Preventing obesity through prenatal nutrition

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

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

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

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

References

  1. Lee H, Lee D, Guo G, and Harris KM. “Trends in body mass index in adolescence and young adulthood in the United States: 1959-2002.” J Adolescent Heath DOI:10.1016/jadolheath2011.04.019 (2011)
  2. Donahue SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gilman MW, and Oken E. “Prenatal fatty acid status and child adiposity at age 3.” Am J Clin Nutr 93: 780-788 (2011)
  3. Korotkova M, Gabrielsson BG, Holmang, A, Larrson BM, Hanson LA, and Strandvik B. “Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids.” Am J Physiol Regul Integr Comp Physiol 288: R575-579 (2005)
  4. Ailhaud G, Guesnet P, and Cannane SC. “An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?” Br J Nutr 100: 461-470 (2008)
  5. Massiera L, Barbry P, Guesnet P, Joly A, Luquet S, Moreihon-Brest C, Moshen-Kanson T, Amri E-Z, and Ailhaud G. “A western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations.” J Lipid Res 51: 2352-2361 (2010)
  6. Massiera Saint-Marc P, Seydoux J, Murata T, Kobayshi T, Narumiya S, Guesnet P, Amri E-Z, Negrel R, and Alhaud G. “Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?’ J Lipid Res 44: 271-279 (2003)

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

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.

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.

The dangers of over-analyzing too much data in prostate study

In the last week there has been a constant buzz about an online pre-publication of a new research article that suggests that high concentrations of omega-3 fatty acids promote aggressive prostate cancer (1). Well, that really isn’t the case, in spite of the press reports. That’s why you have to carefully read the article before jumping to conclusions.

Prostate cancer, like all cancers, is driven by cellular inflammation. The level of cellular inflammation is defined by the AA/EPA ratio of isolated serum phospholipids. When you analyze the data correctly in that article, you find that there was no difference in the AA/EPA ratio between the low-aggressive, high- aggressive, or control group. In fact, all the groups had the same elevated AA/EPA ratio of 18.8. Since I like to have individuals try to maintain an AA/EPA ratio of less than 3, all of these groups could be considered to be inflamed.

Not surprisingly, when you look at either EPA or AA levels separately in each group, they are identical. It’s only when you look at the DHA levels, do you see a small difference statistically, but it’s meaningless clinically. There was a 2.5 percent increase in the DHA levels in the high-aggressive group compared to the control group. In the paper, authors state their error in measuring DHA is ± 2.4 percent. Call me crazy, but I don’t see the big difference between the reported results and their error measurements. To further cloud the results, the authors also find that the levels of trans-fatty acids are lower in the aggressive prostate cancer patients than the controls. So I guess if you wanted to take their data at face value, DHA makes prostate cancer more aggressive and trans-fatty acids found in junk foods make prostate cancer less aggressive.

I believe this is simply a case of over-interpretation of massive amounts of collected data. If you get enough data points, you can always make some type of correlation, but that’s all it is. At some point you also have to allow common sense to enter the final analysis.

Nonetheless, let’s say their data might be correct. How could excess DHA increase the aggressiveness of any cancer? Well, it might decrease the levels of dihomo gamma linolenic acid (DGLA) as I have explained in many of my books (2-5). DGLA is the building block for a powerful group of anti-inflammatory eicosanoids, and its formation is inhibited by DHA. Depressing DGLA levels would reduce the body’s ability to hold back the inflammation that drives the tumor. Unfortunately, with all the data they accumulated, they forgot to publish the changes in the DGLA levels in the various groups. Oops.

So even if there were not any changes in the AA/EPA ratio between groups, a depression of DGLA levels in the aggressive prostate cancer group would easily explain the clinical observation. Unfortunately, that interpretation requires an extensive background in understanding eicosanoid biochemistry, which is not easily found in academic clinical-research centers.

This is not the first time that the potential benefits of DHA are in question. In the largest cardiovascular intervention study ever done, it was demonstrated that adding high levels of EPA to the diet of Japanese patients with high cholesterol levels (who already with a very low AA/EPA ratio of 1.6), dramatically decreased their likelihood of future cardiovascular events (6). This reduction was only correlated with increases in EPA levels as well as with a decrease in the AA/EPA ratio from an already low 1.6 to an even lower 0.8 (7). The levels of DHA in these patients had no significance for predicting future cardiovascular events.

Likewise other studies using DHA alone to treatment post-partum depression, improve neurological functioning of children or treating Alzheimer’s have also been found to be negative (8,9).

It’s not that DHA is bad, it just doesn’t do much to reduce cellular inflammation. DHA does a lot of other useful things, but reducing cellular inflammation in not one of them.

References

  1. Brasky TM, Till C, White E, Neuhouser ML, Song X, Goodman P, Thompson IM, King EB, Albanes D, and Kristal AR. “Serum phospholipid fatty acids and prostate cancer risk.” Amer J Epidem 173: doi 10:1093/aje/kwr9027 (2011)
  2. Sears, B. “The Zone.” Regan Books. New York, NY (1995)
  3. Sears, B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  4. Sears, B. “The Anti-inflammation Zone.” Regan Books. New York, NY (2005)
  5. Sears, B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  6. Matsuzaki M, Yokoyama M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, and Matsuzawa Y. “Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated patients with coronary artery disease.” Circ J 73:1283-1290 (2009)
  7. Itakura H, Yokoyama M, Matsuzaki M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, and Matsuzawa Y. “Relationships between Plasma Fatty Acid Composition and Coronary Artery Disease.” J Atheroscler Thromb 18:99-107 (2011)
  8. Makrides M, Gibson RA, McPhee AJ, Yelland L, Quinlivan J, and Ryan P. “Effect of DHA supplementation during pregnancy on maternal depression and neurodevelopment of young children: a randomized controlled trial.” JAMA 304; 1675-1683 (2010)
  9. Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, and Aisen PS. “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.” JAMA 304: 1903-1911 (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.

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.

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.