Astonishingly, a baby with a heavy surrogate mother and a thin biological mom may harbor a greater risk of becoming obese than a baby with a slim surrogate mom and a heavy biological one.
The Role of Epigenetics in the Obesity Epidemic
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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
Identical twins don’t just share DNA; they also shared a uterus. Might that also help account for some of their metabolic similarities? Fetal overnutrition, evidenced by an abnormally large birth weight, seems to be a strong predictor of obesity in childhood and later in life. Could it be you are what your mom ate?
A dramatic illustration from the animal world is the cross breeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but in the pony uterus they come out much smaller (thank heavens for the poor pony). This is presumably the same reason why the mule (donkey dad and mare) is larger than the hinny (stallion and donkey mom). The way you test this in people is to study the size of babies from surrogate mothers after in vitro fertilization.
Who do you think most determines the birth weight of a test-tube baby—the donor mom who provided all the DNA, or the surrogate mom who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby born to an obese surrogate mother with a skinny biological mom may harbor a greater risk of becoming obese than a baby from a big biological mom born to a slim surrogate. The researchers conclude “the environment provided by the human mother is more important than her genetic contribution to birth weight.”
The most compelling data comes from comparing obesity rates in siblings born to the exact same mother before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity (affecting 35 percent of those born before the weight loss compared to 11 percent born after). The researchers conclude “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.”
But wait. Mom had the same DNA before and after surgery. She passed the same genes down. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted that the greatest error he committed “has been not allowing sufficient weight to the direct action of the environment, like food…independently of natural selection.” We finally figured out the mechanism by which this can happen: epigenetics.
Epigenetics (literally meaning “above genetics”) layers an extra level of information on top of the DNA sequence that can be both affected by our surrounds and potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb depending on the weight of the mother, or even your grandmother. Since all the eggs in your infant daughters’ ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity.
Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to exclusive breastfeeding, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula. The breastfeeding data is controversial though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that doesn’t fit some goal for the greater good (in this case, preferably publishing breastfeeding studies showing more positive results)––but of course that’s coming from someone who works for an infant formula company. Breast is best regardless; its role in the childhood obesity epidemic just remains arguably uncertain.
Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition.
Please consider volunteering to help out on the site.
- Campbell MK. Biological, environmental, and social influences on childhood obesity. Pediatr Res. 2016;79(1-2):205-11.
- Walton A, Hammond J. The maternal effects on growth and conformation in shire horse-shetland pony crosses. Proc R Soc B. 1938;125(840):311-35.
- Brooks AA, Johnson MR, Steer PJ, Pawson ME, Abdalla HI. Birth weight: nature or nurture?. Early Hum Dev. 1995;42(1):29-35.
- Waterland RA. Epigenetic mechanisms affecting regulation of energy balance: many questions, few answers. Annu Rev Nutr. 2014;34:337-55.
- Smith J, Cianflone K, Biron S, et al. Effects of maternal surgical weight loss in mothers on intergenerational transmission of obesity. J Clin Endocrinol Metab. 2009;94(11):4275-83.
- Wang Z, Wang Q, Liu Y. You are what your parents ate: a Darwinian perspective on the inheritance of food effects. Trends Food Sci Technol. 2016;54:204-7.
- Mcallister EJ, Dhurandhar NV, Keith SW, et al. Ten putative contributors to the obesity epidemic. Crit Rev Food Sci Nutr. 2009;49(10):868-913.
- Finch CE, Loehlin JC. Environmental influences that may precede fertilization: a first examination of the prezygotic hypothesis from maternal age influences on twins. Behav Genet. 1998;28(2):101-6.
- Keith SW, Redden DT, Katzmarzyk PT, et al. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes (Lond). 2006;30(11):1585-94.
- Luque V, Closa-monasterolo R, Escribano J, Ferré N. Early Programming by Protein Intake: The Effect of Protein on Adiposity Development and the Growth and Functionality of Vital Organs. Nutr Metab Insights. 2015;8(Suppl 1):49-56.
- Cope MB, Allison DB. White hat bias: examples of its presence in obesity research and a call for renewed commitment to faithfulness in research reporting. Int J Obes (Lond). 2010;34(1):84-8.
- Horta BL, Bahl R, Martinés JC, Victora CG. Evidence on the long-term effects of breastfeeding: systematic reviews and meta-analysis. World Health Organization. 2007.
- Katzmarzyk PT, Barlow S, Bouchard C, et al. An evolving scientific basis for the prevention and treatment of pediatric obesity. Int J Obes (Lond). 2014;38(7):887-905.
Video production by Glass Entertainment
Motion graphics by Avocado Video
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
Identical twins don’t just share DNA; they also shared a uterus. Might that also help account for some of their metabolic similarities? Fetal overnutrition, evidenced by an abnormally large birth weight, seems to be a strong predictor of obesity in childhood and later in life. Could it be you are what your mom ate?
A dramatic illustration from the animal world is the cross breeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but in the pony uterus they come out much smaller (thank heavens for the poor pony). This is presumably the same reason why the mule (donkey dad and mare) is larger than the hinny (stallion and donkey mom). The way you test this in people is to study the size of babies from surrogate mothers after in vitro fertilization.
