Are you what your ancestors ate? The idea that the eating habits of our parents and even grandparents could determine our diet, food choices, body metabolism and a variety of other important characteristics is not new. Scholars have been kicking the idea around for centuries. The idea has gotten new life in the last twenty years.

Is it really true that our parents transmit their eating habits to us and their experiences with food are sent along through our genes? The notion has been aptly summarized in this question. Are you what your grandmother ate? Did grandma set us up to get fat around the middle because she ate too much pasta during her pregnancies? Here, we’ll look at the evidence that supports the idea that we are what our ancestors ate.

Nature Versus Nurture

If you took an introductory psychology class, you’ll remember the nature versus nurture debate. Sir Francis Galton, who favored nature over nurture, is credited with the phrase, but genetic transmission wasn’t understood in 1869. Now, we would relabel the dichotomy as genes versus experience.

Picture of Sir Francis Galton who crystalized the discussion of nature versus nurture.

Sir Francis Galton wrote Hereditary Genius in 1869 and English Men: Their Nature and Nurture in 1874

Picture from the Library of Congress

Which Is More Important, Nature or Nurture?

A well known twentieth century psychologist, Donald Hebb, said this question was like asking which feature of a rectangle—length or width was the more important. Nature and nurture interact and both are important in determining our body size, metabolism, and diet.

I Don’t Like the Idea that I Am What My Ancestors Ate

The idea that my mother’s fondness for chocolate and every other sweet thing under the sun might have been passed down to me was unsettling because I thought my genes were not affected by my mother’s food choices and her life experiences. I didn’t not want to believe that I was gaining weight because of what my grandmothers ate, and I chose to believe that chromosomes from my mom and dad got together, and I as the result of that pairing have a unique and individual genetic make up. Boy was I wrong!

Intergenerational Transfer of Nutritional Status

Studies which examined the health of people who were exposed to famine during World War II provided the first clues suggesting an answer to the question of whether we are what are ancestors ate. Populations which were exposed to malnutrition during gestation passed the negative effects on to the following generations, and this was true although the following generations were never malnourished.

How was it possible for a malnourished grandmother to change the course of the lives of future generations? We are coming to believe that undernutrition during a famine can reprogram genes, that the changes are durable, and they can be passed to the next generation. The process by which adverse experiences of the mother changes the genetic message sent to her young is called fetal reprogramming.

Fetal reprogramming is the process by which the same genotype can give rise to several phenotypes depending upon the environment.

Veenendaal et al. 2013
Generational Transmission

There are two basic types of generational transfer of reprogrammed information about diet– intergenerational and transgenerational.

  • Intergenerational transmission is transfer of acquired genetic information from F0/P1 to F1 (mother to child)
  • Transgenerational transmission is transfer of acquired genetic information from F0/P1 to F1 to F2 to F3 (mother to granddaughter, to great granddaughter).

The generations are labeled in the figure below.

Pictures of three generations of women showing how generations are labeled in epidemiological research.
How to Prove Transgenerational Transmission

To prove that the nutritional experiences of a parent are reprogramming the metabolism of a fetus in the womb, a researcher must show three things:

  • The exposure event which changes the genetic structure of the F1 is controlled and defined.
  • The experience of an ancestor is still present in the F3 generation.
  • Confounding factors in the offspring’s experience such as socioeconomic status or family food preferences are controlled.
David Barker
Photo of David Barker, an epidemiologist and scientist who is credited with the field Developmental Origins of Health and Disease

Credited with the field of Developmental Origins of Health and Disease

David Barker

Barker and colleagues studied famine events in Europe (Hales & Barker, 2001; Kaati et al., 2007; Roseboom et al, 2000). They observed that babies born during the famine were smaller at birth and throughout their lives. Those people exposed to famine during their fetal life were more likely to have high blood pressure, obesity, and heart disease as older adults. To explain these data, Barker advanced the Intergenerational Influences Hypothesis, but this hypothesis was then renamed the Developmental Origins of Health and Disease.

Low birth weight inevitably leads to a number of adult medical conditions including metabolic syndrome, cardiovascular disease, and other health-related phenotypes, which are all programmed prenatally and modified by a limited nutrient supply during the early stages of development.

Developmental Origins of Health and Disease Defined
A general introduction to Developmental Origins of Health and Disease
Famine Events

There are a number of well-studied famine events. We look at a few of these to see if malnourishment associated with famines reprogram the genetic makeup of a fetus.


