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).
- 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)
- 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)
- 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)
- 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)
- Chalon S. “Omega-3 fatty acids and monoamine neurotransmission.” Prostaglandins Leukot Essent Fatty Acids 75: 259-269 (2006)
- 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)
- 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)
- 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.