Who do you think most determines the birth weight of a test-tube baby—the donor mom who provided all the DNA, or the surrogate mom who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby born to an obese surrogate mother with a skinny biological mom may harbor a greater risk of becoming obese than a baby from a big biological mom born to a slim surrogate. The researchers conclude “the environment provided by the human mother is more important than her genetic contribution to birth weight.”
The most compelling data comes from comparing obesity rates in siblings born to the exact same mother before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity (affecting 35 percent of those born before the weight loss compared to 11 percent born after). The researchers conclude “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.”
But wait. Mom had the same DNA before and after surgery. She passed the same genes down. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted that the greatest error he committed “has been not allowing sufficient weight to the direct action of the environment, like food…independently of natural selection.” We finally figured out the mechanism by which this can happen: epigenetics.
Epigenetics (literally meaning “above genetics”) layers an extra level of information on top of the DNA sequence that can be both affected by our surrounds and potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb depending on the weight of the mother, or even your grandmother. Since all the eggs in your infant daughters’ ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity.
Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to exclusive breastfeeding, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula. The breastfeeding data is controversial though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that doesn’t fit some goal for the greater good (in this case, preferably publishing breastfeeding studies showing more positive results)––but of course that’s coming from someone who works for an infant formula company. Breast is best regardless; its role in the childhood obesity epidemic just remains arguably uncertain.
Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition.
Please consider volunteering to help out on the site.
- Campbell MK. Biological, environmental, and social influences on childhood obesity. Pediatr Res. 2016;79(1-2):205-11.
- Walton A, Hammond J. The maternal effects on growth and conformation in shire horse-shetland pony crosses. Proc R Soc B. 1938;125(840):311-35.
- Brooks AA, Johnson MR, Steer PJ, Pawson ME, Abdalla HI. Birth weight: nature or nurture?. Early Hum Dev. 1995;42(1):29-35.
- Waterland RA. Epigenetic mechanisms affecting regulation of energy balance: many questions, few answers. Annu Rev Nutr. 2014;34:337-55.
- Smith J, Cianflone K, Biron S, et al. Effects of maternal surgical weight loss in mothers on intergenerational transmission of obesity. J Clin Endocrinol Metab. 2009;94(11):4275-83.
- Wang Z, Wang Q, Liu Y. You are what your parents ate: a Darwinian perspective on the inheritance of food effects. Trends Food Sci Technol. 2016;54:204-7.
- Mcallister EJ, Dhurandhar NV, Keith SW, et al. Ten putative contributors to the obesity epidemic. Crit Rev Food Sci Nutr. 2009;49(10):868-913.
- Finch CE, Loehlin JC. Environmental influences that may precede fertilization: a first examination of the prezygotic hypothesis from maternal age influences on twins. Behav Genet. 1998;28(2):101-6.
- Keith SW, Redden DT, Katzmarzyk PT, et al. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes (Lond). 2006;30(11):1585-94.
- Luque V, Closa-monasterolo R, Escribano J, Ferré N. Early Programming by Protein Intake: The Effect of Protein on Adiposity Development and the Growth and Functionality of Vital Organs. Nutr Metab Insights. 2015;8(Suppl 1):49-56.
- Cope MB, Allison DB. White hat bias: examples of its presence in obesity research and a call for renewed commitment to faithfulness in research reporting. Int J Obes (Lond). 2010;34(1):84-8.
- Horta BL, Bahl R, Martinés JC, Victora CG. Evidence on the long-term effects of breastfeeding: systematic reviews and meta-analysis. World Health Organization. 2007.
- Katzmarzyk PT, Barlow S, Bouchard C, et al. An evolving scientific basis for the prevention and treatment of pediatric obesity. Int J Obes (Lond). 2014;38(7):887-905.
Video production by Glass Entertainment
Motion graphics by Avocado Video
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Title
The Role of Epigenetics in the Obesity Epidemic
LicenseCreative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Content URLDoctor's Note
A few weeks ago, I had a video about The Best Diet for Weight Loss & Disease Prevention. But what triggered the whole obesity epidemic? It’s a multitude of factors, and I covered many of them in my 11-video series on the epidemic:
- The Role of Diet vs. Exercise in the Obesity Epidemic
- The Role of Genes in the Obesity Epidemic
- The Thrifty Gene Theory: Survival of the Fattest
- Cut the Calorie-Rich-And-Processed Foods
- The Role of Processed Foods in the Obesity Epidemic
- The Role of Taxpayer Subsidies in the Obesity Epidemic
- The Role of Marketing in the Obesity Epidemic
- The Role of Food Advertisements in the Obesity Epidemic
- The Role of Personal Responsibility in the Obesity Epidemic
- The Role of Corporate Influence in the Obesity Epidemic
- The Role of the Toxic Food Environment in the Obesity Epidemic
There are other ways by which we are what our moms ate:
- Heart Disease May Start in the Womb
- Maternal Diet May Affect Stress Responses in Children
- The Effect of Animal Protein on Stress Hormones, Testosterone, and Pregnancy
If you haven’t yet, you can subscribe to my videos for free by clicking here. Read our important information about translations here.
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