Severe food shortages were common during and after World War I and during World War II. Look at a Hunger Map produced in 1918 by America Food Pledge.

Hunger Map of Europe in 1918 when starvation was rampant in Europe due to the war.

Famine and Food Shortage Map in 1918.

The people of the United States were asked to have meatless, wheatless, and porkless days so that food could be sent to the war torn countries of Europe.

Magazine ad around the time of WWI encouraging Americans to eat less and send food to Europe where starvation was rampant.

Wasting Food is the “greatest crime in Christendom.”

The Netherlands

The most influential research comes from the epidemiological studies of the survivors of the Dutch Hunger War. This famine event was circumscribed, affected the entire Dutch population, and has been carefully studied into the F3 generation (or for more than 50 years). The famine lasted approximately one year (1944-1945) when the Nazis, frustrated by Dutch resistance, cut off most food supplies to the country.

To read more about the Dutch Hunger War, follow the link.

Sweden, the Overkalix Studies
Picture of northern lights in Sweden when famine was common and good genetic histories were available.

Overkalix, a remote collection of tiny villages, in northern Sweden. Image from Sled Dog Tours.

Winters in Overkalix are six months long, and residents of the area had led a precarious existence for generations. During the winter months, residents and their livestock depended upon rye and barley harvests. A failed harvest meant a hard famine would follow.

Periods of relative famine have been documented in the area since the 1800’s. Residents of Overkalix meticulously recorded births, deaths, and family lineages in the area as well as details of every harvest. Researchers were able to reconstruct the nutrition available to generations of families in the area (Bygren et al. 2001; Bygren et al., 2014). Their first sample was 94 people born during a famine year of 1905.

I’m Not the Only One!
Picture of L. O. Bygren, his son, and his grandson. Three generatiobs. Bygren pioneered epigenetic studies in Sweden which showed intergenerational transfer of nutritional stressors.

Dr. Bygren struggled for years to get his research on transgenerational transmission published.

L. O. Bygren, his son, and his grandson

Scientists strongly disputed Bygren’s results. It just couldn’t be possible that what a grandmother or grandfather ate or whether or not they smoked in 1905 changed the life expectancy and the illness risks of their children and grandchildren. To read more about Bygren’s 10-year struggle to get the Overkalix data published, go to this blog.

The Great Chinese Famine

The Great Chinese Famine happened between 1959 and 1961. The exact number of deaths is unknown, but estimates suggest there were 30 million premature deaths. Millions more survived the famine after experiencing severe malnutrition (Wang et al., 2018). The major causes of the famine were the policies of the Great Leap Forward and several natural disasters (droughts and floods).

In the second half of 1959, I took a long distance bus from Xinyang to Luoshan and Sushi. Out of the window, I saw one corpse after another in the ditches. On the bus, no one dared mention the dead. In one county, Guangshan, one third of the people had died. … I had seen people who had told the truth being destroyed. Did I dare write it?

Lu Baoguo, Xinhua reporter.
Hungry Ghosts: Mao’s Secret Famine
Hungry Ghosts: Mao's Secret Famine. Shows cover of book by Jasper Becker published in 1992 describing the famine which killed millions and which was engineered by Mao and helped by ,nature.

Jasper Becker, Bureau Chief for the South China Morning Post, published this book on the Great Chinese Famine of 1959-1961.

Major Health Problems Caused by Undernutrition

Early epidemiological studies of those affected by the famine in the Netherlands looked at birth factors such as weight, height, and general health. As years passed, researchers focused their attention on metabolic and cardiovascular diseases. Still later, researchers looked at other health problems including brain and emotional development.

Malnutrition during fetal life has a profound effects on the following health issues in later adult life:

  • More likely to have diabetes and metabolic syndrome.
  • More likely to be overweight or obese.
  • More likely to have cardiovascular problems including hypertension.
  • More likely to have kidney problems.
  • Increased incidence of breast cancer.
  • More likely to have learning disabilities.
  • More likely to have mental health issues such as anxiety or schizophrenia later in life (Edwards, 2018).
Fetal Reprogramming of Obesity, Diabetes, and Metabolic Syndrome

Wow! That’s quite a list of negative outcomes of fetal malnutrition. Too much to tackle in a post. Let’s peel off a chunk and look at the earliest epidemiological research findings on obesity, diabetes, and the metabolic syndrome.

