it would appear that this initial enhancement of PYY release is being compromised. As a result, those patients regain the lost weight.

So maybe gastric bypass is not the best long-term solution (and definitely not a cost-effective one in those patients that regain much of their lost weight) for solving the current epidemic of diabetes. So what's the alternative? One solution would be an anti-inflammatory diet that supplies adequate protein to stimulate PYY release as well as control the levels of cellular inflammation in the pancreas, the underlying reason why insufficient insulin levels are secreted in the first place (2).

Call me crazy, but this dietary approach appears far more cost-effective.

References

  1. Christou NV, Look D, and MacLean LD. “Weight gain after short- and long-limb gastric bypass in patients followed for longer than 10 years.” Ann Surg 244: 734-740 (2006)
  2. Donath MY,Boni-Schnetzler M, Ellingsgaard H, and Ehses JA. “Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.” Physiology 24: 325-331 (2009)

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.