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.

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This entry was posted in Zone Diet and tagged , , , , , , by Dr. Barry Sears. Bookmark the permalink.

About Dr. Barry Sears

Dr. Barry Sears is a leading authority on the impact of the diet on hormonal response, genetic expression, and inflammation. A former research scientist at the Boston University School of Medicine and the Massachusetts Institute of Technology, Dr. Sears has dedicated his research efforts over the past 30 years to the study of lipids. He has published more than 30 scientific articles and holds 13 U.S. patents in the areas of intravenous drug delivery systems and hormonal regulation for the treatment of cardiovascular disease. He has also written 13 books, including the New York Times #1 best-seller "The Zone". These books have sold more than 5 million copies in the U.S. and have been translated into 22 different languages.

18 thoughts on “Obesity starts in the womb

  1. What is your thoughts on high blood levels of DHA connected to a higher chance of aggressive prostate cancer

  2. Hi Dr. Sears,

    I am beginning to understand the consequences of Omega 6. However, why is there so much Omega 6 in our food? Does the body need some Omega 6? Also, can you eat something that will diminish the effects of Omega 6 or is this the wrong way to think about Omega 6?

    • The body requires about 0.5% of total calories as omega-6 fatty acids. Currently the average American consumes about 8% of their total calories as omega-6 fatty acids. The reason is that omega-6 fatty acids are now the cheapest form of calories known and they make processed foods taste much better.

      The best way to reduce the inflammatory impact of omega-6 fatty acids is try to keep them out of the diet. This can be done by eating a diet rich in food ingredients that were common more than 10,000 years ago. Another way to keep the total fat intake to less than 50 grams per day using primarily olive oil and to follow a low-glycemic load diet that inhibits the insulin stimulation of omega-6 fatty acids into arachidonic acid. Finally, one can increase in the intake of EPA and DHA to counteract the inflammatory impact of increased omega-6 fatty acid consumption.

  3. With regard to the Harvard study, it would be useful to know if they collected a diet history from the mothers. Might it be that low levels of EPA/DHA were associated with a diet high in omega-6′ fatty acids? The socio-economic status of the mothers pose another variable. I question the degree to which obesity is genetic since genetics account for less than 50% of expression.

    Beyond epigenetics and fetal programming one must consider the significant changes in lifestyle and activity levels that have occurred in the last three decades. Children and adults are more sedentary than ever. This isn’t genetics, it is lifestyle. Our bodies evolve and reprogram throughout our life based on our environment and exposures. It isn’t so simple as A = B. I wish it were.

    • Your points are well taken, but that’s why I return to the animal models using genetically identical animals under highly controlled laboratory conditions. The fact that such changes can be observed in only three generations is quite frightening.

  4. What boggles my mind is the tremendous confusion about fats and which ones are good for people. I was noticing at the health food store and some websites that think fat is king and others who think it is totally evil. I hate that. If my great grandparents lived long healthy lives eating traditional ancient diets for their culture why not just stick to ancient foods and even their preparation methods. If Japanese and Chinese people eat soy in tiny amounts (compared to Americans) prepared in a very ancient ways then something they observed about it long ago tells us worlds about that product, they observed it was not favorable. And we have had so many people give animal products a bad rap it has caused much confusion.

    • Dietary habits are usually based on hundreds, if not thousands of years, of observation of what type of agricultural, processing,and cooking technologies are available and how they affect health. That’s why they call them “old wife’s tales”.

      It is only after World War II that people started to abdicate their diet to major food companies. Come to think about it that’s about three generations of humans.

  5. Dr. Sears, there was a study done in the Netherlands a long time ago, in which scientist examined the DNA structure of our soy beans. Their findings were that large amounts of the strands were missing. They recommended eating soy grown in Asia because they have not hybridized the soy. Is this true

    • I am not aware of that study, but we have been practicing genetic engineering with plants over the past 10,000 years. It is called cross-breeding. Now we have the technology to speed that process up at a much faster rate.

  6. Unfortunately, soy and soy products are promoted in the US as healthy foods (as opposed to red meat). Usually, this has to do with saturated fat and hormones in the meat as the evil actors. Most of this back and forth comes from the soy industry and those making money from it. But this is not the subject of the day. The subject is the mother’s food intake (during pregnancy) influencing the diet preferences of the child.

    I believe this is possible, but it is hard to isolate the consequences of what happens in the mother’s womb from what the infant is fed soon after birth. If the baby’s mother is a junk food addict, maybe breast feeding is the culprit, and it has something to do with the early formation of an acquired taste or an early onset craving with a physiological basis.

    Something to think about; mothers usually start their babies on fruit as their introduction to solid food, thus establishing an early preference for sweets (mostly fructose). My daughter’s pediatrician started her on meat and vegetables – she didn’t really know the difference – and to this day, 40 years later, she hardly ever eats sweets. Also, she has never had a problem with weight even though many in her family have.

    So the nature vs. nurture argument rears its ever-present head here, and the problem is most likely a combination of the two. After reading Dr. Sears’ argument however, I think that this “mother’s diet makes kids fat” proposition makes sense.

    • Epigenetic programming not only takes place in the womb but also during early childhood and in the elderly. Our dietary choices for the fetus and the young child (neither of each are very good cooks) will play a significant role in determining their future metabolic programming.

  7. Considering the potential depletion of the mother’s store of DHA and micronutrients by the developing embryo, and then the head trauma of the birth process, what are your recommended nutritional guidelines for prenant and lactating mothers? How much “extra activity” protein and how much omega three fats? If the mother is highly active, such as a Nigerian or migrant farm worker, I could imagine more than 15 blocks of protein a day, maybe a more.

    What are your guidelines, especially after she starts lactating?

    • I usually recommend 2.5 grams per day of omega-3 fatty acids during pregnancy and also during breast-feeding. Breast-feeding requires more energy and therefore calorie requirements will be higher. This helps explain why breast-feeding mothers appear to shed excess body fat at a faster rate than mothers who are not breast feeding. If you have very low levels of body fat, then the extra energy required for breast feeding will have to come from increased calorie intake.

  8. I continually see Dr. Sears blaming obesity on everything except the amount of food people eat.
    I believe the amount of food people eat is the main culprit, hence calories. Notice in Dr. Sears first 3 paragraphs above that he says nothing about the amount of food, just the types of food.
    I said before, in another of Dr. Sears blogs, that you can buy Dr. Sears prepared balanced foods and get fat by eating too much.

    • It remains a balance of satiety and hunger hormones being integrated in the hypothalamus. One of the best ways to disturb that subtle balance is by the over-consumption of calories regardless of how well they are balanced.

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