First, we need to nail down some terms.

Obesity + insulin resistance = metabolic syndrome

Bays & Scinta, 2015

You probably thought like I once did that you know what obesity is. It’s fat people, right. Well, you’re sort of right but let’s look at the medical definition of obesity. Read the definition of obesity carefully. It’s packed with information (Bays & Scinta, 2015).

Obesity is

  • Chronic, relapsing, multi-factorial, neurobehavioral disease.
  • The increased body fat promotes adipose tissue dysfunction.
  • The increased body fat causes abnormal fat mass physical forces (e.g., secondary damage to joints).
  • The increased body fat causes metabolic, biochemical, and immunological health consequences.
  • The cause of the disease of obesity is complex and involves the integration of extragenetic, genetic, and epigenetic pathologies.
Insulin Resistance

The term insulin resistance is tossed about like we really understand what it is. No matter how often the concept was explained to me, I couldn’t make sense of it. I found a definition on that finally cleared my brain haze. I hope this metaphor will stick in my brain and maybe in yours.

Insulin resistance is loss of ability of cells to respond to the action of insulin. Insulin is trying to transport glucose from the bloodstream into muscles and other tissues. It is as if insulin is “knocking” on the door of muscle. In the normal metabolism, the muscle hears a knock, opens up, and lets glucose in. But with insulin resistance, the muscle cannot hear the knocking of the insulin (the muscle is “resistant”). Like the Little Richard song, “I hear you knockin’ but you can’t come in.”

The pancreas reacts to the glucose piling up outside the cells by making more insulin. Due to the higher levels of insulin in the blood, the insulin knocks louder. When the pancreas can no longer keep up with the insulin arms race, blood glucose levels in the blood rise to abnormal levels even in the fasting state.
I hear you Knockin’
Little Richard performing at a charity event.
Metabolic Syndrome

Metabolic Syndrome has at least three of the five typical phenotypes as follows: 1) elevated abdominal obesity, 2) elevated fasting glucose, 3) elevated blood pressure, 4) elevated fasting triglycerides, and 5) reduced high-density lipoprotein cholesterol.

Fetal Undernutrition and Obesity

The 50 year follow-up of the grandchildren of the survivors of the Dutch famine revealed that the higher rates of obesity seen in the offspring were also present in the grandchildren (Carey, 2012). Undernutrition in the womb of ancestors had altered the courses of the of generations.

A study of survivors of Swedish famine showed similar increases in obesity. Kaati et al. (2007) examined 15,000 Swedish men and women born between 1915 and 1929 . The grandchildren of people born during the famine were more likely to have diabetes and a shorter life span. Both types he result of the grandmothers’ exposure to undernutrition even though the grandchildren had never experienced undernutrition.

Undernutrition and Metabolic Syndrome

Ning and colleagues (2019) did a meta-analysis of studies which looked at the relationship between famine exposure in the Great China Famine in early life and adulthood Metabolic Syndrome. Famine exposure during fetal life caused a moderate increase in risk of metabolic syndrome in adult years.

Undernutrition and Diabetes

Wang and colleagues (2018) examined the diabetes risk of more than 4,000 adults who had been exposed to the famine event in China during fetal development. The diabetes risk of people who had been exposed to famine during early life was increased by 37%.

These associations support that fetal-stage exposed famine has an adverse influence on the burden of diabetes in adulthood.

Wang et al., 2018
Bah Humbug!

You might be muttering to yourself about now. The epidemiologic studies don’t prove that the experiences in the womb are transmitted to later generations via inheritance. Maybe what’s really happening is a shared environmental characteristic such as socioeconomic status which affects what parents of several generations fed their children after they’re born.

Animal research to the rescue. Animal research provides the strongest evidence that transgenerational transfer of nutritional adversity in the womb exists. Transmission of nutritional information acquired during early development can be transmitted across as many as 20 generations (Galler, 2014).

Animal Research, Unpacking
Metabolic Syndrome and Diabetes

Animal research has shown the following:

  • Glucose metabolism and the endocrine functions of the pancreas are altered when rat pups are malnourished in the womb (Reusens and Pinhiero, 2006.
  • Prenatal malnutrition was linked to diabetes in the adult offspring (F1) and the next generation (F2) (Aets and Van Assche, 2006; Galler, 2014).
  • Insulin resistance is affected by prenatal malnutrition (Thamotheron et al., 2007)

Thus pre-and post natal malnutrition in the rat have been implicated in an increased risk of transgenerational diabetes (Galler, 2014).

Transgenerational Obesity

In agreement with human studies, the offspring of malnourished mice, rats, sheep, and non-human primates are more likely to become obese (Galler, 2014; Zhu et al., 2019). Look at the picture of the mice below.

Two mice with identical diets but one had adequate nutrition during fetal development and the other did not. Undernutrition in the womb produces obesity and metabolic problems which last for generations.

Mice of same the age. Fat mouse had deficient diet in the womb. Normal weight mouse had adequate nutrition.

What’s Going On?

How does maternal diet during early development change our lives and those of the generations which follow us? I thought our genetic code was set, a kind of biological Rosetta Stone. Most scientists agree, so far, that our genetic code is not altered by adverse events during fetal development.

However, it is apparent that something is happening to the way our genetic code is expressed. That something else is an epigenetic process in which genes are turned off or on and proteins are expressed depending upon conditions in the womb (Jing et al., 2020).

Epigenetics Defined

Epigenetics literally means “above” or “on top of” genetics. The term refers to external modifications of DNA that turn genes “on” or “off”. These modifications do not change the DNA sequence, but they affect how cells “read” genes.
Are You What Your Ancestors Ate?

We are what our ancestors ate in more ways than we ever thought possible. We are also what our ancestors experienced in more ways than we ever thought possible. These adverse conditions ranging from environmental toxins such as drugs, chemicals and poorly controlled diabetes to emotional distress can change the way in which our genetic information is translated.

A Plea to Expectant Parents

You are not eating for two, but you are eating for future generations.

Although there is much to learn, please take your diet seriously both before and after pregnancy. Also remember that both parents are pregnant and that the eating habits of the father can alter the future health of generations to come. We’ll get to that in another post.

Review of the Fetal Programming of Obesity

Watch this video to review many of the concepts in this post as well as a few others.

Stay Tuned to This Channel

We have many unanswered questions which we will tackle in future posts:

  • What roles do fathers play in the transfer of epigenetic changes across generations?
  • What does overnutrition in the womb do to the fetus and future generations?
  • Why do people who are exposed to adverse conditions in the womb get fat?
  • How do anthropologists look at obesity?
  • How does fetal adversity affect functions beyond the metabolism? Specifically, we want to look at the brain, the immune system, and the cardiovascular system.
  • How do adverse conditions in the womb cause lasting changes in the offspring?
  • Can anything be done to undo the epigenetic programing which makes us fat?

Our Book on Carbohydrate Addiction

Check out our book on Carbohydrate Addiction, Confessions of a Carbohydrate Addict. Coping with carbohydrate addiction led us to the huge literature on the origins of obesity. To learn more follow the link.


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Bays, H., & Scinta, W. (2015). Adiposopathy and epigenetics: an introduction to obesity as a transgenerational disease. Current Medical Research and Opinion, 31(11), 2059-2069. doi:10.1185/03007995.2015.1087983

Bresler, D. E., Ellison, G., & Zamenhof, S. (1975). Learning deficits in rats with malnourished grandmothers. Dev Psychobiol, 8(4), 315-323. doi:10.1002/dev.420080405

Bygren, L. O., Kaati, G., & Edvinsson, S. (2001). Longevity determined by paternal ancestors’ nutrition during their slow growth period. Acta Biotheor, 49(1), 53-59. doi:10.1023/a:1010241825519

Bygren, L. O., Tinghog, P., Carstensen, J., Edvinsson, S., Kaati, G., Pembrey, M. E., & Sjostrom, M. (2014). Change in paternal grandmothers’ early food supply influenced cardiovascular mortality of the female grandchildren. BMC Genet, 15, 12. doi:10.1186/1471-2156-15-12

Galler, J., Rabinowitz, Danielle Galler. (2014). The intergenerational effects of early adversity. Progress in molecular biology and translational science, 128, 177-198. doi:10.1016/B978-0-12-800977-2.00007-3

Hales, C. N., & Barker, D. J. (2001). The thrifty phenotype hypothesis. Br Med Bull, 60, 5-20. doi:10.1093/bmb/60.1.5

Hanafi, M. Y., Saleh, M. M., Saad, M. I., Abdelkhalek, T. M., & Kamel, M. A. (2016). Transgenerational effects of obesity and malnourishment on diabetes risk in F2 generation. Mol Cell Biochem, 412(1-2), 269-280. doi:10.1007/s11010-015-2633-6

Jing, J., Wang, Y., Quan, Y., Wang, Z., Liu, Y., & Ding, Z. (2020). Maternal obesity alters C19MC microRNAs expression profile in fetal umbilical cord blood. Nutrition & Metabolism, 17, 52-52. doi:10.1186/s12986-020-00475-7

Kaati, G., Bygren, L. O., Pembrey, M., & Sjostrom, M. (2007). Transgenerational response to nutrition, early life circumstances and longevity. Eur J Hum Genet, 15(7), 784-790. doi:10.1038/sj.ejhg.5201832

King, V., Dakin, R. S., Liu, L., Hadoke, P. W. F., Walker, B. R., Seckl, J. R., . . . Drake, A. J. (2013). Maternal Obesity Has Little Effect on the Immediate Offspring but Impacts on the Next Generation. Endocrinology, 154(7), 2514-2524. doi:10.1210/en.2013-1013

Ning, F., Ren, J., Song, X., Zhang, D., Liu, L., Zhang, L., . . . Diabetes Prevention Program, O. (2019). Famine Exposure in Early Life and Risk of Metabolic Syndrome in Adulthood: Comparisons of Different Metabolic Syndrome Definitions. J Diabetes Res, 2019, 7954856. doi:10.1155/2019/7954856

Pinheiro, A. R., Salvucci, I. D., Aguila, M. B., & Mandarim-de-Lacerda, C. A. (2008). Protein restriction during gestation and/or lactation causes adverse transgenerational effects on biometry and glucose metabolism in F1 and F2 progenies of rats. Clin Sci (Lond), 114(5), 381-392. doi:10.1042/cs20070302

Reusens, B., Remacle, C. (2006). Programming of the endocrine pancreas by the early nutritional environment. The International Journal of Biochemistry and Cell Biology, 38(5-6), 913-922.

Roseboom, T. J., van der Meulen, J. H. P., Osmond, C., Barker, D. J. P., Ravelli, A. J. C., Schroeder-Tanka, van Montfrans, G. A., Michels, R. P. J., Bicker, O. P. (2000). Coronary heart disease after prenatal exposure to the Dutch famine, 1944-45. Heart, 84, 595-598.

Shasa, D. R., Odhiambo, J. F., Long, N. M., Tuersunjiang, N., Nathanielsz, P. W., & Ford, S. P. (2015). Multigenerational impact of maternal overnutrition/obesity in the sheep on the neonatal leptin surge in granddaughters. Int J Obes (Lond), 39(4), 695-701. doi:10.1038/ijo.2014.190

Thamotharan, M., Garg, M., Oak, S., Rogers, L. M., Pan, G., Sangiorgi, F., . . . Devaskar, S. U. (2007). Transgenerational inheritance of the insulin-resistant phenotype in embryo-transferred intrauterine growth-restricted adult female rat offspring. Am J Physiol Endocrinol Metab, 292(5), E1270-1279. doi:10.1152/ajpendo.00462.2006

Wang, Z., Zou, Z., Yang, Z., Dong, Y., Song, J., Dong, B., . . . Arnold, L. (2018). The association between fetal-stage exposure to the China famine and risk of diabetes mellitus in adulthood: results from the China health and retirement longitudinal study. BMC Public Health, 18(1), 1205. doi:10.1186/s12889-018-6134-x

Zhu, Z., Cao, F., & Li, X. (2019). Epigenetic Programming and Fetal Metabolic Programming. Front Endocrinol (Lausanne), 10, 764. doi:10.3389/fendo.2019.00764

Linda J. Gummow

Linda J. Gummow

L. J. Gummow, Ph.D. and Robert E. Conger, Ph.D. are Clinical Psychologists. L. J. lost 25% of her body weight by following by reducing carbohydrates. In the process, she learned that much of what we're taught about weight loss is wrong. She and her co-author researched weight loss diets and the results show that sugar consumption is our public health enemy number one. R. E.

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